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Key words: Relaxation, Caldesmon, Tropomyosin, HSP27. Paper-14167567.
Beta-tropomyosin mutations alter tropomyosin isoform composition. Paper-14429327.
Cap disease due to mutation of the beta-tropomyosin gene ( TPM2). Paper-13750956.
The results showed that TM and GDH co-pelleted with F-actin. Paper-9514002.
Like TPM1, PDCD4 and maspin also reduced invasiveness of MDA-MB-231 cells. Paper-12760329.
A de novo mutation in alpha-tropomyosin that causes hypertrophic cardiomyopathy. Paper-216170.
Cap disease caused by heterozygous deletion of the beta-tropomyosin gene TPM2. Paper-13260998.
Mutation of L27 to E or G in the Tmod helix reduces TM affinity. Paper-10741987.
A protein of 10 kD was found to bind to GST/ TM2, but not to GST. Paper-8151862.
Mutations in the beta-tropomyosin ( TPM2) gene--a rare cause of nemaline myopathy. Paper-9345083.
MicroRNA-21 targets the tumor suppressor gene tropomyosin 1 ( TPM1). Paper-13214255.
TM and CaD are known to play crucial role in actomyosin interaction promoting contraction. Paper-14167567.
Polycystin-2 associates with tropomyosin-1, an actin microfilament component. Paper-9659022.
Preincubation of CSMC with VIP exhibited a decrease in phosphorylation of TM and CaD. Paper-14167567.
Sequence-tagged sites (STSs) were developed for the human alpha-tropomyosin gene TPM4. Paper-558525.
Tropomyosin requires an intact N-terminal coiled coil to interact with tropomodulin. Paper-9438629.
In the SIF system, MHC was also easily decomposed, while TM and actin were resistant to digestion. Paper-15545611.
In SIF system, MHC was easily decomposed, while TM and actin were similarly resistant to digestion. Paper-15238284.
TM and CaD are known to play crucial role in actomyosin interaction promoting contraction. Paper-15904441.
Molecular basis of tropomyosin binding to tropomodulin, an actin-capping protein. Paper-13416887.
Simultaneous silencing of TPM1 with siRNA only partially recapitulates the effect of miR-21 ASO. Paper-13840804.
Myo1 message disappears with a delay while the expression level of Tpm2 is strongly reduced. Paper-1980497.
In the SIF system, MHC was easily decomposed, while TM and actin were similarly resistant to digestion. Paper-15302807.
Preincubation of CSMC with VIP exhibited a decrease in phosphorylation of TM and CaD. Paper-15904441.
New morphologic and genetic findings in cap disease associated with beta-tropomyosin ( TPM2) mutations. Paper-13478977.
A tropomyosin 1 induced defect in cytokinesis can be rescued by elevated expression of cofilin. Paper-14473590.
A mutation in the alpha tropomyosin gene TPM3 associated with autosomal dominant nemaline myopathy. Paper-196265.
The level of miR-21 is reversely correlated with TPM1 and PTEN expression and apoptosis of cancer cells. Paper-13840804.
We also report that the phosphorylation of tropomyosin-1 mediated by DAP kinase occurs on Ser283. Paper-12571479.
Exon selection in alpha-tropomyosin mRNA is regulated by the antagonistic action of RBM4 and PTB. Paper-11280634.
We sequenced eight genes: MYH7, MYBPC3, TNNT2, TNNI3, TPM1, MYL3, MYL2, and ACTC. Paper-14314646.
cAMP and bFGF negatively regulate tropomyosin expression in rat cultured astroblasts. Paper-185069.
Similarly, alpha-actin and alpha-tropomyosin polypeptide synthesis remained close to the level of untreated cells. Paper-22744.
Assignment of the human beta tropomyosin gene ( TPM2) to band 9p13 by fluorescence in situ hybridisation. Paper-288254.
The nebulette repeat domain is necessary for proper maintenance of tropomyosin with the cardiac sarcomere. Paper-14470282.
We also describe the correlation between TPM1 and DCN expression and the presence of KRAS mutations in CRC. Paper-13995610.
Analysis of cardiac performance revealed impaired cardiac function in TM180 and TM180/ AE3 mutants. Paper-15610521.
Biochemical and immunohistochemical studies on tropomyosin and glutamate dehydrogenase in the chicken liver. Paper-9514002.
The present study investigated the role of tropomyosin in TGF-beta1-mediated cell motility and invasion. Paper-12550835.
Structure and tropomyosin binding properties of the N-terminal capping domain of tropomodulin 1. Paper-10741987.
Novel mutation in the alpha-tropomyosin gene and transition from hypertrophic to hypocontractile dilated cardiomyopathy. Paper-8624666.
Assignment of the human alpha-tropomyosin gene TPM4 to band 19p13.1 by fluorescence in situ hybridization. Paper-558525.
A missense mutation in the alpha-tropomyosin gene ( TPM3) has been associated with NEM1 in one family. Paper-2091956.
Mutations in beta-tropomyosin ( TPM2) have recently been identified as an important cause of neuromuscular disorders. Paper-14429327.
The coiled-coil interactions of TM-5 with other low and high molecular weight TM isoforms were studied. Paper-587245.
Both methods suggest that Tm is synthesized and accumulated at a greater rate than myosin heavy chain. Paper-5848257.
Further experiments targeted the interacting domains to G821-R878 of PC2 and A152-E196, a common segment of TM-1 and TM-1a. Paper-9659022.
Adenovirus mediated expression of cofilin is able to relieve the tropomyosin 1 induced effects on cytokinesis. Paper-14473590.
Congenital myopathy with nemaline rods and cap structures caused by a mutation in the beta-tropomyosin gene ( TPM2). Paper-13430706.
Tropomodulin- binding site mapped to residues 7-14 at the N-terminal heptad repeats of tropomyosin isoform 5. Paper-8390224.
