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The binding of this variant HRG to plasminogen was normal. Paper-7820690.
Type 3 cystatins; fetuins, kininogen and histidine-rich glycoprotein. Paper-13656386.
CD36- TSP- HRGP interactions in the regulation of angiogenesis. Paper-13446260.
Soluble HPRG did not significantly influence plasminogen activation. Paper-946808.
Complex formation of platelet thrombospondin with histidine-rich glycoprotein. Paper-4759299.
Fluctuations of HRG caused only minor changes in free plasminogen concentrations. Paper-4598471.
In addition, HRG was able to displace biologically active bFGF from the ECM. Paper-139834.
HRG in plasma behaved as a uniform fraction with respect to plasminogen binding. Paper-6131183.
Importantly, plasminogen interacted specifically with GAG- bound HPRG. Paper-1360803.
Plasma histidine-rich glycoprotein and plasminogen in patients with liver disease. Paper-4933441.
HRG had inhibitory effects on DS as well, as was observed from assaying HC II activity. Paper-4989012.
Both clusterin and HRG are regulators of the membrane attack complex (C5b-C9) of complement. Paper-473049.
We found that binding of HRGP to TSP-1 was similarly mediated by TSP type I repeats. Paper-8689729.
Histidine-rich glycoprotein and plasminogen plasma levels in term and preterm newborns. Paper-6686994.
Modulation of heparin cofactor II activity by histidine-rich glycoprotein and platelet factor 4. Paper-4988137.
Their results show that HRG, like PF 4, has an affinity, not only for heparin, but also for DS. Paper-7331981.
In contrast, HPRG abrogates the stimulatory effects of fibrinogen on Plg activation in solution. Paper-10911023.
Histidine-rich glycoprotein inhibits the antiangiogenic effect of thrombospondin-1. Paper-8689729.
Effects of histidine-proline-rich glycoprotein on plasminogen activation in solution and on surfaces. Paper-10911023.
The heparin-neutralizing ability of HRG in the thrombin inhibition by PCI was not affected by Ca2+. Paper-7523895.
HRG specifically interacted with mitochondrial ATP synthase with a dissociation constant of 66 nM. Paper-13734756.
The newborns had significantly lower plasminogen and HRG levels when compared with those of the adults. Paper-6686994.
No species differences were found, as either rabbit or human HPRG bound readily to rabbit or human PLG. Paper-172840.
The effect of HRG caused the level of free plasminogen to be only 50-60% of the level of total plasminogen. Paper-4598471.
ERK activation remained elevated for 2 h following high doses of HRG which induce differentiation. Paper-1577501.
Furthermore, truncated HRGP, devoid of the heparin-binding and histidine-rich domain, was not antibacterial. Paper-12428358.
The data indicate a close link among HRG-beta stimulation, HER signaling, and AP-1 activation. Paper-13051552.
The unique features present in the cloned cDNA indicate that p43 is a novel member of the HRGP family of proteins. Paper-1959727.
High affinity interaction between histidine-rich glycoprotein and the cell surface type ATP synthase on T-cells. Paper-13734756.
Etiolated seedlings subjected to a pulse of red light accumulated PvPRP1, GRP, and HRGP mRNAs in the hypocotyls. Paper-11716321.
Identification of histidine-rich glycoprotein, a potential autoantigen, in human and rat brain preparations. Paper-13422005.
Association of purified skeletal-muscle AMP deaminase with a histidine-proline-rich-glycoprotein-like molecule. Paper-1171373.
We have recently reported the association of an HPRG-like protein with rabbit skeletal muscle AMP deaminase ( AMPD). Paper-1718190.
In severe (Child C) cirrhosis, HRG level, total plasminogen level, and free plasminogen level were all decreased. Paper-6307177.
HPRG also augments the increase in Plg activation caused by fibrinogen fragments either in solution or on GAG surfaces. Paper-10911023.
However, free plasminogen not bound to histidine-rich glycoprotein was not significantly different between these two groups. Paper-5903091.
These mRNA changes include differential regulation of transcripts derived from the GRP and HRGP multigene families. Paper-11716321.
The formation of the thrombospondin- histidine-rich glycoprotein complex was specific, concentration dependent, and saturable. Paper-4759299.
In HRG-alpha the N-terminal residues 2-6 form a well-defined beta strand rather than being disordered as found for hEGF. Paper-555501.
Three members of the human cystatin gene superfamily, AHSG, HRG, and KNG, map within one megabase of genomic DNA at 3q27. Paper-220647.
Levels of thrombospondin-4 (900%; p < 0.001) and alpha2-macroglobulin (300%, p < 0.05) mRNA increased substantially in the HRG. Paper-11443917.
This was associated with significant increases in plasma plasminogen and a concomitant reduction in histidine-rich glycoprotein. Paper-4618902.
Other newly discovered modulators of the fibrinolytic system include histidine-rich glycoprotein, tetranectin and thrombospondin. Paper-5398889.
The biological activity of partially purified rat NDF/ HRG was examined and found to be the same as that of the pure growth factor. Paper-514890.
In fact, HRG is 10 times less effective than PF 4 in neutralizing the 50% antithrombin activity of HC II in the presence of DS. Paper-7331981.
In contrast, a transient 5 min peak of ERK activation in response to doses of HRG which induce proliferation was observed. Paper-1577501.
We conclude that histidine-rich glycoprotein and platelet factor 4 can regulate the antithrombin activity of heparin cofactor II. Paper-4988137.
No correlation between HRGP level and t-PA- mediated plasminogen activation was observed.(ABSTRACT TRUNCATED AT 250 WORDS) Paper-7862153.
The interactions between the streptococcal protein and the plasma proteins were further characterized using purified clusterin and HRG. Paper-473049.
This investigation will be continued to clarify the role of HRG, HC II, AT III, and heparin in the prevention of thrombi formation. Paper-4989012.
Acceleration of plasminogen activation by tissue plasminogen activator on surface- bound histidine-proline-rich glycoprotein. Paper-946808.
Familial association of high levels of histidine-rich glycoprotein and plasminogen activator inhibitor-1 with venous thromboembolism. Paper-7862153.
The ternary complex model implies that, HRG being responsible for efficient G protein activation, it should be as stable as possible. Paper-10490383.
Histidine-proline-rich glycoprotein ( HPRG), also known as histidine-rich glycoprotein, is a major plasminogen-binding protein. Paper-946808.
Platelet factor 4 abolishes the activation of heparin cofactor II by dermatan sulfate, but plasma histidine-rich glycoprotein does not. Paper-11924208.
Heparin cofactor II, histidine-rich glycoprotein, alpha 2-macroglobulin, pre-kallikrein and factor XII had no discriminative power. Paper-6740051.
