scholarly journals Organization and chromosomal localization of the human ECEL1 (XCE) gene encoding a zinc metallopeptidase involved in the nervous control of respiration

2000 ◽  
Vol 346 (3) ◽  
pp. 611-616 ◽  
Author(s):  
Olivier VALDENAIRE ◽  
Elisabeth ROHRBACHER ◽  
An LANGEVELD ◽  
Anja SCHWEIZER ◽  
Carel MEIJERS
Keyword(s):  
Critical Role ◽  
Phylogenetic Study ◽  
Control Of Respiration ◽  
Chromosome 2 ◽  
Converting Enzyme ◽  
Gene Encoding ◽  
Nervous Control ◽  
Zinc Metalloprotease ◽  
Endothelin Converting Enzyme

ECEL1 (endothelin-converting enzyme-like 1; previously known as XCE) is a putative zinc metalloprotease that was identified recently on the basis of its strong identity with endothelin-converting enzyme. Although the physiological function of ECEL1 is unknown, inactivation of the corresponding gene in mice points to a critical role of this protein in the nervous control of respiration. In the present study we have characterized the human ECEL1 gene. It was located to region q36-q37 of chromosome 2 and shown to be composed of 18 exons spanning approx. 8 kb. The structure of the ECEL1 gene displays some striking similarities with those of genes of related metallopeptidases, supporting the hypothesis that they are all derived from a common ancestor. A short phylogenetic study describing the relationship between the various members of this gene family is also presented.

Endothelin-converting enzyme-like I (ECEL1; ‘XCE’): a putative metallopeptidase crucially involved in the nervous control of respiration

2000 ◽  
Vol 28 (4) ◽  
pp. 426-430 ◽  
Author(s):  
O. Valdenaire ◽  
A. Schweizer
Keyword(s):  
Physiological Function ◽  
Control Of Respiration ◽  
Converting Enzyme ◽  
Specific Expression ◽  
Nervous Control ◽  
Zinc Metalloprotease ◽  
Neonatal Lethality ◽  
Its Gene ◽  
Endothelin Converting Enzyme ◽  
The Central Nervous System

Endothelin-converting enzyme-like 1 (ECEL1) is a putative zinc metalloprotease that was recently identified on the basis of its strong similarity to endothelin-converting enzyme 1. The physiological function of ECEL1 remains unknown so far; the failure to identify a substrate for ECEL1 could be related to the endoplasmic reticulum subcellular localization found by immunofluorescence in recombinant systems. However, clues to the function of ECEL1 were provided by the in-activation of its gene in mice, which resulted in neonatal lethality. The phenotype of homozygous ECEL1− mice, together with the very specific expression profile of its mRNA in the central nervous system, suggests that ECEL1 is crucially involved in the nervous control of respiration.

scholarly journals The 3’UTR of the orb2 gene encoding the Drosophila CPEB translation factor plays a critical role in spermatogenesis

2020 ◽  
Author(s):  
Rudolf A. Gilmutdinov ◽  
Eugene N. Kozlov ◽  
Ludmila V. Olenina ◽  
Alexei A. Kotov ◽  
Justinn Barr ◽  
...  
Keyword(s):  
Deletion Mutant ◽  
Critical Role ◽  
Self Regulation ◽  
Biological Processes ◽  
Apparent Effect ◽  
Gene Encoding ◽  
Cytoplasmic Polyadenylation ◽  
Polarized Cells ◽  
Biological Context

AbstractCPEB proteins are conserved translation regulators involved in multiple biological processes. One of these proteins in Drosophila, Orb2, is a principal player in spermatogenesis. It is required for meiosis and spermatid differentiation. During the later process orb2 mRNAs and proteins are localized within the developing spermatid. To evaluate the role of orb2 mRNA 3’UTR in spermatogenesis, we used the CRISPR/Cas9 system to generate a deletion of the orb2 3’UTR, orb2R. This deletion disrupts the process of spermatid differentiation, but has no apparent effect on meiosis. While this deletion appears to destabilize the orb2 mRNA and reduce the levels of Orb2 protein, this is not the primary cause of the differentiation defects. Instead, differentiation appears to be disrupted because orb2 mRNAs and proteins are not properly localized within the differentiating spermatids. Other transcripts and proteins involved in spermatogenesis are also mislocalized in orb2R spermatids.Author summaryThe conserved family of cytoplasmic polyadenylation element binding (CPEB) proteins can activate or repress translation of target mRNAs, depending on the specific biological context, through interaction with special cytoplasmic polyadenylation element (CPE) sequences. These proteins function mainly in highly polarized cells. Orb2, one of the two Drosophila melanogaster CPEB proteins, is predominantly expressed in the testes and is crucial for spermatogenesis. The 3’UTR of orb2 transcript contains multiple CPE-like motifs, which is indicative of orb2 self-regulation. We have generated a deletion that removes the greater portion of 3’UTR. While this deletion causes a reduction in the levels of orb2 mRNA and the protein, this does not appear to be responsible for the defects in spermatogenesis observed in the deletion mutant. Instead, it is the mislocalization of the mRNA and protein in the developing spermatids.

