Endothelin 1

EDN1
Available structures
PDB	Ortholog search: PDBe RCSB
List of PDB id codes
	1EDN, 1EDP, 1T7H, 1V6R, 6DK5, 5GLH
Identifiers
Aliases	EDN1, ARCND3, ET1, HDLCQ7, QME, endothelin 1, PPET1
External IDs	MGI: 95283 HomoloGene: 1476 GeneCards: EDN1
Gene location (Human)
Chr.	Chromosome 6 (human)[1]
End	12,297,194 bp[1]
Gene location (Mouse)
Chr.	Chromosome 13 (mouse)[2]
End	42,307,990 bp[2]
RNA expression pattern
	More reference expression data
Gene ontology
Molecular function	• hormone activity; • receptor binding; • cytokine activity; • endothelin B receptor binding; • GO:0001948 protein binding; • endothelin A receptor binding;
Cellular component	• cytoplasm; • Weibel-Palade body; • basal part of cell; • extracellular region; • rough endoplasmic reticulum lumen; • extracellular; • transport vesicle;
Biological process	• skeletal system development; • response to amino acid; • positive regulation of cytosolic calcium ion concentration involved in phospholipase C-activating G-protein coupled signaling pathway; • negative regulation of cellular protein metabolic process; • positive regulation of MAP kinase activity; • regulation of sensory perception of pain; • vasoconstriction; • body fluid secretion; • positive regulation of sarcomere organization; • positive regulation of cardiac muscle hypertrophy; • cell surface receptor signaling pathway; • cellular response to drug; • multicellular organism aging; • artery smooth muscle contraction; • cellular response to interferon-gamma; • positive regulation of chemokine-mediated signaling pathway; • phosphatidylinositol 3-kinase signaling; • response to leptin; • positive regulation of mitotic nuclear division; • cellular response to hypoxia; • response to muscle stretch; • cellular response to calcium ion; • cellular response to transforming growth factor beta stimulus; • positive regulation of renal sodium excretion; • blood vessel morphogenesis; • negative regulation of blood coagulation; • response to nicotine; • in utero embryonic development; • neutrophil chemotaxis; • heart development; • positive regulation of prostaglandin secretion; • vein smooth muscle contraction; • cartilage development; • rhythmic excitation; • protein kinase C-activating G-protein coupled receptor signaling pathway; • cellular response to glucocorticoid stimulus; • branching involved in blood vessel morphogenesis; • negative regulation of hormone secretion; • positive regulation of smooth muscle contraction; • negative regulation of nitric-oxide synthase biosynthetic process; • positive regulation of prostaglandin-endoperoxide synthase activity; • positive regulation of urine volume; • positive regulation of JUN kinase activity; • leukocyte activation; • membrane depolarization; • negative regulation of transcription from RNA polymerase II promoter; • response to ozone; • respiratory gaseous exchange; • positive regulation of heart rate; • regulation of blood pressure; • response to lipopolysaccharide; • response to prostaglandin F; • regulation of vasoconstriction; • cellular response to interleukin-1; • response to salt; • positive regulation of cell size; • middle ear morphogenesis; • nociception; • prostaglandin biosynthetic process; • dorsal/ventral pattern formation; • phospholipase D-activating G-protein coupled receptor signaling pathway; • positive regulation of odontogenesis; • regulation of pH; • positive regulation of smooth muscle cell proliferation; • protein kinase C deactivation; • histamine secretion; • maternal process involved in parturition; • GO:0007243 intracellular signal transduction; • response to hypoxia; • neural crest cell development; • regulation of systemic arterial blood pressure by endothelin; • nitric oxide transport; • positive regulation of cell migration; • response to testosterone; • positive regulation of cytosolic calcium ion concentration; • epithelial fluid transport; • positive regulation of nitric oxide biosynthetic process; • cell-cell signaling; • cellular response to tumor necrosis factor; • response to activity; • response to dexamethasone; • superoxide anion generation; • positive regulation of endothelial cell migration; • cellular response to peptide hormone stimulus; • cellular response to fatty acid; • peptide hormone secretion; • cellular response to mineralocorticoid stimulus; • positive regulation of cell proliferation; • inositol phosphate-mediated signaling; • positive regulation of hormone secretion; • negative regulation of smooth muscle cell apoptotic process; • response to drug; • calcium-mediated signaling; • response to transforming growth factor beta; • positive regulation of transcription from RNA polymerase II promoter; • positive regulation of sequence-specific DNA binding transcription factor activity; • positive regulation of cell growth involved in cardiac muscle cell development; • positive regulation of neutrophil chemotaxis; • regulation of receptor activity; • G-protein coupled receptor signaling pathway; • adenylate cyclase-inhibiting G-protein coupled receptor signaling pathway; • regulation of glucose transport; • negative regulation of gene expression; • positive regulation of NIK/NF-kappaB signaling; • positive regulation of vascular smooth muscle cell proliferation;
	Sources:Amigo / QuickGO
Orthologs
	1906
	13614
	ENSG00000078401
	ENSMUSG00000021367
	P05305
	P22387
	NM_001168319; NM_001955
	NM_010104
	NP_001161791; NP_001946; NP_001161791; NP_001946
	NP_034234
	Wikidata
View/Edit Human	View/Edit Mouse

