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CPE is thus not essential for sorting proinsulin to granules. Paper-1231629.
Antisera to the N- and C-terminal regions of CPE do not recognize CPD. Paper-382371.
This demonstrates that CPE is required for normal SP proteolytic processing. Paper-1589568.
To study the mechanisms of CPE, we examined induction of iNOS and COX-2. Paper-13312781.
Of these 150 genes, all but two, HMG14 and carboxypeptidase E, were upregulated with age. Paper-10157043.
Role of carboxypeptidase E in processing of pro- islet amyloid polypeptide in {beta}-cells. Paper-11060452.
The mutation resulted in a loss of CpE activity that correlated with aberrant proinsulin processing. Paper-655326.
The CPH tumours expressed similar amounts of c-myc and c-raf-1 mRNA, and neither expressed N-myc or L-myc. Paper-39641.
Our data are consistent with a deficit in CpE activity affecting the maturation of both pro- NT and pro- MCH. Paper-655326.
We conclude that stomach CPE activity is essential for gastric secretory activity and for challenged gastrin release. Paper-1706536.
These results demonstrate that the CPE mutation differentially affects CCK processing in these two cell types. Paper-1593634.
Polyadenylation activity correlates with p82 binding in wild-type and CPE-mutant RR 3' UTR RNAs. Paper-1718368.
Alkaline phosphatase expression by MDFC was increased by CPE (1.0 microgram/ml), in comparison to the control. Paper-1153815.
CPE clearly induced phosphorylation of IkappaBalpha, suggesting a role as an NF-kappaB activator. Paper-13312781.
Both modulations of iNOS and COX-2 expression by CPE were evaluated by Western immunoblotting and RT-PCR. Paper-13312781.
Beta-cell lines derived from transgenic Cpe(fat)/Cpe(fat) mice are defective in carboxypeptidase E and proinsulin processing. Paper-1216471.
Proinsulin targeting to the regulated pathway is not impaired in carboxypeptidase E-deficient Cpefat/Cpefat mice. Paper-1231629.
Interaction between secretogranin III and carboxypeptidase E facilitates prohormone sorting within secretory granules. Paper-11537480.
A major difference between the two enzymes is the molecular masses; CPE is 50,000-56,000, whereas CPD is approximately 180,000. Paper-382371.
Transcriptional regulators Cph1p and Efg1p mediate activation of the Candida albicans virulence gene SAP5 during infection. Paper-9183487.
Ca2+ depletion also decreased proteolytic maturation of the prohormone convertases PC1, PC2 and carboxypeptidase H. Paper-1003876.
For example, three CPE-like proteins contain a Tyr in place of Glu300 (equivalent to Glu270 of carboxypeptidase A and B). Paper-1831938.
Sorting and activity-dependent secretion of BDNF require interaction of a specific motif with the sorting receptor carboxypeptidase e. Paper-11297511.
Effect of carboxypeptidase E deficiency on progastrin processing and gastrin messenger ribonucleic acid expression in mice with the fat mutation. Paper-978415.
A bi-directional carboxypeptidase E-driven transport mechanism controls BDNF vesicle homeostasis in hippocampal neurons. Paper-12918165.
Enhancement was blocked by GEMSA, a specific inhibitor of CPE activity, and could be duplicated by other carboxypeptidases, including CPD, CPB, or CPM. Paper-1296622.
Altered biosynthesis and secretion of pro-opiomelanocortin in the intermediate and anterior pituitary of carboxypeptidase E-deficient, Cpe(fat)/ Cpe(fat)mice. Paper-8268722.
In contrast, carboxypeptidase H or peripherin do not induce a similar protective effect, suggesting that GAD has a critical role in the diabetogenic response. Paper-8115394.
(35)S labeling experiments demonstrated that activity-dependent secretion of BDNF from cortical neurons was obliterated in CPE knockout mice. Paper-11297511.
Carboxypeptidase E deficiency as seen in the fat/fat mice is associated with reduced antral somatostatin content but tripling of the progastrin product. Paper-2101134.
A spontaneous point mutation in the coding region of the carboxypeptidase E ( CPE) gene in Cpe(fat)/Cpe(fat) mice affects proinsulin processing. Paper-1216471.
These results demonstrate that CPE is required for the correct processing of arginine- and glycine-extended CCK in all major regions of the mouse brain. Paper-1878218.
The obesity susceptibility gene Cpe links FoxO1 signaling in hypothalamic pro-opiomelanocortin neurons with regulation of food intake. Paper-14037253.