Although fibrinogen, plasminogen, and alpha 2-antiplasmin were present in culture supernatants, histidine-rich glycoprotein was not detected. Paper-4271120.
Familial elevation of plasma histidine-rich glycoprotein. A case associated with recurrent venous thrombosis and high PAI-1 levels. Paper-7495610.
HRGP mRNAs are abundant in outer and inner phloem regions, while GRP mRNAs are present mostly in primary xylem and in the cambium region. Paper-89993.
Histidine-rich glycoprotein binds to DNA and Fc gamma RI and potentiates the ingestion of apoptotic cells by macrophages. Paper-9579646.
Interaction of histidine-proline-rich glycoprotein with plasminogen: effect of ligands, pH, ionic strength, and chemical modification. Paper-172840.
In contrast to HRG, there was no significant difference in the heparin-neutralizing ability of PF4 in the presence or absence of 1 mM Ca2+. Paper-7523895.
The His6 epitopes did not affect the native infectivity of Ad5 vectors. Paper-11232471.
In this work we characterized extensively the circumstances under which HPRG accelerates plasminogen activation and the specificity of this effect. Paper-946808.
The immobilized N- and C-terminal domains, but not the histidine-proline-rich domain of HPRG, also bound plasminogen and stimulated its activation. Paper-946808.
At saturation the relative molar stoichiometry of Plg:TPA was 3:1 within the TSP-containing complexes and 1:1 within HRGP-containing complexes. Paper-5126593.
Of the ligands of HPRG tested, mesoheme (20 microM) but not heparin (M(r) 10,000, 10 microM) inhibits the formation of the HPRG- PLG complex. Paper-172840.
The hormone group showed an increase in plasminogen level to about 150% of normal, while the concentration of HRG was decreased to about 75% of normal. Paper-4117132.
In fetuses, euglobulin clot lysis time (ECLT) was significantly shortened, plasminogen level was low and histidine-rich glycoprotein undetectable. Paper-7103045.
Modified crossed immunoelectrophoresis to study with whole plasma the reversible complex formation of histidine-rich glycoprotein with plasminogen. Paper-6131183.
Decreased levels of histidine-rich glycoprotein ( HRG) and increased levels of free plasminogen in women on oral contraceptives low in estrogen. Paper-4117132.
The authors studied the interaction of DS and low molecular weight DS, in a purified system with HRG, platelet factor 4 ( PF 4), and with HC II. Paper-7331981.
A sequential study of plasma histidine-rich glycoprotein and plasminogen in patients with acute myocardial infarction and deep vein thrombosis. Paper-4598471.
Evidence for the interaction between (-)-epigallocatechin gallate and human plasma proteins fibronectin, fibrinogen, and histidine-rich glycoprotein. Paper-878748.
Histidine-rich glycoprotein inhibits the antithrombin activity of heparin cofactor II in the presence of heparin or dermatan sulfate. Paper-4988338.
Plasminogen binding by alpha 2-antiplasmin and histidine-rich glycoprotein does not inhibit plasminogen activation at the surface of fibrin. Paper-7453301.
Western blot analysis showed that complement C8, C9, factor D, and S-protein in diluted serum were bound by nylon membrane-immobilized HRG. Paper-60940.
Locations of the introns in HRG gene coding for cystatin domains are essentially identical with those of cystatin SN, SA and C, and kininogen genes. Paper-5801313.
TIE1 and TIE2 mRNA levels were unaltered in the LRG, whereas transcription levels of both genes were increased by 2.5-fold in the HRG (p < 0.01). Paper-11443917.
Clexane (M(r) = 4,500) also bound antithrombin III, but both histidine-rich glycoprotein and vitronectin were quantitatively significant neutralising proteins. Paper-7820698.
P123 did not cross- link to plasminogen, histidine-rich glycoprotein, fibronectin, or plasma globulins other than fibrinogen/fibrin. Paper-1708261.
Effects of zinc and calcium ions on the heparin-neutralizing abilities of histidine-rich glycoprotein ( HRG) and platelet factor 4 ( PF4) were examined. Paper-7523895.
The concentration of serum HRG decreased during the last trimester of pregnancy reaching a nadir at the 36-37th week ( HRG 49 +/- 14 g/l, mean +/- SD). Paper-4359302.
The tripartite interactions among CD36, TSR domains and HRGP in tissues may play an important role in regulating physiological and pathological angiogenesis. Paper-13446260.
In blood drawn into streptokinase or into urokinase, HRG (78 kDa) was degraded producing peptides ranging in apparent molecular weight from 67 to 9 kDa. Paper-5100843.
Histidine-proline-rich glycoprotein ( HPRG) is an abundant multidomain plasma protein evolutionarily related to high-molecular-weight kininogen. Paper-9552588.
The characteristic sequence motifs of hydroxyproline-rich glyco-proteins ( HRGP) are present in the cDNA corres-ponding to the N-terminal domain of the mature p43. Paper-1959727.
HRGP colocalized with TSP-1 in the stroma of human breast cancer specimens, and this interaction masked the antiangiogenic epitope of TSP-1. Paper-8689729.
In contrast, VEGF- induced proliferation was not affected by HRGP or HRGP330, demonstrating the central role of cell migration during tube formation. Paper-12078379.
Indeed, both HRG and PF4, at physiological concentrations, were shown to effectively inhibit the binding of 125I- aFGF and 125I- bFGF to ECM. Paper-139834.
The HRG/Con A- induced morphological changes of MOLT-4 cells were specifically inhibited by a monoclonal antibody against the beta-subunit of ATP synthase. Paper-13734756.
These data indicate that sustained activation of the MEK/ ERK pathway is both essential and sufficient for HRG-induced differentiation of AU565 cells. Paper-1577501.
The additional complement of zinc in hyperzincemic plasma was localized within fractions containing zinc-binding proteins such as albumin, transferrin and HRG. Paper-4220541.
Presence in human skeletal muscle of an AMP deaminase- associated protein that reacts with an antibody to human plasma histidine-proline-rich glycoprotein. Paper-1718190.
Binding of anti-CD14 mAb MY4 to human monocytes was almost completely abolished by 0.3 microM HRGP and KGP treatments for 15 min, and 1 microM RGP2 for 30 min. Paper-8401526.
The mean (+/- SD) pretreatment concentration of histidine-rich glycoprotein was 1.08 +/- 0.24 U/ml, which was almost identical with the normal reference values. Paper-6906191.
In moderate (Child B) cirrhosis, both HRG levels and total plasminogen levels were reduced, resulting in a normal amount of free plasminogen in circulation. Paper-6307177.