These data indicate the importance of the nebulette- TPM interactions in the maintenance and stability of the thin filaments. Paper-14470282.
Among the cytoskeleton-associated proteins that were highly expressed in Prdx6-deficient LECs was tropomyosin (Tm)2beta. Paper-14216845.
A mutation in the alpha tropomyosin gene TPM3 associated with autosomal dominant nemaline myopathy NEM1. Paper-346061.
Furthermore, although calponin also binds to tropomyosin, ATPase inhibition was not dependent on the presence of tropomyosin. Paper-11924.
Altogether, the aforementioned 6 mutations found in MYBPC3, TPM1, and MYH7 accounted for 61% of familial and 40% of all HCM cases. Paper-10231908.
Diastolic ventricular dysfunction as a marker for hypertrophic cardiomyopathy in a family with a novel alpha-tropomyosin mutation. Paper-10027011.
Polarization of specific tropomyosin isoforms in gastrointestinal epithelial cells and their impact on CFTR at the apical surface. Paper-10115537.
Coordinate expression of alpha-tropomyosin and caldesmon isoforms in association with phenotypic modulation of smooth muscle cells. Paper-1056539.
We have previously cloned the human E-Tmod cDNA, identified its TM-binding region, and mapped its gene to chromosome 9q22. Paper-8577467.
Systematic analysis of tropomodulin/ tropomyosin interactions uncovers fine-tuned binding specificity of intrinsically disordered proteins. Paper-15888898.
From these results, we propose two hypotheses on the physiological roles of the interaction between TM and GDH in nonmuscle cells. Paper-9514002.
Treatment of these cells with demethylating agent 5-aza-2'-deoxycytidine (5-aza-dC) increased mRNA levels of TPM1 with no effect on TPM2. Paper-11093251.
These include alpha-actin (ACTA1), alpha- and beta- tropomyosin ( TPM3 and TPM2), troponin T ( TNNT1), and nebulin ( NEB). Paper-10660953.
The slow alpha-tropomyosin ( TPM3) gene has to date been associated with few cases of both dominant and recessive nemaline myopathies. Paper-13175967.
Contraction is associated with phosphorylation of small heat shock protein, HSP27 concomitant with the phosphorylation of TM and CaD. Paper-14167567.
Phosphorylated HSP20 modulates the association of thin-filament binding proteins: caldesmon with tropomyosin in colonic smooth muscle. Paper-15407653.
We identified a new TM-1 splicing isoform in kidney and heart (TM-1a) that differs from TM-1 in the C terminus and interacted with PC2. Paper-9659022.
Following 5 days of T3 treatment, the synthetic rates of Tm and MHC are 266 and 70 times the control values, respectively. Paper-5848257.
Tmod1- TM control of actin filament length is hypothesized to regulate spectrin-actin lattice organization and membrane stability. Paper-15427499.
A missense mutation, Glu41Lys, in the beta-tropomyosin gene TPM2 was identified in both patients but was absent in their healthy relatives. Paper-13430706.
Thin-filament regulation of actomyosin interaction is modulated by two actin binding regulatory proteins tropomyosin ( TM) and caldesmon ( CaD). Paper-14167567.
Contraction is associated with phosphorylation of the small heat shock protein HSP27, concomitant with the phosphorylation of TM and CaD. Paper-15904441.
RESULTS: We detected significant previously undescribed underexpression in CRC for genes SLC26A3, TPM1 and DCN, with a suggested tumour suppressor role. Paper-13995610.
When searching for chromosomal abnormalities, we found deletion of the TPM1 gene in one case of CRC, but no deletions of DCN and SLC26A3 were found. Paper-13995610.
Indirect double immunofluorescence experiments showed partial co-localization of PC2 and TM-1 in transfected mouse fibroblast NIH 3T3 cells. Paper-9659022.
In this study, we have identified several amino acid residues on Tmod-1 that are important for its interaction with TM5 (a nonmuscle TM isoform). Paper-11310064.
Vimentin, two of the tropomyosin isoforms, a protein with M(r) approximately 90,000 and a protein with M(r) approximately 200,000 were found to be degraded. Paper-7276768.
TGF-beta induction of stress fibers in epithelial cells requires high molecular weight tropomyosins encoded by TPM1 and TPM2 genes. Paper-11093251.
Fine mapping of five human skeletal muscle genes: alpha-tropomyosin, beta-tropomyosin, troponin-I slow-twitch, troponin-I fast-twitch, and troponin-C fast. Paper-887373.
Expression of internal deletions of nebulette verifies that a site between module 10 and 15 is important for TPM maintenance within the sarcomeric lattice. Paper-14470282.
Histidine-proline rich glycoprotein ( HPRG) binds and transduces anti-angiogenic signals through cell surface tropomyosin on endothelial cells. Paper-10533417.
BACKGROUND: Two missense mutations in the gene for alpha-tropomyosin have been described that segregate with hypertrophic cardiomyopathy in single families. Paper-216170.
Cleavage of human and mouse cytoskeletal and sarcomeric proteins by human immunodeficiency virus type 1 protease. Actin, desmin, myosin, and tropomyosin. Paper-80782.
Thin-filament regulation of actomyosin interaction is modulated by two actin-binding regulatory proteins: tropomyosin ( TM) and caldesmon ( CaD). Paper-15904441.
Presence of activating KRAS mutations correlates significantly with expression of tumour suppressor genes DCN and TPM1 in colorectal cancer. Paper-13995610.
We examined the localization of TM and GDH by immunohistochemistry and revealed that they were distributed in the cytoplasm of the adult chicken liver. Paper-9514002.
Mapping the tropomyosin isoform 5 binding site on human erythrocyte tropomodulin: further insights into E-Tmod/ TM5 interaction. Paper-11467341.
Thyroid hormone induces synthesis and accumulation of tropomyosin and myosin heavy chain in limb buds of premetamorphic tadpoles. Paper-5848257.