Endothelin 1 (ET-1), also known as preproendothelin-1 (PPET1), is a potent vasoconstrictor that in humans is encoded by the EDN1 gene and produced by vascular endothelial cells. The protein encoded by this gene is proteolytically processed to release a secreted peptide termed endothelin 1. Endothelin 1 is one of three isoforms of human endothelin.

Source

Preproendothelin is precursor of the peptide ET-1. Endothelial cells convert preproendothelin to proendothelin and subsequently to mature endothelin, which the cells release.[5]

Clinical significance

Long term ET-1 exposure has been associated with hypertrophic cardiomyopathy.[6]

Endothelin-1 receptor antagonists (Bosentan) are used in the treatment of pulmonary hypertension. Inhibition of these receptors prevents pulmonary vasculature constriction and thus decreases pulmonary vascular resistance.

References

GRCh38: Ensembl release 89: ENSG00000078401 - Ensembl, May 2017
GRCm38: Ensembl release 89: ENSMUSG00000021367 - Ensembl, May 2017
"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
Boulpaep EL, Boron WF (2009). Medical physiology: a cellular and molecular approach. Saunders/Elsevier. ISBN 978-1-4160-3115-4.
Archer CR, Robinson EL, Drawnel FM, Roderick HL (August 2017). "Endothelin-1 promotes hypertrophic remodelling of cardiac myocytes by activating sustained signalling and transcription downstream of endothelin type A receptors". Cellular Signalling. 36: 240–254. doi:10.1016/j.cellsig.2017.04.010. PMC 5486433. PMID 28412414.

External links

Overview of all the structural information available in the PDB for UniProt: P05305 (Endothelin-1) at the PDBe-KB.

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.

[refGRCh38Ensembl-1] GRCh38: Ensembl release 89: ENSG00000078401 - Ensembl, May 2017

[refGRCm38Ensembl-2] GRCm38: Ensembl release 89: ENSMUSG00000021367 - Ensembl, May 2017

[3] "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[4] "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.

[isbn1-4160-3115-4-5] Boulpaep EL, Boron WF (2009). Medical physiology: a cellular and molecular approach. Saunders/Elsevier. ISBN 978-1-4160-3115-4.

[6] Archer CR, Robinson EL, Drawnel FM, Roderick HL (August 2017). "Endothelin-1 promotes hypertrophic remodelling of cardiac myocytes by activating sustained signalling and transcription downstream of endothelin type A receptors". Cellular Signalling. 36: 240–254. doi:10.1016/j.cellsig.2017.04.010. PMC 5486433. PMID 28412414.

Endothelin 1

Source

Clinical significance

References

Further reading

External links