These data suggest that heparan sulfate is the predominate cell-surface ligand for HRG and that mammalian heparanase is a potential regulator of HRG binding. Paper-10346184.
In addition, VEGF- mediated endothelial cell tubular morphogenesis in a three-dimensional collagen matrix was inhibited by HRGP and HRGP330. Paper-12078379.
In contrast, the amount of transforming growth factor beta2 transcript increased only in the HRG (330%; p < 0.01), whereas it remained unchanged in the LRG (-80%). Paper-11443917.
The expression of c-Jun and c-Fos and the level of the phosphorylated c-Jun were markedly increased after HRG-beta treatment in MCF-7/ HER2 cells. Paper-13051552.
In the present paper we report that Rac1 is an essential player for mediating the induction of cyclin D1 and p21(Cip1) by HRG in breast cancer cells. Paper-12704493.
The activation of Glu-plasminogen in alpha 2-AP-depleted plasma containing a normal concentration of HRGP produced a time-dependent increase in the generation of plasmin. Paper-7453301.
Plg activators did not influence binding of Plg to histidine-rich glycoprotein or of histidine-rich glycoprotein to TSP, demonstrating specificity. Paper-5411521.
Our data suggest that HRG-beta- induced MMP-7 expression was regulated by HER2- mediated AP-1 activation in MCF-7 cells. Paper-13051552.
Fibrinogen, which has been previously shown to bind to absorbed thrombospondin, did not inhibit the formation of the thrombospondin- histidine-rich glycoprotein complex. Paper-4759299.
Thrombospondin and histidine-rich glycoprotein are two proteins with diverse biological activities which have been associated with human platelets and other cell systems. Paper-4759299.
In both cases, there were no significant modifications of three proteins with high heparin affinity (antithrombin III, heparin cofactor II, histidine-rich glycoprotein). Paper-5734470.
These studies suggest that HRGP can modulate the antiangiogenic activity of TSP-1, and identify a potential mechanism of resistance to the antiangiogenic effect of TSP-1. Paper-8689729.
Hypothetically, the tandem repetitions of a consensus histidine-rich penta-peptide sequence in HRG may provide a highly charged area that interacts with complement components. Paper-60940.
The results of the immunological analysis reported here demonstrate that an antibody against human plasma HPRG reacts with an AMPD preparation from human skeletal muscle. Paper-1718190.
Histidine-rich glycoprotein complexed with thrombospondin was capable of binding heparin and neutralizing the anticoagulant activity of heparin in plasma. Paper-4759299.
Interestingly, HRG interfered with the ability of D10 cells to adhere to tissue culture plastic, as well as to laminin-, collagen- or fibronectin-coated culture dishes. Paper-602733.
We have shown previously that HRGP binds with high affinity to thrombospondin-1 ( TSP-1), a homotrimeric glycoprotein that is a potent inhibitor of angiogenesis. Paper-8689729.
Our results indicate that Ava II and Hinc II polymorphisms at the LDLR locus contribute to the variability of total cholesterol and LDL-C levels in HRG individuals. Paper-2090477.
The 5 years event-free survival rate for all patients was 73% (s.e. 2%); for SRG, MRG and HRG patients 85% (s.e. 3%), 73% (s.e. 3%) and 39% (s.e. 7%), respectively. Paper-9473794.
The stoichiometry and dissociation constant (KD) of the complex were determined from the equilibrium distribution of fluorescein-isothiocyanate-labeled PLG in the presence of HPRG. Paper-172840.
Subsequent treatment of GAG-positive Chinese hamster ovary cells with mammalian heparanase or bacterial heparinase III, but not chondroitinase ABC, abolished HRG binding. Paper-10346184.
These observations demonstrate that HPRG can act as either a positive or negative effector of Plg activation in vitro and may serve as a modulator of fibrinolysis in vivo. Paper-10911023.
By removing N-linked sugars with N-glycanase, it could be demonstrated that the difference between the two forms of HRG is caused by an extra carbohydrate group at Asn 184 in form 1. Paper-675806.
However, interactions of TSPs with growth factors, proteases, histidine-rich glycoprotein, and other cell-surface receptors on EC have the potential to modulate CD36-mediated effects. Paper-10020181.
At least two binding sites for HPRG, tropomyosin and heparan sulfate proteoglycans (HSPs), were identified on the surface of FGF-2-activated endothelial cells. Paper-10533417.
At their physiological concentrations, the presence of alpha 2-plasmin inhibitor more markedly decreased the binding of plasminogen to fibrin than histidine-rich glycoprotein. Paper-4590954.
To study the reversible complex formation between the plasma protein histidine-rich glycoprotein ( HRG) and plasminogen, crossed immunoelectrophoresis of HRG was modified. Paper-6131183.
Although the biological function of histidine-rich glycoprotein ( HRG) is unknown, it may serve as an antifibrinolytic agent by interfering with the binding of plasminogen to fibrin. Paper-4970642.
A plasminogen binding protein ( histidine-rich glycoprotein), plasmin inhibitors and activator inhibitors appear to contribute to the regulation of the initial phase of fibrinolysis. Paper-6580946.
We studied the levels of both HRG and plasminogen in patients with different degrees of liver cirrhosis to assess the role of HRG in enhanced fibrinolysis in these patients. Paper-6307177.
HRGP/HRGP330 treatment of endothelial cells induced disruption of actin stress fibers, a process reversed by treatment of cells with the FAK inhibitor geldanamycin. Paper-12078379.
In contrast, the addition of 1.5 microM- HRGP to HRGP-depleted plasma containing a normal amount of alpha 2-AP produced only a modest (17%) decrease in the amount of plasmin(ogen) bound. Paper-7453301.
The purpose of this study was to assay the plasma levels of tPA, PAI, histidine-rich glycoprotein ( HRG), and other fibrinolytic proteins in 15 severely stressed newborns. Paper-7491617.
Addition of PLG shifts the S-value of 125I- labeled HPRG from 4.8S to 6.8S, providing the first direct evidence that HPRG associates with the zymogen form of plasmin in solution. Paper-172840.
Using an enzyme-linked immunosorbent assay, we have demonstrated that purified human platelet thrombospondin formed a complex with purified human plasma histidine-rich glycoprotein. Paper-4759299.
The H84 mutant viruses incorporated wild-type levels of CypA and viral RNAs and showed nearly normal signals in virus entry assays. Paper-11241051.
Unlike other stimulators of plasminogen activation, the effect of HPRG on fibrinolysis is modulated by factors that influence the equilibrium between solution and surface-bound HPRG. Paper-946808.