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.
The mobility of the crosslinked product on SDS-PAGE gels indicated the formation of a 1:1 complex between S100A2 and TM and the interaction was Ca2+ dependent. Paper-1013518.
In addition, these findings provide the strongest genetic evidence that mutations in the alpha-tropomyosin gene are directly responsible for hypertrophic cardiomyopathy. Paper-216170.
This length may be in part attributed to a "molecular ruler" made of erythrocyte tropomodulin ( E-Tmod) and tropomyosin ( TM) isoforms 5 or 5b. Paper-11467341.
In this patient, we demonstrate heterozygosity for a de novo CGT-CAT (Arg167His) mutation in a constitutively expressed exon (exon 5) of slow alpha-tropomyosin ( TPM3). Paper-9651439.
The binding of the 10-kD protein to GST/ TM2 was dependent on the presence of Ca2+ and inhibited by molar excess of free TM2 in a competition assay. Paper-8151862.
Thus, in the TM180 cardiomyopathy model, loss of AE3 had no apparent anti-hypertrophic effect and led to more rapid decompensation and heart failure. Paper-15610521.
Moreover, we found underexpression of the TPM1 gene in a case of CRCs without KRAS mutations, showing that TPM1 might serve as an alternative path of development of CRC. Paper-13995610.
For alpha-tropomyosin, regulation of splicing by PTB and U2AF primarily affected the joining of exons 1-3 with no dramatic increases in 1-2 splicing being detected. Paper-422261.
Coding sequence rare variants identified in MYBPC3, MYH6, TPM1, TNNC1, and TNNI3 from 312 patients with familial or idiopathic dilated cardiomyopathy. Paper-15251240.
These genes--cardiac beta myosin heavy chain, alpha tropomyosin, and troponin T--code for proteins that are integral components of the sarcomere. Paper-291485.
Leucine 135 of tropomodulin-1 regulates its association with tropomyosin, its cellular localization, and the integrity of sarcomeres. Paper-11310064.
These results suggest that HPRG binds to endothelial cell surface tropomyosin which at least partially mediates the antiangiogenic effects of HPRG. Paper-10533417.
CONCLUSIONS: miR-21 is an independent prognostic indicator for TSCC, and may play a role in TSCC development by inhibiting cancer cell apoptosis partly via TPM1 silencing. Paper-13840804.
In erythrocytes, the E-Tmod/ TM complex contributes to the formation of the short actin protofilament, which in turn defines the geometry of the membrane skeleton. Paper-8577467.
In vitro biochemical methods, including GST pull-down, blot overlay and microtiter binding assays, confirmed the interaction between PC2 and the two TM-1 isoforms. Paper-9659022.
The 1q22-->q23 localization of TPM3 is within the NEM1 locus associated with autosomal dominant nemaline myopathy, making TPM3 a candidate for this disorder. Paper-137796.
Loss of AE3 had no effect on hypertrophy; however, survival of TM180/ AE3 double mutants was sharply reduced compared with TM180 single mutants. Paper-15610521.
Indirect immunofluorescence localization detects the accumulation of both MHC and Tm in the developing thigh region within 24 h of T3 treatment. Paper-5848257.
Here we demonstrate that expressions of alpha-tropomyosin and caldesmon isoforms are coordinately regulated in association with phenotypic modulation of smooth muscle cells. Paper-1056539.
Tropomodulin is a globular protein that caps the pointed end of actin filaments by complexing with the N-terminus of a tropomyosin ( TM) molecule. Paper-8390224.
Furthermore, the in vivo interaction between the endogenous PC2 and TM-1 was demonstrated also by reciprocal co-IP using native human embryonic kidney cells and human adult kidney. Paper-9659022.
Earlier studies identified two regions in Tmod1 that bind the N terminus of TM, though the ability of different isoforms to bind the two sites is controversial. Paper-13416887.
The relative expression of the corresponding S1 MHC and S1 Tm isoforms was measured in the same samples with PCR primers designed according to previously identified sequences. Paper-10444444.
The N-terminal "KRK ring" may participate in balancing electrostatic force with hydrophobic interaction in dimerization of TM and its binding to E-Tmod. Paper-11467341.
The results indicate that the K178E mutation has a localized effect on a structure that is critical to the regulatory function of the second actin- Tm binding region of cTnI. Paper-11503960.
By binding to the N-terminus of tropomyosin ( TM) and actin, E-Tmod blocks the elongation and depolymerization of the actin filaments at the pointed end. Paper-8577467.
The tropomodulin ( Tmod) family of proteins that cap the pointed, slow-growing end of actin filaments require tropomyosin ( TM) for optimal function. Paper-13416887.
Quantitative immunochemical determinations indicate that within 24 h of T3 treatment, synthesis of Tm and MHC are increased 23-fold and 6-fold, respectively. Paper-5848257.
Tropomodulin-1 ( Tmod-1) is a well defined actin-capping protein that interacts with tropomyosin ( TM) at the pointed end of actin filaments. Paper-11310064.
Erythrocyte tropomodulin ( E-Tmod or Tmod1) of 41 kDa is a tropomyosin (TM)-binding protein that caps the slow-growing end of the actin filaments. Paper-15392722.
Transmitral Doppler flow indexes suggested impaired diastolic filling in the PLB/N27A mice, but improved LV diastolic function in the PLB/KO mice and TM-180 mutants. Paper-10955912.
We show that the interactions of Wt- tpm3 with actin and tropomyosin are comparable to those of fast alpha tropomyosin isolated from chicken striated muscle. Paper-9528201.
We conclude that Tm isoforms Tm5a and/or Tm5b mark an apical population of microfilaments that can regulate the insertion and/or retention of CFTR into the plasma membrane. Paper-10115537.
In contrast to EDNRB, signaling through EDNRA induced cell rounding, which correlated with FAK inhibition and TM1 and RhoA protein destabilization in the presence of tenascin-C. Paper-13329874.