Levels of PAM mRNA generally changed in parallel with levels of PAE mRNA; in contrast, levels of carboxypeptidase-E mRNA were unaffected by any of the secretagogues tested. Paper-6524496.
Live-cell imaging showed that the velocity and distance of movement of fluorescent protein-tagged CPE- or BDNF-containing vesicles were reduced in both directions. Paper-12918165.
It is concluded that in CPE-deficient Cpefat/Cpefat mice, proinsulin is efficiently routed to the regulated pathway and its release can be effectively stimulated by secretagogues. Paper-1231629.
During inhibition of stimulated secretion with glucocorticoids or cobalt ions, secretion of PAM activity, enkephalin convertase activity, and immunoactive hormone fell in parallel. Paper-4777409.
Cholecystokinin ( CCK) amide concentrations were reduced over 85% in all the major brain regions of carboxypeptidase E (Cpe)(fat)/Cpe(fat) mice in comparison to control mice. Paper-1878218.
Modeling and binding studies showed interaction of the acidic residues in the BDNF motif with two basic residues in the sorting receptor, carboxypeptidase E ( CPE). Paper-11297511.
We have reported previously that CPE activity was absent in the antrum of the stomach and that processing of progastrin to the amidated biologically active form of gastrin is reduced. Paper-1706536.
Together, the data indicate that posttranslational processing of CPE occurs in secretory granules and that this activity may be mediated by a prohormone convertase-like enzyme. Paper-7832342.
We investigated the binding of SgIII and CPE because they frequently localize close to the periphery of SGs, and they bind each other in mouse corticotrope-derived AtT-20 cells. Paper-11537480.
NPY activation is complex, requiring sequential actions of a prohormone convertase ( PC), carboxypeptidase H, and peptidylglycine alpha-amidating mono-oxygenase. Paper-476677.
These results indicate that CPE is needed for processing progastrin to gastrin in the stomach and that amidated gastrin exerts an inhibitory feedback effect on gastrin mRNA levels. Paper-978415.
To investigate the importance of this position, Glu300 of rat CPE was converted into Gln, Lys, or Tyr, and the proteins expressed in Sf9 cells using the baculovirus system. Paper-1831938.
The secretion of insulin/ proinsulin from NIT-2 and -3 cells is significantly elevated by secretagogues, indicating that CPE is not required for sorting proinsulin into the regulated pathway. Paper-1216471.
New evidence shows that interaction between a motif in the tertiary structure of BDNF and the sorting receptor carboxypeptidase E directs this neurotrophin to the regulated secretory pathway. Paper-10790000.
The Cpe fat pituitary exhibited elevated levels of SgIII and CgA, which suggests that they compensate for a sorting function of CPE for POMC and its intermediates to ACTH. Paper-11537480.
Our results show that Cpe and Carboxypeptidase D ( Cpd), another carboxypeptidase with a very similar function, are strictly co-localized in the mouse placenta from late mid-gestation to term. Paper-12360091.
The presence of mutant carboxypeptidase E in granules supports a potential role for its involvement as a sorting/retention receptor in the trafficking of proinsulin to the regulated secretory pathway. Paper-9739530.
Most secretory pathway peptides were much lower in Cpe(fat/fat) mouse brain, relative to WT mouse brain, indicating that CPE plays a major role in their biosynthesis. Paper-13512353.
In contrast, levels of enkephalin convertase activity, cell protein, lactate dehydrogenase, fumarase, and lysosomal carboxypeptidase did not decline in response to chronic glucocorticoid exposure. Paper-4777409.
Taking all this together, we conclude that CPE isolated from Curcuma xanthorrhiza stimulates the immune functions of macrophages, which is mediated in part by specific activation of NF-kappaB. Paper-13312781.
Carboxypeptidase D is a potential candidate to carry out redundant processing functions of carboxypeptidase E based on comparative distribution studies in the rat central nervous system. Paper-1908515.
CPE was rapidly secreted from the astrocytes after a 30-min lag time, presumably reflecting transport through the endoplasmic reticulum and Golgi apparatus, followed by constitutive secretion. Paper-7354272.
An obese mouse, called Cpe(fat)/Cpe(fat), has a missense mutation in carboxypeptidase E ( CPE) with no pancreatic CPE activity and a reduced processing of pancreatic proinsulin to insulin. Paper-978415.