No differences were observed in prekallikrein, high-molecular-weight kininogen, alpha 2-antiplasmin, alpha 2-macroglobulin, antithrombin III, and histidine-rich glycoprotein plasma levels. Paper-4603222.
Structurally, HRG is a modular protein consisting of an N-terminal cystatin-like domain (N1N2), a central histidine-rich region (HRR) flanked by proline-rich sequences, and a C-terminal domain. Paper-10346184.
Each of cystatin-like domains I and II of HRG is encoded by three exons, exons I to III and exons IV to VI, respectively, like those of other members of the cystatin superfamily. Paper-1876309.
Interestingly, the proliferative effect of HRG was impaired not only when the expression of Rac1 or cyclin D1 was inhibited, but also when cells were depleted of p21(Cip1) using RNAi. Paper-12704493.
IgG from most APS patients bound to HRGP, which shares distinct biochemical properties with beta2- GPI, is present in the brain and may be an important autoantigen. Paper-13422005.
Histidine-proline-rich glycoprotein ( HPRG) has long been known to associate with plasminogen ( Plg) in solution, but the consequences of this interaction have not been defined. Paper-10911023.
Expression of HRGP in rat and human brain was established by RT-PCR studies and a partial sequence of rat brain HRGP was obtained showing 68% homology with the human protein. Paper-13422005.
Like platelet factor 4, but unlike histidine-rich glycoprotein, S protein/ vitronectin readily neutralized the anticoagulant activities of heparan sulfate of Mr approximately 20,000. Paper-5738260.
Plasma levels of plasminogen and histidine-rich glycoprotein ( HRG) increased and decreased, respectively, whereas an increase in von Willebrand factor was observed in the treatment group. Paper-137987.
In assays performed in vitro of endothelial cell migration and tube formation, and in vivo corneal angiogenesis assays, HRGP inhibited the antiangiogenic effect of TSP-1. Paper-8689729.
Group 1 includes individuals who were at low risk for exposure to M. tuberculosis ( LRG) and Group 2 includes individuals who were likely to have been exposed to M. tuberculosis infections ( HRG). Paper-13631116.
Similar pH-dependent antimicrobial activities were demonstrated for peptides derived from histidine-rich and heparin- binding regions of human kininogen and histidine-rich glycoprotein. Paper-13434293.
Thus, the peptide (GHHPH)4, derived from the histidine-rich region of HRGP and containing such a heparin-binding motif, was antibacterial for E. faecalis in the presence of Zn2+ or at low pH. Paper-12428358.
The method can be used to assess several aspects of reversible complex formation between plasma proteins, as demonstrated for plasminogen binding of HRG and alpha 2-antiplasmin in whole plasma. Paper-6131183.
We have recently identified several plasma proteins having anti-angiogenic properties, including Histidine-Proline-Rich Glycoprotein ( HPRG) and activated high-molecular-weight kininogen (HKa). Paper-10609103.
The process is regulated by physiological inhibitors, of which alpha 2-antiplasmin, histidine-rich glycoprotein and plasminogen activator inhibitor are reported to be of major physiological significance. Paper-6885500.
Extensive similarity among the NH2-terminal sequences of alpha 2-HS glycoprotein and human histidine-rich glycoprotein suggest that the latter protein is another candidate protein of this new family. Paper-6390164.
Modulation of protein C inhibitor activity by histidine-rich glycoprotein and platelet factor 4: role of zinc and calcium ions in the heparin-neutralizing ability of histidine-rich glycoprotein. Paper-7523895.
These results indicate that HPRG has independent binding sites for heparin and PLG and confirm that one or more lysine residues of HPRG are involved in its recognition by PLG. Paper-172840.
Affinity chromatography of human plasma on Sepharose coupled with the protein specifically absorbed two plasma proteins which were identified as clusterin and histidine-rich glycoprotein ( HRG). Paper-473049.
Thus, HRG, PF4, aFGF, and bFGF all interact with the same HS chains on the 3T3 cell surface, either binding to the same or binding to adjacent saccharide sequences on the chains. Paper-139834.
Histidine-rich glycoprotein ( HRG) reduces by complex formation with plasminogen the amount of "free" plasminogen in circulation and is therefore considered an inhibitor of fibrinolysis. Paper-6307177.
Simultaneous determinations of HRG and total plasminogen combined with a calculation of free plasminogen might yield valuable information when evaluating patients for the availability of plasminogen. Paper-4933441.
The results show a previously undisclosed antibacterial activity of HRGP and suggest that the histidine-rich and heparin- binding domain of HRGP mediates the antibacterial activity of the protein. Paper-12428358.
The interaction of the conserved C-terminal lysine of HPRG with the high affinity lysine binding site of plasminogen is necessary and sufficient to accelerate plasminogen activation. Paper-946808.
Purified HRG or HRG in sera increased the number of HMDM-containing apoptotic cells and accelerated the ingestion, while neutralization or depletion of HRG from sera reduced this effect. Paper-9579646.
However, some divergence is observed between the sequence of one of the fragments liberated from AMP deaminase by a more extensive trypsinization and rabbit plasma HPRG in the region containing residues 472-477. Paper-1171373.
We conclude that TSP1 contains a high-affinity binding site for polyhistidine and this is likely to be the molecular basis for the observed binding of TSP1 to histidine-rich glycoprotein. Paper-8571596.
High levels of histidine-rich glycoprotein ( HRGP) and plasminogen activator inhibitor-1 ( PAI-1) have been claimed to contribute to the hypofibrinolytic state observed in patients with venous thrombosis. Paper-7862153.
Because of the reduction of free plasminogen levels in severe liver cirrhosis, we propose that the decrease in HRG levels in liver cirrhosis plays no role in enhanced fibrinolysis in these patients. Paper-6307177.
On the basis of these findings, it is proposed that HRG and PF4 may act as positive regulators of FGF activity by displacing FGF from the ECM or basement membrane and making FGF available to responsive cells. Paper-139834.
The measured upwelling radiance was converted to % reflectance; and we integrated the hyperspectral reflectance to match the Red and NIR bands of three satellite sensors: Landsat 7 ETM, SPOT 5 HRG, and ASTER. Paper-13548169.
TNF-alpha production by monocytes after HRGP and KGP treatments was decreased at 1 ng/ml, but not at 20 microg/ml LPS, indicating that gingipains inhibited a CD14-dependent cell activation. Paper-8401526.
Inhibition of thrombin by heparin cofactor II and heparin was completely prevented by purified histidine-rich glycoprotein at the ratio of 13 micrograms histidine-rich glycoprotein/microgram heparin. Paper-4988137.