In endothelial cells, oxidative stress quickly activates the extracellular-signal-regulated kinase ( ERK) MAP kinase, which results in the phosphorylation of tropomyosin. Paper-12571479.
An approximately 105/110-kDa 4.1R isoform appears to occur in vivo in a supramolecular complex with major sarcomeric proteins, including myosin, alpha-actin, and alpha-tropomyosin. Paper-8474539.
Concomitant to the decrease of TnC mRNAs in antisense oligomer-treated cells, the steady-state levels of alpha-actin and alpha-tropomyosin mRNAs were also reduced by approximately 20 to 40%. Paper-22744.
NMR and circular dichroism were used to determine the structure of a peptide containing residues 1-92 of tropomodulin (Tmod1(1-92)) and to define its TM binding site. Paper-10741987.
METHODS: Lewis rats were immunized with bovine alpha- TPM and another group of rats was treated with neutralizing anti- tumor necrosis factor-alpha ( TNF-alpha) antibodies. Paper-12578881.
RESULTS: In the SGF system, proteins such as actin and myosin heavy chain ( MHC) were rapidly degraded within a short period of time, while TM was relatively resistant to pepsin digestion. Paper-15545611.
The altered events include the EGFR, LR, FAS, intracellular Ca(2+) , OPN secretion, caspace-3, gelsolin, Tm-4, Tm-1, and adherens junction proteins, E-cadherin and β-catenin. Paper-16107622.
The ionophore had little or no effect on the synthesis of total myotube proteins, but caused a marked decrease in the synthesis of MHC, LC1f, LC2f, Ac, TM, and Dm after 48 h. Paper-4873091.
Zero-length chemical crosslinking with 1-ethyl-3-[3-(dimethyl amino)propyl]carbodiimide (EDC) indicated an association of the Ca2+-binding protein S100A2 with tropomyosin ( TM) in vitro. Paper-1013518.
HnRNP G acts via a specific sequence to repress the skeletal muscle-specific exon (SK) of human slow skeletal alpha-tropomyosin, TPM3, and stimulates inclusion of the alternative non-muscle exon. Paper-9899039.
CONCLUSIONS: De novo mutations in the alpha-tropomyosin gene can result in hypertrophic cardiomyopathy that may appear to be sporadic but in subsequent generations gives rise to familial disease. Paper-216170.
Co-immunoprecipitation (co-IP) studies using 3T3 cells and Xenopus oocytes co-expressing PC2 and TM-1 (or TM-1a) revealed in vivo association between the protein pairs. Paper-9659022.
In unstimulated cells, tropomyosin-1 was found diffuse in the cells, whereas it quickly colocalized with actin and stress fibers upon stimulation of ERK by H(2)O(2) or by expression of MEK(CA). Paper-9704463.
We found homozygosity in two of the families at 1q12-21.2, a region encompassing the gamma-tropomyosin gene ( TPM3) encoding slow skeletal muscle alpha-tropomyosin, a known NM gene. Paper-12916390.
Using a yeast two-hybrid screen, we identified a specific interaction between the PC2 cytoplasmic C-terminal domain and tropomyosin-1 ( TM-1), a component of the actin microfilament complex. Paper-9659022.
DAP kinase mediates the phosphorylation of tropomyosin-1 downstream of the ERK pathway, which regulates the formation of stress fibers in response to oxidative stress. Paper-12571479.
Our data demonstrate the possible interaction of S100A2 with TM that is not bound to the microfilaments and indicate a differentiation-related function for S100A2 in LLC PK1 cells. Paper-1013518.
In SGF system, proteins such as actin and the original band of myosin heavy chain ( MHC) were rapidly degraded within a short period of time, while TM was relatively resistant to pepsin digestion. Paper-15238284.
TM180/ AE3 double mutants were more severely affected and exhibited little response to β-adrenergic stimulation, a likely consequence of their more rapid progression to heart failure. Paper-15610521.
Taken together, these results suggest that SRF and Barx1b are coordinately involved in the SMC-specific transcription of the beta- TM gene in the upper digestive organs and their attached arteries. Paper-8840504.
In the SGF system, proteins such as the original band of myosin heavy chain ( MHC) and actin were rapidly degraded within a short period of time, while TM was relatively resistant to pepsin digestion. Paper-15302807.
The circular dichroism changes in the Tmod upon binding and modeling of the Tmod sequences suggest that the interface between TM and Tmod includes a three- or four-stranded coiled coil. Paper-9438629.
The affinity of model peptides derived from the N-terminus of different TM isoforms to protein fragments that correspond to the two TM- binding sites of different Tmod isoforms were analyzed. Paper-15888898.
We conclude that tropomyosin 1 and cofilin play antagonistic roles within the contractile ring and that the balance between tropomyosin 1 and cofilin expression is important for cytokinesis. Paper-14473590.
The functional consequence of the sequence differences is reflected in more effective inhibition of actin filament elongation by full-length alpha-TMs than gamma- TM in the presence of Tmod1. Paper-13416887.
TM-5 and TM-4 were capable of dimerizing with each other as well as with other low molecular weight isoforms (TM-5a and TM-5b), but not with the HMW isoforms ( TM-1, TM-2, and TM-3). Paper-587245.
Furthermore, CSMC preincubated with VIP showed a reduced association of TM with HSP27 and with phospho-HSP27 (ser78) while there was reduced dissociation of TM from CaD and from phospho- CaD. Paper-14167567.
Accompanying these changes, the levels of the expression of high molecular weight tropomyosin ( TM) isoforms, especially TM1 and TM2, were significantly increased in the TGFbeta1-treated cells. Paper-1319794.
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.
Tropomyosin phosphorylation was also induced by expression of a constitutively activated form of MEK1 (MEK(CA)), which confirms that its phosphorylation resulted from the activation of ERK. Paper-9704463.