Microarray-based transcriptional profiling of Cpe mutant placentas identified only a very small number of genes with altered expression, including Dtprp, which belongs to the prolactin gene family. Paper-12360091.
Two CPE-containing synaptonemal complex protein mRNAs, which interact with CPEB in vitro and in vivo, contained shortened poly(A) tails and mostly failed to sediment with polysomes in the null mice. Paper-9090968.
Although the transgenic mice were born in the expected frequency, 21 of 22 proSAAS transgenic Cpe (fat/fat) mice died between 11 and 26 weeks of age, presumably due to greatly elevated blood glucose. Paper-10232068.
The fat mutation maps to mouse chromosome 8, very close to the gene for carboxypeptidase E ( Cpe), which encodes an enzyme ( CPE) that processes prohormone intermediates such as proinsulin. Paper-346049.
Secretogranin III ( SgIII) and carboxypeptidase E ( CPE) bind specifically to cholesterol-rich secretory granule ( SG) membranes. Paper-11537480.
After genetic knockout of PC2 or its helper protein 7B2, but not after mutation of carboxypeptidase E, endoproteolytic processing decreased, as indicated by appearance of intermediate-sized processing products. Paper-9587575.
Upon stimulation with a beta-adrenergic agonist, a phorbol ester, a calcium ionophore, or forskolin, the secretion of DCE activity was increased; this rise was parallel to the secretion of CPE activity and ACTH. Paper-7200422.
This study examines the role of carboxypeptidase E ( CPE) in processing pro tachykinin to form the final bioactive amidated undecapeptide, substance P ( SP) in various rat brain regions. Paper-1589568.
In the brain, bioactive CCK was markedly reduced (7.9+/-1.0 pmol/g in fat/fat mice vs. 82.5+/-11.2 pmol/g in controls), but the concentration of the CPE substrate, glycylarginine-extended CCK, was elevated 105-fold. Paper-1593634.
In our study, overexpression of the cytoplasmic tail of the carboxypeptidase E ( CPE) found in BDNF vesicles significantly reduced localization of BDNF in neurites of hippocampal neurons. Paper-12918165.
Carboxypeptidase E ( CPE) is a sorting receptor that directs the prohormone pro-opiomelanocortin ( POMC) to the regulated secretory pathway, and is also a prohormone processing enzyme in neuro/endocrine cells. Paper-9350870.
In a competitive pull-down assay, excessive SgIII led to a decrease in CPE- bound POMC-derived intermediate molecules, and SgIII pulled-down by anti-ACTH antibody increased proportionately. Paper-11537480.
CPE significantly increased the phagocytosis of macrophages and the release of NO, H2O2, TNF-alpha, and PGE2 in a dose-dependent manner, and showed a similar activity to lipopolysaccharide (LPS). Paper-13312781.
While treatment with IFN-alpha or IFN-gamma alone has weak antiviral action, HSV-2 plaque formation, viral replication and the onset of viral CPE in Vero cells are synergistically inhibited by interferon combination. Paper-12078073.
In the present study, we investigated the effect of CPE on nitric oxide (NO), hydrogen peroxide (H2O2), tumor necrosis factor-alpha ( TNF-alpha), and prostaglandin E2 ( PGE2) production in RAW 264.7 cells. Paper-13312781.
However, this mutant produced filaments in the tongues of immunosuppressed gnotobiotic piglets and when embedded in agar, demonstrating that an Efg1p- and Cph1p-independent pathway for promotion of filamentous growth exists. Paper-1909046.
No measurable secretion of cytosolic, mitochondrial, or lysosomal marker enzymes was detected, indicating that the secretion of PAM activity and enkephalin convertase activity was specific and not a result of cell damage or lysis. Paper-4777409.
Thus, the CPE cytoplasmic tail binds dynactin that recruits kinesins or dynein for driving bi-directional transport of BDNF vesicle to maintain vesicle homeostasis and secretion in hippocampal neurons. Paper-12918165.
Carboxypeptidase H ( CPH; EC 3.4.17.10) removes basic residues from the carboxyterminus of the products of endoproteolytic cleavage of prohormones and is generally essential in the formation of substrates for PAM. Paper-7208111.
Substance P has numerous functions in the brain; therefore, SP deficiency due to the CPE mutation may contribute to the obese phenotype or even to other phenotypes not yet described in Cpe(fat)/Cpe(fat) mice. Paper-1589568.