The fourfold-greater increase in aerobic fitness and markedly differing gene expression profile in the HRG indicates that these ECM genes may be critical for physiological adaptation to exercise in humans. Paper-11443917.
The purpose of this study was to measure the plasma levels of HRG and plasminogen in three groups of patients: normal adults (n = 48), normal term newborns (n = 43), and normal premature newborns (n = 18). Paper-6686994.
In contrast, native HPRG bound to hydrazide or nickel chelate surfaces strongly stimulated the activation of plasminogen by tissue plasminogen activator, but not by urokinase or streptokinase. Paper-946808.
Thus, under conditions of local acidosis (e.g. ischemia or hypoxia), HPRG can co-immobilize plasminogen at the cell surface as well as compete for heparin with other proteins such as antithrombin. Paper-1360803.
The sample consists of the adenosine monophosphate deaminase ( AMPD) histidine proline rich glycoprotein ( HPRG) complex that contains 3-4 Zn(II) ions per dimer of approximately 320 kDa molecular weight. Paper-9822831.
Specifically, Plg complexed with HPRG on a GAG surface is more readily activated by tissue-type Plg activator than free Plg, with a 10-fold difference in apparent catalytic efficiency (kcat/Km). Paper-10911023.
Complex formation was detected by a specific binding enzyme-linked immunosorbent assay ( ELISA) which demonstrated simultaneous binding of fluid-phase Plg and HRGP to TSP adsorbed to microtitration wells. Paper-5079045.
The plasma concentrations of histidine-rich glycoprotein and plasminogen were measured and those of free plasminogen calculated in 34 patients with acute myocardial infarction treated with thrombolytic drugs. Paper-6906191.
On the significance of antithrombin-III, alpha 2-macroglobulin, alpha 2-antiplasmin, histidine-rich glycoprotein, and protein C in patients with acute myocardial infarction and deep vein thrombosis. Paper-4855883.
RESULTS: neuropilin-1 (800%; p < 0.001) and VEGF receptor 2 (300%; p < 0.01) transcript abundance increased only in the HRG, whereas levels of VEGF receptor 1 mRNA actually declined in the LRG (p < 0.05). Paper-11443917.
A selective binding of the anti- HPRG antibody to Type IIB muscle fibers was detected, suggesting a preferential association of the novel protein to the AMPD isoenzyme contained in the fast-twitch glycolytic fibers. Paper-1718190.
Partial purification of the activating factor present in RMT-conditioned medium yielded a heparin-binding growth factor with biochemical properties similar to those of neu differentiation factor/heregulin ( NDF/ HRG). Paper-514890.
Translocation of tropomyosin to the surface of HUVEC occurred in response to FGF-2, and the anti-angiogenic activity of HPRG in a Matrigel plug model was partially inhibited by soluble tropomyosin. Paper-10533417.
We tested this hypothesis by comparing the effects of histidine-rich glycoprotein and 6-aminohexanoic acid in an in vitro assay of fibrin-dependent plasmin production mediated by tissue plasminogen activator. Paper-8472816.
Histidine-rich glycoprotein ( HRG) has been reported to be a fibrinolysis regulating protein due to its capacity to bind to the high affinity lysine binding sites of plasminogen. Paper-4933441.
Isolation and characterization of a human plasma protein with affinity for the lysine binding sites in plasminogen. Role in the regulation of fibrinolysis and identification as histidine-rich glycoprotein. Paper-3673509.
Levels of both HRG and plasminogen were higher in the stressed group but the ratio of HRG to plasminogen was the same as that in the normal control newborns (1:3), suggesting an insignificant effect of HRG. Paper-7491617.
The ratio of bound antithrombin, histidine-rich glycoprotein and vitronectin to GAG was negatively correlated with the Orgaran concentration in plasma, implying that the efficacy of Orgaran may not be linearly related to dose. Paper-8228496.
In this study, we show that heregulin-beta ( HRG-beta) stimulation remarkably induced MMP-7 promoter activity and significantly enhanced the expression and activity of MMP-7 in MCF-7 cells overexpressing HER2. Paper-13051552.
S protein/ vitronectin efficiently neutralized oligosaccharides of Mr 2,400-7,200, unlike the two other physiologically occurring heparin neutralizing proteins histidine-rich glycoprotein and platelet factor 4. Paper-5738260.
Furthermore, HRGP inhibited interleukin 2 receptor expression on activated T cells, causing decreased T cell interferon-gamma release and altered T cell-dependent inhibition of erythropoiesis. Paper-6450931.
The results suggest that zinc markedly potentiates the binding of HRG to T cells, and that HRG and zinc may play an important role in regulating the adhesion of T cells to other cells and the extracellular matrix. Paper-602733.
These results provide direct evidence that HRG belongs to a supergene family that includes cystatin SN, SA and C, and kininogen, and also demonstrate high conservation of the intron-exon organization among this supergene family. Paper-5801313.
We have shown that a fragment released from the central histidine/ proline-rich (His/Pro-rich) domain of HRGP blocks endothelial cell migration in vitro and vascularization and growth of murine fibrosarcoma in vivo. Paper-12078379.
This structural difference correlates with functional data which suggest that the N-terminal region of the HRG-alpha EGF-like domain is responsible for the observed receptor specificity differences between HRG-alpha and EGF. Paper-555501.
Recently we identified a circulating protein, histidine-rich glycoprotein ( HRGP), that contains a CD36 homology domain and that acts as a soluble decoy to block the anti-angiogenic activities of TSPs, thereby promoting angiogenesis. Paper-13446260.
All three parametres showed wide individual variations, but with decreasing functional capacity of the liver the individual levels of plasminogen were reduced earlier than those of HRG leading to decreased amounts of free plasminogen. Paper-4933441.
In addition, we found that HRG activates NF-kappaB (nuclear factor kappaB) in a Rac1- and MEK-dependent fashion, and inhibition of NF-kappaB abrogates cyclin D1/p21(Cip1) induction and proliferation by HRG. Paper-12704493.
Protonation of two histidine residues ( His83 and His87) in helix C of hGM-CSF appears to act as a pH-dependent molecular switch to control the interaction with GAGs. Paper-10751595.
The plasma proteins alpha 2-plasmin inhibitor and histidine-rich glycoprotein were compared directly with respect to their effectiveness in inhibiting the binding of plasminogen to fibrin under the same experimental conditions. Paper-4590954.
The association of plasma histidine-proline-rich glycoprotein ( HPRG) with plasminogen ( PLG) was examined using a sucrose density gradient assay in order to evaluate the effects of several relevant conditions on complex formation. Paper-172840.