Role of endothelin-converting enzyme, chymase and neutral endopeptidase in the processing of big ET-1, ET-1(1-21) and ET-1(1-31) in the trachea of allergic mice

2002 ◽  
Vol 103 (s2002) ◽  
pp. 353S-356S ◽  
Author(s):  
Benjamin A. DE CAMPO ◽  
Roy G. GOLDIE ◽  
Arco Y. JENG ◽  
Peter J. HENRY
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Response Curve ◽  
Histological Analysis ◽  
Neutral Endopeptidase ◽  
Converting Enzyme ◽  
Rightward Shift ◽  
Endothelin Converting Enzyme ◽  
Mast Cell Chymase

The present study examined the roles of endothelin-converting enzyme (ECE), neutral endopeptidase (NEP) and mast cell chymase as processors of the endothelin (ET) analogues ET-1(1–21), ET-1(1–31) and big ET-1 in the trachea of allergic mice. Male CBA/CaH mice were sensitized with ovalbumin (10µg) delivered intraperitoneal on days 1 and 14, and exposed to aerosolized ovalbumin on days 14, 25, 26 and 27 (OVA mice). Mice were killed and the trachea excised for histological analysis and contraction studies on day 28. Tracheae from OVA mice had 40% more mast cells than vehicle-sensitized mice (sham mice). Ovalbumin (10µg/ml) induced transient contractions (15±3% of the Cmax) in tracheae from OVA mice. The ECE inhibitor CGS35066 (10µM) inhibited contractions induced by big ET-1 (4.8-fold rightward shift of dose-response curve; P<0.05), but not those induced by either ET-1(1–21) or ET-1(1–31). The chymase inhibitors chymostatin (10µM) and Bowman-Birk inhibitor (10µM) had no effect on contractions induced by any of the ET analogues used. The NEP inhibitor CGS24592 (10µM) inhibited contractions induced by ET-1(1–31) (6.2-fold rightward shift; P<0.05) but not ET-1(1–21) or big ET-1. These data suggest that big ET-1 is processed predominantly by a CGS35066-sensitive ECE within allergic airways rather than by mast cell-derived proteases such as chymase. If endogenous ET-1(1–31) is formed within allergic airways, it is likely to undergo further conversion by NEP to more active products.

scholarly journals The Role of Endothelin-Converting Enzyme-1 in the Development of α 1 -Adrenergic-Stimulated Hypertrophy in Cultured Neonatal Rat Cardiac Myocytes

Circulation ◽  
1999 ◽  
Vol 99 (2) ◽  
pp. 292-298 ◽  
Author(s):  
Satoshi Kaburagi ◽  
Koji Hasegawa ◽  
Tatsuya Morimoto ◽  
Makoto Araki ◽  
Tatsuya Sawamura ◽  
...  
Keyword(s):  
Cardiac Myocytes ◽  
Neonatal Rat ◽  
Converting Enzyme ◽  
Endothelin Converting Enzyme ◽  
Neonatal Rat Cardiac Myocytes ◽  
Rat Cardiac Myocytes

scholarly journals Organization and chromosomal localization of the human ECEL1 (XCE) gene encoding a zinc metallopeptidase involved in the nervous control of respiration

2000 ◽  
Vol 346 (3) ◽  
pp. 611 ◽  
Author(s):  
Olivier VALDENAIRE ◽  
Elisabeth ROHRBACHER ◽  
An LANGEVELD ◽  
Anja SCHWEIZER ◽  
Carel MEIJERS
Keyword(s):  
Chromosomal Localization ◽  
Control Of Respiration ◽  
Gene Encoding ◽  
Nervous Control

Abstract 443: Transcription Factor E2F2 Regulates Vessel Contractile Function and Blood Pressure via Isoform-specific Expressions of Endothelin Converting Enzyme-1

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Gangjian Qin ◽  
Yan Zhu ◽  
Raj Kishore ◽  
Deepika Dinesh ◽  
Tina Thorne ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Contractile Function ◽  
Critical Role ◽  
Alternative Promoters ◽  
Converting Enzyme ◽  
Aortic Artery ◽  
Endothelin Converting Enzyme ◽  
Reporter Assays ◽  
E2f Transcription Factors ◽  
Cycle Regulation

E2F transcription factors play critical roles in cell cycle regulation but their cardiovascular specific functions are not well defined. Recent studies have revealed a polymorphism in Endothelin Converting Enzyme-1b (ECE-1b) promoter (C-338A), located within E2F consensus site, which is strongly associated with blood pressure (BP) values in hypertensive women. ECE-1, with four isoforms ECE-1a/b/c/d expressed by the use of alternative promoters, is the major enzyme that catalyzes the biogenesis of the potent vessel-constricting peptide endothelin-1 (ET-1) from its inactive precursor Big-ET-1. The role of E2Fs in ECE-1 bioactivity and BP regulation, however, is unknown. Here we provide evidence that E2F2- but not E2F1-deficient mice display an elevated arterial BP. Loss of E2F2 leads to an aortic artery hypercontractility in response to Big-ET-1, indicating an increased ECE-1 bioactivity. ECE-1b promoter-reporter assays, combined with either E2F2 overexpression or knockdown, confirm that E2F2 regulates ECE-1b transcription. The incorporation of C-338A polymorphism in the promoter confers a higher basal level of the promoter activity and blunts the induction of ECE-1b by E2F2. Among all four isoforms, ECE-1b has been suggested to localize in the late endosome and heterodimerize with cell surface ECE-1a/c/d isoforms for lysosomal degradation, thereby down-regulating their activities. Indeed, we found that knockdown of E2F2 leads to a reduced cytosolic however an increased plasma membrane ECE-1 immunoactivity, corroborating with the hypercontractility of E2F2-deficient vessels. These data indicate that in the normal “non-proliferating” vessels, E2F2 plays a critical role in the maintenance of vascular tone. Deregulated E2F2 activity may contribute to the pathogenesis of hypertension.

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