Effects on posttranslational processing enzymes were evaluated by measuring levels of the mRNAs encoding carboxypeptidase-E and peptidyl-glycine-alpha-amidating monooxygenase ( PAM); cellular levels of PAM activity were also measured. Paper-6524496.
These data provide evidence that the lack of carboxypeptidase E, the sorting receptor, results in the intracellular misrouting and secretion of pro-opiomelanocortin and growth hormone via the constitutive pathway in the pituitary of Cpefat mice. Paper-1012345.
Recently, a receptor to which these sorting signals bind has been identified as the membrane form of carboxypeptidase E ( CPE) and localized to the Golgi apparatus, where sorting occurs, specifically at the trans-Golgi network. Paper-12778894.
The levels of several pituitary peptides were significantly reduced in the proSAAS transgenic Cpe (fat/fat) mice relative to non-transgenic Cpe (fat/fat) mice, suggesting that the transgene inhibited prohormone convertase 1 in these mice. Paper-10232068.
Secretion of peptidyl-glycine alpha-amidating monooxygenase ( PAM) activity and enkephalin convertase (a carboxypeptidase B-like enzyme) activity from AtT-20 mouse corticotrope tumor cells was compared with secretion of pro-ACTH/endorphin-derived peptides. Paper-4777409.
Using a technique to identify substrates of the peptide processing enzyme carboxypeptidase E ( CPE), several novel peptides were detected in the brain and pituitary of Cpe(fat)/Cpe(fat) mice and found to be derived from a single precursor, termed proSAAS. Paper-8959052.
The mutant CPE as well as prohormone convertase 2 were secreted into the medium in a stimulated manner by treatment with the physiological secretagogue, glucagon-like peptide-1, consistent with its presence in granules of the regulated secretory pathway. Paper-9739530.
Since CPE converts many prohormones to hormones, a deficiency of biologically active cholecystokinin is a likely contributor to enhanced susceptibility to cholelithiasis through compromising gallbladder contractility and small intestinal motility. Paper-9232882.
Following a 15-min pulse with [35S]Met, both soluble and membrane-bound forms of CPE were identified, indicating that the posttranslational processing event that generates these forms of CPE occurs in the endoplasmic reticulum or early Golgi apparatus. Paper-7832342.
NK activity was studied against the 51Cr-radiolabelled Moloney virus-induced lymphoid cell line YAC 1, while IFN titres were determined by the inhibition of cytopathology of vesicular stomatitis virus on L929 cells, scored for CPE after 24 h from viral infection. Paper-4325688.
Several proSAAS-derived peptides were previously identified in the brain and pituitary of the Cpe(fat)/Cpe(fat) mouse based on the accumulation of C-terminally extended peptides due to the absence of enzymatically active carboxypeptidase E, a peptide-processing exopeptidase. Paper-8699975.
Analysis of anterior pituitaries from AQP1 knockout mice showed reduced prohormone convertase 1/3, carboxypeptidase E, and ACTH levels compared to wild-type mice demonstrating that our results observed in AtT20 cells can be extended to the animal model. Paper-12943853.
Adult carboxypeptidase E-deficient fat/fat mice have a near-total depletion of brain CCK 8 accompanied by a massive accumulation of glycine and arginine extended CCK: identification of CCK 8 Gly as the immediate precursor of CCK 8 in rodent brain. Paper-1878218.
Because the inhibitory potency of proSAAS-derived peptides towards prohormone convertase 1 is much greater in the absence of carboxypeptidase E activity, the proSAAS transgene was also expressed in carboxypeptidase E-deficient Cpe (fat/fat) mice. Paper-10232068.
From this, we successfully identified six putative caspase substrates, including five novel proteins ( ABCF1, AKAP1, CPE, DOPEY1 and GOPC1) that may be targeted specifically by the initiator caspases 8 and 10 during the early stages of apoptosis. Paper-12750584.
Carboxypeptidase E ( CPE) has important functions in processing of endocrine pro-peptides, such as pro-insulin, pro-opiomelanocortin, or pro-gonadotropin-releasing hormone, as evidenced by the hyper-pro-insulinemia, obesity, and sterility of Cpe mutant mice. Paper-12360091.
The biosynthesis and secretion of pro-opiomelanocortin ( POMC) was examined in the pituitary of Cpe(fat)/ Cpe(fat)mice, which are deficient in carboxypeptidase E, a sorting receptor for the regulated secretory pathway (Cool D R, Normant E, Shen F S, et al. Cell 1997; 83: 73-83). Paper-8268722.