We have recently established that HRG (heregulin beta1) promotes breast cancer cell proliferation and migration via cross-talk with EGFR ( EGF receptor) that involves the activation of the small GTPase Rac1. Paper-12704493.
However, by immunoprecipitation of relatively undiluted serum with anti- HRG IgG beads, HRG was found to coprecipitate with S-protein and plasminogen, which suggested that HRG may complex with these proteins in serum. Paper-60940.
The sera levels of proteins, such as the 10 kDa subunit of vitronectin, alpha 1-acid glycoprotein, apolipoprotein B100, fragment of factor H, and histidine-rich glycoprotein were observed to be different between AD and controls. Paper-10543981.
In contrast, histidine-rich glycoprotein had no effect on inhibition of thrombin by heparin cofactor II and dermatan sulfate at ratios of less than or equal to 128 micrograms histidine-rich glycoprotein/microgram dermatan sulfate. Paper-4988137.
A similar effect was also apparent in the corresponding euglobulin fractions (554 +/- 169 fmol versus 754 +/- 310 fmol), the latter lacking the plasminogen- binding proteins alpha 2-antiplasmin and histidine-rich glycoprotein, but containing Lp(a). Paper-7191890.
In the present study, we identified the alpha-subunit of ATP synthase as one of the HRG-binding proteins on the surface of T-cells by HRG-derived glycopeptide affinity chromatography and by a peptide mass finger printing method. Paper-13734756.
In the nephrotic syndrome heparin-sensitivity correlated with albumin and triglyceride concentrations but not with antithrombin III, platelet factor 4, cholesterol, fibrinogen, heparin cofactor II or histidine-rich glycoprotein. Paper-5638990.
HRGP suppressed proliferation of antigen receptor (CD3)- triggered T cells induced by interleukin 2; this suppression was specifically reversed by prior incubation of HRGP with affinity-purified anti- HRGP IgG. Paper-6450931.
Using immunological methods we have measured the concentrations in plasma of HRG and total plasminogen and calculated the amounts of plasminogen not bound to HRG (free plasminogen) in 28 patients with moderate to severe liver disease. Paper-4933441.
These results strongly suggest that the cell surface ATP synthase functions as a binding protein for HRG on MOLT-4 cells, which is required for the morphological changes observed in MOLT-4 cells following treatment with HRG/Con A. Paper-13734756.
In contrast, the enzyme model suggests that although a limited stabilization of HRG facilitates GDP release, HRG should not be "too stable" as this might trap the G protein in an inactive state and actually hinder G protein activation. Paper-10490383.
The binding of plasminogen to fibrin is regulated by histidine-rich glycoprotein, and the primary physiological inhibitor of generated plasmin is alpha 2-antiplasmin and especially the plasminogen-binding form of this immediate plasmin inhibitor. Paper-7873914.
Two molecular forms of plasminogen, Glu- and Lys-plasminogen, induced a dose-dependent reduction of the electrophoretic mobility of HRG, with a half maximal retardation for both plasminogens at 0.50-0.55 microM of added plasminogen to the agarose gel. Paper-6131183.
This review describes the properties of four structurally related, abundant plasma proteins denoted fetuin-A/alpha-2-Heremans Schmid-glycoprotein ( AHSG), fetuin-B ( FETUB), kininogen ( KNG) and histidine-rich glycoprotein ( HRG). Paper-13656386.
Here we show that HPRG adsorbed to a glycosaminoglycan (GAG) surface also binds Plg with a Kd value of 0.7 micromol/l. Moreover, we present evidence that HPRG acts as a modulator of the activation of Plg by tissue-type Plg activator. Paper-10911023.
Taken together, these findings establish a central role for Rac1 in the control of HRG- induced breast cancer cell-cycle progression and proliferation through up-regulating the expression of cyclin D1 and p21(Cip1). Paper-12704493.
Many of them, including thrombospondin-1 ( TSP-1), histidine-rich glycoprotein, kininogen 1, and alpha 2 macroglobulin ( alpha2M), are well-known glycoproteins involved in the regulation of inflammation, angiogenesis, and tissue remodeling. Paper-12192611.
Utilizing a standard procedure for the isolation of serum beta2- GPI we purified a 100 kD human brain protein, which was found by peptide sequencing to have full homology with the serum protein, histidine-rich glycoprotein ( HRGP). Paper-13422005.
Because histidine-rich glycoprotein binds to the kringle 1-3 domain of plasminogen, it may affect fibrinolysis by reducing fibrin-dependent plasmin production, and in this way it could be mechanistically analogous to 6-aminohexanoic acid. Paper-8472816.
According to the criteria used to evaluate the adequacy of the admission to the hospital, twentyeight patients were classified in the HRG, with an appropriate admission, whilst fourteen (33%) were in the LRG, with an inappropriate admission to the hospital. Paper-11770264.
The relative abundance of wound induced RNAs was confirmed by using two well identified wound inducible gene probes of hydroxyproline-rich glycoproteins ( HRGP) and proteinase inhibitor I. The selectively separated wound induced mRNA was used to make cDNA probes. Paper-324289.
While neither ligand inhibited complex formation of the other with TSP, 10 mM epsilon-amino-n-caproic acid selectively blocked incorporation of Plg into the complex, suggesting that TSP contains independent binding sites for Plg and HRGP. Paper-5079045.
We have shown that HRGP binds specifically to human T lymphocytes but not sheep erythrocytes and have demonstrated a 56-kDa HRGP- binding protein on the T cell surface which is distinct from the CD2 sheep erythrocyte receptor. Paper-6450931.
The levels of alpha 2-macroglobulin, antithrombin-III and HRG were within the normal range in plasma from reactors, the level of C1-esterase inhibitor was slightly increased (116%), and the level of alpha 1-antitrypsin was higher than normal (124%). Paper-5413930.
RNA-polymerase chain reaction analysis demonstrated that RMT cells expressed mRNA for NDF/ HRG, and western-blot analysis confirmed the presence of the 45-kDa secreted form of NDF/ HRG in conditioned medium from the growth factor-independent RMT cells. Paper-514890.
Chemical modification of the single histidine residue ( His15) located in helix A of WT mGM- CSF with diethyl pyrocarbonate totally abolished binding to immobilized heparin. Paper-10751595.
Furthermore, the HRG- plasminogen interaction is lysine-dissociable and involves predominately the amino-terminal domain of HRG, and the fifth kringle domain of plasminogen, but not the carboxyl-terminal lysine of HRG. Paper-10643946.
In contrast to histidine-rich glycoprotein, purified platelet factor 4 prevented inhibition of thrombin by heparin cofactor II in the presence of either heparin or dermatan sulfate at the ratio of 2 micrograms platelet factor 4/micrograms glycosaminoglycan. Paper-4988137.