Extracellular signal-regulated kinase mediates phosphorylation of tropomyosin-1 to promote cytoskeleton remodeling in response to oxidative stress: impact on membrane blebbing. Paper-9704463.
Tropomodulin binds to tropomyosin ( TM) and to the pointed end of actin filaments and "caps" the pointed end (i.e., inhibits its polymerization and depolymerization). Paper-10741987.
Complementary DNAs (cDNA) encoding an S2 isoform of myosin heavy chain ( MHC) and an S2 isoform of tropomyosin ( Tm) were isolated from the superficial abdominal flexor muscles of adult lobsters. Paper-10444444.
Transforming growth factor beta1 increases the expressions of high molecular weight tropomyosin isoforms and vinculin and suppresses the transformed phenotypes in human lung carcinoma cells. Paper-1319794.
Serum response factor and Barx1b bound each other directly, coordinately transactivated the beta- TM gene in differentiated SMCs and heterologous cells, and formed a ternary complex with a CArG probe. Paper-8840504.
We propose that phosphorylation of tropomyosin-1 downstream of ERK by contributing to formation of actin filaments increases cellular contractility and promotes the formation of focal adhesions. Paper-9704463.
The NMR and CD studies show that there is an increase in alpha-helix upon Tmod1- TM complex formation, indicating that intrinsically disordered regions of the two proteins become ordered upon binding. Paper-13416887.
METHODS AND RESULTS: The presence or absence of an alpha-tropomyosin mutation and the haplotypes of the flanking chromosomal regions were determined for members of a family with hypertrophic cardiomyopathy. Paper-216170.
The 10-kD protein was isolated from an extract of NIH 3T3 cells transformed by v-Ha-ras by affinity chromatography on a GST/ TM2 truncation mutant followed by SDS-PAGE and electroelution. Paper-8151862.
We identified, for the first time, death-associated protein kinase 1 ( DAP kinase 1) as the kinase that phosphorylates tropomyosin-1 in response to ERK activation by hydrogen peroxide (H(2)O(2)). Paper-12571479.
RESULTS: Six recombinant crustacean proteins: TM, AK, SCP, a novel MLC, troponin C (TnC), and triosephosphate isomerase ( TIM) bound IgE in ImmunoCAP analysis. Paper-16176518.
We describe two patients, a woman and her daughter, with muscle weakness and distal arthrogryposis (DA) type 2B, caused by a heterozygous missense mutation, R133W, in TPM2, the gene encoding beta- TM. Paper-13141569.
Rabbit antisera evoked by a purified fragment of type 5 M protein crossreacted with myosin, but not alpha-tropomyosin, actin, or myosin light chains. Paper-5110213.
To test these hypotheses we crossed AE3-null mice, which appear phenotypically normal, with a hypertrophic cardiomyopathy mouse model carrying a Glu180Gly mutation in α- tropomyosin ( TM180). Paper-15610521.
Index patients were screened for mutations in all coding regions of 10 sarcomere genes ( MYH7, MYL3, MYBPC3, TNNI3, TNNT2, TPM1, ACTC, CSRP3, TCAP, and TNNC1) and five exons of TTN. Paper-13640748.
Furthermore, cells expressing increased levels of tropomyosin 1 usually fail to complete cytokinesis and this is accompanied by reduced accumulation of actin depolymerising factor/ cofilin in the contractile ring. Paper-14473590.
The mutation identified in this patient is an in-frame deletion (c.415_417delGAG) of one codon in exon 4 of TPM2 removing a single glutamate residue (p.Glu139del) from the beta-tropomyosin protein. Paper-13260998.
Immunoprecipitation studies using anti-beta-actin antibody revealed that several actin-binding proteins implicated in cells include formin-2 (FMN-2), caldesmon ( CaD), tropomyosin ( Tm), and profilin. Paper-14183455.
During metamorphosis the adult-type area gradually expanded from dorsal to ventral slides with an anteroposterior gradient with increase in adult-type (adult-type MHC and beta- TM-positive) muscle fibers. Paper-7964170.
FABP5, PABPC1, DDX5, SF3B1, EIF3S6 and Cks2 expression levels were significantly increased, and TPM2 and TAGLN were significantly decreased, in superficial bladder cancer compared with normal bladder tissue. Paper-16009376.
Furthermore, CSMC preincubated with VIP showed a reduced association of TM with HSP27 and with phospho-HSP27 (ser78) whereas there was reduced dissociation of TM from CaD and from phospho- CaD. Paper-15904441.
The short actin filaments in the red blood cell (RBC) membrane skeleton are capped at their pointed ends by tropomodulin 1 ( Tmod1) and coated with tropomyosin ( TM) along their length. Paper-15427499.
Knowing the residues responsible for isoform-specific affinity creates a tool suitable for studying the influence of Tmod/ TM interactions on sarcomere assembly in muscle cells or actin dynamics in non-muscle cells. Paper-15888898.
The apparent TM association constant ( Ka) was taken as the free concentration at half saturation and was found to be 3 microM for TM-5 compared to 2 microM for TM-5b at an F-actin concentration of 42 microM. Paper-587245.
In this study we undertook a systematic analysis of the specificity of the tropomodulin ( Tmod) interaction with tropomyosin ( TM) to show that affinities of different Tmod isoforms to TM are isoform-dependent. Paper-15888898.
In order to detect novel mutations we screened the sarcomeric protein genes beta-myosin heavy chain ( MYH7), myosin-binding protein C ( MYBPC3), troponin T (TNNT2), and alpha-tropomyosin ( TPM1) in 46 young patients with DCM. Paper-9455291.
Immunofluorescence confocal scanning microscopy indicated that changes in the subcellular distribution of Tm and CaD, in which the diffuse cytosolic staining was shifted to show colocalization with actin stress fibers. Paper-14183455.