Several active site-directed inhibitors also show generally similar potency toward the two enzymes, although guanidinoethylmercaptosuccinic acid is approximately 10-fold more potent, and hippuryl-Arg is approximately 100-fold more potent as an inhibitor of CPD than of CPE. Paper-382371.
We suggest that SgIII and CPE form the separate functional sorting complex by anchoring to cholesterol-rich SG membranes, and POMC-derived peptides are transferred from CPE to SgIII, and subsequently to CgA. Paper-11537480.
An inherited defect in the fat/fat mouse which affects the processing of proinsulin, and probably also many other prohormones, due to a point mutation in carboxypeptidase E has recently been identified and has begun to provide new insights into the functional integration of the individual processing steps. Paper-470538.
Both SgIII and CgA were solubilized from the SGM by Triton X-100 in contrast to the Triton X-100 insolubility of carboxypeptidase E. SgIII and carboxypeptidase E strongly bound to the SGM-type liposome in intragranular conditions, but CgA did not. Paper-10328133.
With respect to the PC pathway, human pituitary expresses PC1/3 and PC2 of ~60-65 kDa, which represent active PC1/3 and PC2; peptide hormone production then utilizes carboxypeptidase E ( CPE) which is present as a protein of ~55 kDa. Paper-13808598.
Taken together, these data suggest that CPE is completely inactive in the Cpefat/Cpefat mice, and that all of the CPE-like activity is due to other carboxypeptidases such as carboxypeptidase D. Levels of Leu-enkephalin in Cpefat/Cpefat mouse brain are approximately 5-fold lower than those in control brain. Paper-796255.
In double-label immunofluorescence microscopy, a portion of the mutant CPE did not colocalize with calnexin, an endoplasmic reticulum marker, but was found in prohormone convertase 2-containing secretory granules, demonstrating that it had escaped degradation and arrived at a post-Golgi compartment. Paper-9739530.
Because studies have identified membrane carboxypeptidase E as a sorting receptor for targeting prohormones to the regulated secretory pathway for processing and secretion, the intracellular routing and secretion of pro-opiomelanocortin/adrenocorticotropin and growth hormone from anterior pituitary cells were investigated in Cpefat mice. Paper-1012345.
To know whether CPE is implicated in proinsulin sorting, pancreatic islets were isolated from CPE-deficient Cpefat/Cpefat mice and Cpefat/+ controls, pulse-labeled ([3H]leucine), and then chased in basal medium (90 min) to examine constitutive secretion followed by medium with secretagogues (60 min) to stimulate regulated secretion. Paper-1231629.
Concordant deregulation of Cpe and Cpd in abnormal placentas of interspecies hybrids before the onset of IHPD phenotype and recapitulation of some phenotypes of IHPD hyperplastic placentas in Cpe mutant placentas suggests that these two genes are causally involved in IHPD and may function as speciation genes in the genus Mus. Paper-12360091.
We show that FoxO1 ablation in pro-opiomelanocortin (Pomc)- expressing neurons in mice (here called Pomc-Foxo1(-/-) mice) increases Carboxypeptidase E ( Cpe) expression, resulting in selective increases of alpha-melanocyte-stimulating hormone (alpha-Msh) and carboxy-cleaved beta-endorphin, the products of Cpe-dependent processing of Pomc. Paper-14037253.
These synonyms are used for gene Cpe (carboxypeptidase E): R74677, Prohormone-processing carboxypeptidase, MGC7101, fat, Enkephalin convertase, Cph-1, Cph1, CPH, CPE, Carboxypeptidase H, carboxypeptidase H, Carboxypeptidase E.
These accession numbers are used for gene Cpe: Q64439 (UNIPROT__AC), Q543R4 (UNIPROT__AC), CAA43550 (NCBI_GENBANK__AC), AAH10197 (NCBI_GENBANK__AC).
Cpe is a homologue of zgc:85981 (zgc:85981) from Danio rerio.
Cpe is a homologue of egl-21 (EGg Laying defective) from Caenorhabditis elegans.
Cpe is a homologue of CPE (carboxypeptidase E) from Homo sapiens.
Cpe is a homologue of CPE (carboxypeptidase E) from Pan troglodytes.
Cpe is a homologue of CPE (carboxypeptidase E) from Gallus gallus.
Cpe is a homologue of CPE (carboxypeptidase E) from Canis lupus familiaris.
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