Decreased expression of beta-tubulin, actin, JCW1, HRGP and GRP and increased expression of sbPRP1, pGE95 and pGE16 in the hypocotyl zone of cell elongation could participate in the reversible growth inhibition observed in water-deficient soybean seedlings. Paper-43980.
Sucrose-density-gradient ultracentrifugation of a mixture of thrombospondin and histidine-rich glycoprotein also revealed the formation of fluid-phase complexes, with an estimated stoichiometry of 1 thrombospondin: 3.5 histidine-rich glycoprotein. Paper-4759299.
Inhibition of Rac function by expressing either the Rac-GAP ( GTPase-activating protein) beta2-chimaerin or the dominant-negative Rac mutant N17Rac1, or Rac1 depletion using RNAi ( RNA interference), abolished the cyclin D1 and p21(Cip1) induction by HRG. Paper-12704493.
The efficacy of this system can be evaluated by plasminogen concentration determinations and by the behavior of factors such as histidine-rich glycoprotein ( HRG) which controls plasminogen activation and alpha 2-antiplasmin which controls plasmin activity. Paper-7290856.
Significant binding was detected when histidine-rich glycoprotein was incubated with thrombospondin immobilized on anti-thrombospondin IgG-coated plates, indicating that the observed complex formation was not due to a thrombospondin interaction with the plastic surface. Paper-4759299.
Pulse-chase experiments in the absence and presence of various proteinase inhibitors revealed that, while wild-type HRG was completely secreted during 4-h chase periods, both the G85E and C223R mutants were only partially secreted and primarily degraded within the cells. Paper-8379322.
Studies using confocal fluorescence microscopy indicated that following incubation of MT4 cells with HRG in the presence of zinc at 4 degrees, the HRG was localized exclusively at the plasma membrane, but was actively internalized after incubation at 37 degrees. Paper-602733.
APC-resistance (FV:Q506), protein C, protein S, antithrombin, heparin cofactor II ( HCII), histidine-rich glycoprotein ( HRGP), and prothrombin (F.II), factor XII (F.XII), plasminogen, homocysteine and lipoprotein (a) (Lp(a)) were investigated. Paper-2085622.
A recent report suggests that histidine-rich glycoprotein binds to the high-affinity lysine- binding sites of plasminogen and that histidine-rich glycoprotein may retard fibrinolysis by interfering with the binding of plasminogen to fibrin [3]. Paper-4048576.
Two other fibrinolytic inhibitor molecules ( alpha-2 plasmin inhibitor antigen and histidine-rich glycoprotein antigen) were also significantly reduced, as well as the two subunits of fibrin stability factor XIII, although only subunit A is known to be susceptible to thrombin action. Paper-79261.
We investigated whether the plasma levels of histidine-rich glycoprotein and free plasminogen were associated with clinical parameters such as the occurrence and time of successful reperfusion, the incidence of reocclusion and the presence and extent of the systemic lytic state. Paper-6906191.
To test the universality of this Soret band splitting for 6-coordinate low-spin heme A systems, we have reconstituted purified heme A with the apo forms of the heme binding proteins, hemopexin, histidine-proline-rich glycoprotein and the H64V/V68H double mutant of human myoglobin. Paper-193858.
This resulted in a considerable relative increase in the concentration of free plasminogen in the hormone group (calculated from the equilibrium: HRG . plasminogen in equilibrium HRG + plasminogen, using KD = 1.0 microM), representing a doubling of that in the normal group. Paper-4117132.
There is a controversy about whether or not histidine-rich glycoprotein ( HRG), the most abundant plasma protein with glycosaminoglycans-neutralizing capacity, is able to prevent the inhibition of human thrombin by heparin cofactor II ( HC II) in the presence of dermatan sulfate (DS). Paper-7331981.
In this study, we demonstrate that HPRG binds with high affinity to FGF-2-stimulated human umbilical vein endothelial cells (HUVEC) and immobilized tropomyosin in a Zn2+ or pH-dependent manner, and that this interaction is mediated by the H/P domain of HPRG. Paper-10533417.
Histidine-rich glycoprotein, and alpha 2-glycoprotein in human plasma, has been shown to interact with heparin, with the high-affinity lysine-binding site of plasminogen, with divalent cations, and is associated with the rosette formation between erythrocytes and lymphocytes. Paper-4498622.
Other causes of inherited thrombophilia include abnormalities in the proteins of the fibrinolytic system, dysfibrinogenemias, deficiency of heparin cofactor II, abnormal thrombomodulin, elevated levels of histidine-rich glycoprotein, and the recently described variation in the prothrombin gene. Paper-1442560.
The activity of the MMP-7 promoter induced by HRG-beta in MCF-7/ HER2 cells could be inhibited by a dominant negative c-Jun mutant TAM67 and by the mutagenesis of the AP-1 site. c-Jun binding to MMP-7 promoter was confirmed by ChIP assays. Paper-13051552.
In a longitudinal study the plasma levels of antithrombin-III, alpha 2-macroglobulin, alpha 2-antiplasmin, histidine-rich glycoprotein, and protein C were followed in two groups of patients with acute myocardial infarction (AMI), one with and one without deep vein thrombosis (DVT). Paper-4855883.
To determine whether plasminogen binding by HRGP may influence plasminogen activation, we studied the fibrinolytic activity of members of this family cohort with a system that detects modifications in plasmin generation by proteins interfering with the binding of plasminogen to fibrin. Paper-7862153.
We have investigated the effects of Ava II (exon 13) and Hinc II (exon 12) polymorphisms at the low-density lipoprotein receptor ( LDLR) gene on circulating lipids of 170 white unrelated individuals presenting a lipid profile with high risk for CHD ( HRG) and 130 controls (CG) from São Paulo City, Brazil. Paper-2090477.
Thrombospondin ( TSP), a multifunctional alpha-granule glycoprotein of human platelets binds fibrinogen, fibronectin, heparin, histidine-rich glycoprotein ( HRGP), and plasminogen ( Plg), and thus, may play an important role in regulating thrombotic influences at vessel surfaces. Paper-5079045.
RESULTS: Seventy patients (14%) were homozygous for the histidine variant ( HH) of CFH, 237 (48%) were heterozygous for the histidine variant (HY), and 186 (38%) were homozygous for the tyrosine variant (YY). Paper-13150089.
We studied factors affecting fibrinolysis in neonates and observed that an important reduction in HRG accompanied the reduced circulating plasminogen levels, with the result that 85% of circulating plasminogen was not bound to HRG and was thus free for binding to fibrin and for activation to plasmin. Paper-7290856.