In addition, we measured the relative proportions of MHC, troponin (Tn) T and I protein isoforms present in the same samples to examine the correlation of these proteins with one another and with the MHC and Tm mRNAs. Paper-10444444.
Immunoprecipitations of [35S]methionine-labeled extracts using S100A2 as well as TM-specific antibodies failed to co-precipitate TM and S100A2, indicating a transient association between these two molecules in solution. Paper-1013518.
The reduction of TM- binding ability was relatively mild (reduced approximately 20-40%) from the G136A Tmod mutant but more substantially (reduced approximately 50-100%) from the I134D, L135E, and L135V Tmod mutants. Paper-11310064.
Glutathione-Sepharose beads bearing GST/ TM2 were incubated with [35S]methionine-labeled NIH 3T3 cell extracts and the materials bound to the fusion proteins were analyzed to identify proteins that interact with TM2. Paper-8151862.
Expression of the three homeobox genes Otx, Cnox1-Pc, and Cnox3-Pc; a specific splice variant of the myosin heavy chain gene ( Myo1); and a tropomyosin ( Tpm2) is stable in isolated and cultured striated muscle tissue. Paper-1980497.
The binding sites of the two Tmod1 peptides on a model TM peptide differ, as defined by comparing (15)N,(1)H HSQC spectra of a (15)N-labeled model TM peptide in both the absence and presence of Tmod1 peptide. Paper-13416887.
We thus propose the crucial physiological relevance of molecular signaling switch ( phosphorylation state of HSP27 and HSP20), which dictates 1) the phosphorylation states of TM and CaD and 2) their dissociations from each other. Paper-15407653.
By radiation hybrid mapping, TPM1 was assigned to chromosome 15q22.1, TPM2 to chromosome 9p13.2-p13.1, TNNI1 to chromosome 1q31.3, TNNI2 to chromosome 11p15.5, and TNNC2 to chromosome 20q12-q13.11. Paper-887373.
Our patient has an identical TPM2 mutation to the first genetically diagnosed cap disease patient, a denovo heterozygous three base pair deletion that removes glutamic acid 139 from the centre of beta-tropomyosin (p.E139del). Paper-13750956.
Myosin heavy chain ( MHC) and tropomyosin ( Tm) have been isolated from limb muscles of the North American bullfrog, Rana catesbeiana, and injected into rabbits to raise monospecific antibodies. Paper-5848257.
Considering previous reports that TM-1 acts as a suppressor of neoplastic growth of transformed cells, it is possible that TM-1 contributes to cyst formation/growth when the anchorage of PC2 to the actin microfilament via TM-1 is altered. Paper-9659022.
Semi-nondenaturing 2D-PAGE revealed that partially purified GDH from the nuclear fraction was associated with TM, but not GDH from the mitochondrial fraction, suggesting preferential binding of TM to GDH. Paper-9514002.
Previous studies have shown that three distinct genes encode six isoforms of tropomyosin ( TM) in rat fibroblasts: the alpha gene encodes TM-2, TM-3, TM-5a, and TM-5b, the beta gene encodes TM-1, and the TM-4 gene encodes TM-4. Paper-587245.
GDH alone also co-precipitated with F-actin, but the amount of GDH sedimenting with F-actin was increased in the presence of chicken liver TM, suggesting that GDH is involved in the regulation of the actin cytoskeleton. Paper-9514002.
These genes include alpha-skeletal actin (ACTA1), beta- tropomyosin ( TPM2), alpha-tropomyosin slow ( TPM3), nebulin ( NEB), troponin I fast (TNNI2), troponin T slow (TNNT1), troponin T fast (TNNT3) and cofilin ( CFL2). Paper-14498662.
This review examines echocardiographic indices of LV diastole (focusing on color M-mode) in mice with abnormal LV relaxation and hypertrophic cardiomyopathy based on genetic alterations of phospholamban and alpha-tropomyosin, respectively. Paper-10955912.
Our finding that tropomyosin-1 is phosphorylated downstream of ERK, an event that modulates its interaction with actin, may lead to further understanding of the role of this protein in regulating cellular functions associated with cytoskeletal remodeling. Paper-9704463.
Three genes are known to cause nemaline myopathy: the genes for nebulin ( NEB) on chromosome 2q22, slow alpha-tropomyosin ( TPM3) on chromosome 1q21 and skeletal muscle alpha-actin ( ACTA1) on chromosome 1q42. Paper-8732933.
We, therefore, screened HCM patients for mutations in six sarcomeric genes: myosin-binding protein C3 ( MYBPC3), MYH7, cardiac troponin T ( TNNT2), alpha-tropomyosin ( TPM1), cardiac troponin I ( TNNI3), and cardiac troponin C ( TNNC1). Paper-9986591.
DNA was obtained after informed consent; specific MHY7, TNNT2, and TPM1 fragments were amplified by polymerase chain reaction; and the mutations were detected by denaturing high-performance liquid chromatography and automated DNA sequencing. Paper-9227578.
These antibodies were used to study the localization and synthesis of myosin heavy chain and tropomyosin in the limb buds of premetamorphic (stage VI-VII) tadpoles treated with triiodothyronine ( T3) to induce metamorphosis. Paper-5848257.
Included in the study are the reduced and oxidized (disulfide cross-linked) forms of alpha alpha- and beta beta-tropomyosin, and the forms of alpha alpha-tropomyosin in which all sulfhydryl groups have been blocked by carboxymethylation or carboxyamidomethylation. Paper-7064013.
Immunoblotting of mouse skeletal and human pectoral muscle myofibrils treated in vitro with human immunodeficiency virus type 1 protease showed that myosin heavy chain, desmin, tropomyosin, and a fraction of the actin were all cleaved. Paper-80782.
Imaging analysis of isolated myocytes revealed reductions in amplitude and decay of Ca(2+) transients in both mutants, with greater reductions in TM180/ AE3 mutants, consistent with the greater severity of their heart failure phenotype. Paper-15610521.
Moreover, the expression of the pseudophosphorylated tropomyosin mutant Ser283Glu triggers by itself the formation of stress fibers in untreated cells, and the effect is maintained in H(2)O(2)-treated cells in which DAP kinase expression is knocked-down by siRNA. Paper-12571479.
Since the N-terminal residues need to overlap with the C-terminus of TM in their head-to-tail association, this investigation elucidates the mechanisms by which the tropomodulin- hTM5 complex is formed and functions in regulating the actin filaments. Paper-8390224.
Reverse transcriptase-polymerase chain reaction ( RT-PCR) and real-time PCR revealed a significant increase in the expression of mRNAs for basic (h1) calponin ( CaP), and alpha-isoform of tropomyosin ( Tm) in hypertrophied DSM compared to controls. Paper-10836999.
The cDNA coding for mouse fibroblast tropomyosin isoform 2 ( TM2) was placed into a bacterial expression vector to produce a fusion protein containing glutathione-S-transferase ( GST) and TM2 ( GST/ TM2). Paper-8151862.
Tropomodulin 1 has two distinct actin-capping regions: a folded C-terminal domain (residues 160-359), which does not bind to TM, and a conserved, N-terminal region, within residues 1-92 that binds TM and requires TM for capping activity. Paper-10741987.
Analysis by electrophoresis revealed that isoforms of myosin heavy chain ( MHC) switched from larval to adult type and adult-specific beta- tropomyosin ( TM) appeared during metamorphosis in addition to preexisting alpha- TM. Paper-7964170.
Overexpression of the nebulette C-terminal linker and/or SH3 domains in chicken cardiomyocytes results in a loss of endogenous nebulette with a concomitant loss of tropomyosin ( TPM) and troponin, as well as a shortening of the thin filaments. Paper-14470282.
Recently, we have reported a novel tropomyosin ( TM) -binding protein, glutamate dehydrogenase ( GDH) and demonstrated by affinity column chromatography that chicken liver TM interacts with GDH in an ATP-dependent manner. Paper-9514002.
These variants were 12 MYBPC3 (myosin-binding protein C) in 13 (4.2%) probands, 8 MYH6 (alpha-myosin heavy chain) in 10 (3.2%), 6 TPM1 ( tropomyosin) in 6 (1.9%), 4 TNNC1 (cardiac troponin C) in 4 (1.3%), and 1 TNNI3 ( cardiac troponin I) in 2 (0.6%). Paper-15251240.
Our finding that tropomyosin-1 is phosphorylated downstream of ERK and DAP kinase and that it helps regulate the formation of stress fibers will aid understanding the role of this protein in regulating the endothelial functions associated with cytoskeletal remodeling. Paper-12571479.
Analysis of the homology of the sense sequence of this oligomer with that of alpha-actin and alpha-tropomyosin mRNAs suggested that reduction in the level of alpha-actin and alpha-tropomyosin mRNAs was not due to direct hybridization of the antisense oligomer to these mRNAs. Paper-22744.
To elucidate the physiological roles of the interaction between TM and GDH, we performed co-sedimentation assays of TM and GDH with F-actin, because it is known that TM exerts its physiological functions by associating with actin filaments. Paper-9514002.
The protein-coding sequences of 9 sarcomere protein genes ( MYH7, MYBPC3, TNNI3, TNNT2, TPM1, MYL2, MYL3, ACTC, and TNNC1), the genes encoding desmin ( DES), and the gamma-2 subunit of AMP kinase ( PRKAG2) were screened for mutations. Paper-14621066.
A model proposed for the binding of Tmod to actin and TM at the pointed end of the filament shows how the Tmod- TM accentuates the asymmetry of the pointed end and suggests how subtle differences among TM isoforms may modulate actin filament dynamics. Paper-13416887.
A large number of mutations in genes coding for the beta-myosin heavy chain (beta-MyHC), cardiac troponin T ( cTnT), cardiac troponin I, alpha-tropomyosin, myosin binding protein C (MyBP-C), and myosin light chain 1 and 2 in patients with HCM have been identified. Paper-1349329.
Patients were genetically screened by capillary electrophoresis single strand conformation polymorphism and subsequently by bidirectional DNA sequencing of conformers in the coding regions of MYH7, MYBPC3, TPM1, ACTC, MYL2, MYL3, TNNT2, CSRP3 and TNNI3. Paper-14009084.
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.
This system can now be used to accurately demonstrate the effect of this (and other disease-associated tropomyosin mutations) on the interactions of tpm3 with the other protein components of the muscle thin filament, including those responsible for differing forms of nemaline myopathy. Paper-9528201.
Here we report the characterization of a cDNA clone encoding the most recent rat fibroblast TM to be identified, herein referred to as TM-5, that is the product of a fourth gene that is homologous to the human hTMnm gene, herein referred to as the rat slow-twitch alpha TM gene. Paper-587245.
Accordingly, diastolic function was assessed in PLB knockout mice ( PLB/KO) and age-matched transgenic mice expressing a mutant, superinhibiting form of PLB ( PLB/N27A), and in mice with cardiac-specific expression a mutant a- tropomyosin ( TM-180). Paper-10955912.
Affinity chromatography of cell extracts on immobilized recombinant TMs, however, confirmed the Ca2+-dependent interaction between S100A2 and both muscle TMs as well as with high and low molecular mass nonmuscle TMs, suggesting that the binding site resides in one of the conserved regions of TM. Paper-1013518.
In this paper the chromosomal localization of the human skeletal muscle genes Troponin-I slow-twitch ( TNNI1), Troponin-I fast-twitch ( TNNI2), and Troponin-C fast ( TNNC2) and the refinement of the position for alpha-Tropomyosin ( TPM1) and beta-Tropomyosin ( TPM2) are reported. Paper-887373.