Inhibition of EGFR, PI3K ( phosphoinositide 3-kinase; kinases required for Rac activation by HRG) or MEK [ MAPK (mitogen-activated protein kinase)/ERK ( extracellular-signal-regulated kinase) kinase] also blocked the up-regulation of cyclin D1 and p21(Cip1) by HRG. Paper-12704493.
Determinations by immunologic methods of histidine-rich glycoprotein ( HRG) and plasminogen, were made in plasma samples collected during one normal or hormone induced cycle in 15 young, normal women and in 11 women using oral contraceptives with 30 micrograms ethinyl estradiol and 150 micrograms levo-norgestrel. Paper-4117132.
This enhancing activity was not due to a nonspecific effect of anionic proteins since other purified serum proteins, of similar size and charge as Gc-globulin ( alpha 1 acid glycoprotein, alpha 2 HS glycoprotein, alpha 2 histidine-rich glycoprotein), could not increase the chemotactic activity of C5a des Arg. Paper-5963406.
A month after stopping the drug, her plasma activities of antithrombin III, protein C, protein S, heparin cofactor II, plasminogen and plasminogen activator inhibitor were normal, but her plasma histidine-rich glycoprotein ( HRG) level was only 21% of the normal level of 109.5 +/- 51.5% (mean +/- 2 SD). Paper-7848516.
Histidine-rich glycoprotein ( HRGP), an abundant heparin-binding protein found in plasma and thrombocytes, exerts antibacterial effects against Gram-positive bacteria ( Enterococcus faecalis and Staphylococcus aureus) and Gram-negative bacteria ( Escherichia coli and Pseudomonas aeruginosa). Paper-12428358.
Moreover, replacement of His15 for an alanine residue significantly reduced the affinity of mGM- CSF for heparin at pH 5.0 and completely blocked heparin binding to a synthetic peptide corresponding to helix A of GM-CSF. Paper-10751595.
The data indicate that zinc is not required for HPRG/ AMPD interaction, both zinc ions being bound to the catalytic subunit of the enzyme, one to the three conserved amino acid residues among those four assumed to be in contact with zinc in yeast AMPD, and the other at the N-terminal region, probably to His-52, Glu-53 and His-57. Paper-13106593.
Because of the known evolutionary and structural relationship of KNG to other members of the cystatin gene superfamily, we tested the physical linkage of the genes encoding alpha-2HS-glycoprotein ( AHSG), KNG, and histidine-rich glycoprotein ( HRG), all of which were previously mapped to the long arm of chromosome 3. Paper-220647.
By use of a signal transduction antibody array representing 400 different signal transduction molecules, we now show that HRGP and the synthetic peptide HRGP330 specifically induce tyrosine phosphorylation of focal adhesion kinase and its downstream substrate paxillin in endothelial cells. Paper-12078379.
In a prospective study of deep vein thrombosis (DVT), detected by the Tc-plasmin test, in 34 patients with acute myocardial infarction sequential determinations were made in plasma by immunologic methods of histidine-rich glycoprotein ( HRG) and total plasminogen and the concentrations of free plasminogen calculated. Paper-4598471.
Eight proteins, transthyretin ( TTHY), ceruloplasmin (CERU), afamin (AFAM), alpha-1-microglobulin ( AMBP), apolipoprotein E ( APOE), serum amyloid P-component ( SAMP), histidine-rich glycoprotein ( HRG) and alpha-1-antitrypsin ( A1AT) were up-regulated and one, clusterin ( CLUS), down-regulated. Paper-12892046.
Subjects were ranked based on improvement in aerobic fitness, and two cohorts were formed (n = 8 per group): the high-responder group ( HRG; peak rate of oxygen consumption increased by +0.71 +/- 0.1 L min(-1); p < 0.0001) while the low-responder group ( LRG; peak rate of oxygen consumption did not change, +0.17 +/- 0.1 L min(-1), ns). Paper-11443917.
In whole plasma in the absence of platelet release, antithrombin III was the most abundant protein bound to therapeutic doses of unfractionated heparin, and histidine-rich glycoprotein its only effective competitor, while both histidine-rich glycoprotein and vitronectin were potentially important modulators of LMW heparin activity. Paper-7889350.
Based on these findings, we have now generated a triple mutant form of murine GM-CSF (mGM- CSF) in which three noncharged residues in helix C of the murine factor (Tyr83, Gln85, and Tyr87) were replaced by the corresponding basic residues present in hGM-CSF ( His83, Lys85, and His87). Paper-10751595.
Anabolic steroids increase the activity of the fibrinolytic system by reducing plasma levels of inhibitors ( plasminogen activator inhibitor type I, histidine-rich glycoprotein, alpha-2-macroglobulin) and increasing plasma levels of tissue-type plasminogen activator activity, plasminogen, and plasmin activity (B beta 15-42 fragment of fibrinogen). Paper-106678.
Since hypervariable regions (HVRs) are nonconserved among hexons of different serotypes, we investigated whether the HVRs could be used for genetic modification of hexon by incorporating oligonucleotides encoding six histidine residues ( His6) into different HVRs in the Ad5 genome. Paper-11232471.
Using radial immunodiffusion serum histidine-rich glycoprotein ( HRG) levels were measured in acquired immune deficiency syndrome (AIDS) patients, in end-stage renal disease ( ESRD) patients after renal transplantation and immunosuppressive steroid therapy, and in asthma and chronic obstructive pulmonary disease ( COPD) patients treated with steroids. Paper-5272042.
To probe factors which might govern hexamer assembly preferences in vivo, we examined the effects of mutations at CA histidine residue 84 ( H84), modeled at the outer edges of NTD hexamers, as well as a nearby histidine ( H87) in the cyclophilin A ( CypA) binding loop. Paper-11241051.
These synonyms are used for gene HRG (histidine-rich glycoprotein): HRGP, HPRG, Histidine-rich glycoprotein, Histidine-proline-rich glycoprotein, DKFZp779H1622.
These accession numbers are used for gene HRG: Q68DR3 (UNIPROT__AC), B2R8I2 (UNIPROT__AC), AAH69574 (NCBI_GENBANK__AC), AAA52694 (NCBI_GENBANK__AC).
HRG is a homologue of HRG (histidine-rich glycoprotein) from Bos taurus.
HRG is a homologue of HRG (histidine-rich glycoprotein) from Pan troglodytes.
HRG is a homologue of HRG (histidine-rich glycoprotein) from Gallus gallus.
HRG is a homologue of Hrg (histidine-rich glycoprotein) from Mus musculus.
HRG is a homologue of Hrg (histidine-rich glycoprotein) from Rattus norvegicus.
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