Mutations in six genes have been reported to cause NM: Nebulin (NEB Pelin 1999), alpha-skeletal muscle actin (ACTA1 Nowak 1999), alpha-slow tropomyosin ( TPM3 Laing 1995), beta- tropomyosin ( TPM2 Donner 2002), slow troponin T (TNNT1 Johnston 2000) and cofilin 2 ( CFL2 Agrawal 2007). Paper-14693429.
In this present study, circular dichroism was used to study the interaction of two designed chimeric proteins, AcTM1aZip and AcTM1bZip, containing the N terminus of a long or a short TM, respectively, with protein fragments containing residues 1 to 130 of erythrocyte or skeletal muscle Tmod. Paper-9438629.
We used model peptides to determine the affinity and define the specificity of the highly conserved N termini of three short, non-muscle TMs (alpha, gamma, delta- TM) for the two Tmod1 binding sites using circular dichroism spectroscopy, native gel electrophoresis, and chemical crosslinking. Paper-13416887.
Phospholamban ( PLB) reversibly inhibits the sarcoplasmic reticulum Ca(2+) ATPase and is a crucial regulator of myocardial relaxation; tropomyosin is a contractile protein that plays a critical role in regulating contractile activity vis-à-vis interactions with the actin and troponin complex. Paper-10955912.
HPRG is evolutionarily, functionally and structurally related to cleaved high molecular weight kininogen (HKa), an anti-angiogenic polypeptide that stimulates apoptosis of proliferating endothelial cells through binding to cell-surface tropomyosin (Zhang J-C, et al. Proc Natl Acad Sci USA 2002; 99: 12224-9). Paper-10533417.
This is the first mutation identified in a constitutively expressed exon of TPM3 in a nemaline myopathy patient, but is similar to recently described mutations in beta- tropomyosin ( TPM2) associated with nemaline myopathy and mutations in fast alpha-tropomyosin ( TPM1) which cause hypertrophic cardiomyopathy. Paper-9651439.
A total of 34 different mutations were identified in 108 patients: 18 mutations in MYBPC3 in 20 patients [ intervening sequence ( intron) 7 + 1G > A and Q1233X were found twice], 13 missense mutations in MYH7 in 14 patients (R807H was found twice), and one amino acid change in TPM1, TNNT2, and TNNI3, respectively. Paper-9986591.
All TM peptides have high affinity for the second Tmod1 binding site (within residues 109-144; alpha- TM, 2.5 nM; gamma- TM, delta- TM, 40-90 nM), but differ >100-fold for the first site (residues 1-38; alpha- TM, 90 nM; undetectable at 10 microM, gamma- TM, delta- TM). Paper-13416887.
The DCM mutations reviewed here are those of the beta-myosin heavy chain (beta-MHC), myosin binding protein-C (MyBP-C), actin, alpha- tropomyosin ( Tm), troponin T (TnT), troponin I (TnI), troponin C (TnC), of the sarcomere, and titin, T-cap, desmin, vinculin, and muscle LIM protein ( MLP) of the cytoskeleton. Paper-11503924.
The genes encode cytoskeletal tropomyosin TM30nm ( TPM3), HS1-binding protein Hax-1 (HAX1), RNA-specific adenosine deaminase (ADAR1), the 34/67-kD laminin receptor (LAMRL6), and the 26S proteasome subunit p31 (PSMD8L), as well as five hitherto uncharacterized proteins ( NICE-1, NICE-2, NICE-3, NICE-4, and NICE-5). Paper-8789069.
Cathepsin D precursor, peroxiredoxin 6 ( PDX6), heat shock protein 27 (HSP27), HSP60, tropomyosin 1 ( TPM1), TPM2, TPM3, TPM4, 14-3-3 protein epsilon, and tumor protein D54 were up-regulated in the highly metastatic variant, whereas alpha B-crystalline (CRAB) was only detected in its parental counterpart. Paper-12022886.
BACKGROUND: Genotype-phenotype correlative studies have implicated 8 particular mutations that cause hypertrophic cardiomyopathy (HCM) as "benign defects," associated with near-normal survival: N232S, G256E, F513C, V606M, R719Q, and L908V of beta-myosin heavy chain ( MYH7); S179F of troponin T ( TNNT2); and D175N of alpha-tropomyosin ( TPM1). Paper-9227578.
An intact coiled coil at the N terminus of the TMs is essential for Tmod binding, as modifications that disrupt the N-terminal helix, such as removal of the N-terminal acetyl group from AcTM1aZip or striated muscle alpha- TM, or introduction of a mutation that causes nemaline myopathy, Met-8-Arg, into AcTM1aZip destroyed Tmod binding. Paper-9438629.
A recessive mutation causing nemaline myopathy among the Old Order Amish has recently been identified in the gene for slow skeletal muscle troponin T. As linkage studies had shown that at least one further gene exists for nemaline myopathy, we investigated another tropomyosin gene expressed in skeletal muscle, the beta-tropomyosin 2 gene. Paper-9345083.
CSMC transfected with 16D-HSP20 cDNA showed significant decreases in 1) phosphorylation of HSP27 (ser78); 2) phosphorylation of PKC-α (ser657); 3) phosphorylation of TM and CaD (ser789); 4) ACh-induced phosphorylation of myosin light chain; 5) ACh-induced association of TM with HSP27; and 6) ACh-induced dissociation of TM from caldesmon ( CaD). Paper-15407653.
These synonyms are used for gene TPM1 (tropomyosin 1 (alpha)): Tropomyosin alpha-1 chain, Tropomyosin-1, TMSA, HTM-alpha, CMH3, CMD1Y, C15orf13, Alpha-tropomyosin.
These accession numbers are used for gene TPM1: Q86W64 (UNIPROT__AC), P10469 (UNIPROT__AC), L02923 (NCBI_GENBANK__AC), CR625156 (NCBI_GENBANK__AC).
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