Angiopoietin 1

Angiopoietin 1 is a type of angiopoietin and is encoded by the gene ANGPT1.

ANGPT1
Available structures PDB Ortholog search: PDBe RCSB List of PDB id codes 4EPU, 4JYO, 4K0V
Identifiers
Aliases	ANGPT1, AGP1, AGPT, ANG1, angiopoietin 1
External IDs	OMIM: 601667 MGI: 108448 HomoloGene: 37447 GeneCards: ANGPT1
Gene location (Human) Chr. Chromosome 8 (human)[1] Band 8q23.1 Start 107,249,482 bp[1] End 107,498,055 bp[1]
Gene location (Mouse) Chr. Chromosome 15 (mouse)[2] Band 15 B3.1|15 16.69 cM Start 42,424,723 bp[2] End 42,676,977 bp[2]
RNA expression pattern More reference expression data
Gene ontology Molecular function • receptor tyrosine kinase binding • GO:0001948 protein binding • receptor binding • Ras guanyl-nucleotide exchange factor activity Cellular component • cell membrane • microvilli • membrane raft • extracellular exosome • extracellular region • intracellular • extracellular Biological process • negative regulation of neuron apoptotic process • negative regulation of protein phosphorylation • negative regulation of endothelial cell apoptotic process • negative regulation of cell adhesion • cell differentiation • haematopoiesis • positive regulation of protein kinase B signaling • heparin biosynthetic process • positive regulation of receptor internalization • regulation of tumor necrosis factor production • transmembrane receptor protein tyrosine kinase signaling pathway • negative regulation of cytokine secretion involved in immune response • sprouting angiogenesis • in utero embryonic development • negative regulation of apoptotic process • positive regulation of peptidyl-serine phosphorylation • MAPK cascade • positive regulation of endothelial cell migration • multicellular organism development • cell-substrate adhesion • protein localization to cell surface • angiogenesis • positive regulation of blood vessel endothelial cell migration • positive regulation of ERK1 and ERK2 cascade • regulation of macrophage migration inhibitory factor signaling pathway • regulation of endothelial cell proliferation • positive regulation of phosphatidylinositol 3-kinase signaling • positive chemotaxis • activation of transmembrane receptor protein tyrosine kinase activity • regulation of protein binding • regulation of skeletal muscle satellite cell proliferation • positive regulation of protein ubiquitination • leukocyte migration • regulation of I-kappaB kinase/NF-kappaB signaling • negative regulation of protein import into nucleus • positive regulation of cell adhesion • glomerulus vasculature development • negative regulation of vascular permeability • Tie signaling pathway • positive regulation of peptidyl-tyrosine phosphorylation Sources:Amigo / QuickGO
Orthologs
Species	Human	Mouse
Entrez	284	11600
Ensembl	ENSG00000154188	ENSMUSG00000022309
UniProt	Q15389	O08538
RefSeq (mRNA)	NM_001146 NM_001199859 NM_001314051 NM_139290	NM_009640 NM_001286062
RefSeq (protein)	NP_001137 NP_001186788 NP_001300980	NP_001272991 NP_033770
Location (UCSC)	Chr 8: 107.25 – 107.5 Mb	Chr 15: 42.42 – 42.68 Mb
PubMed search	[3]	[4]
Wikidata
View/Edit Human View/Edit Mouse

Angiopoietins are proteins with important roles in vascular development and angiogenesis. All angiopoietins bind with similar affinity to an endothelial cell-specific tyrosine-protein kinase receptor. The protein encoded by this gene is a secreted glycoprotein that activates the receptor by inducing its tyrosine phosphorylation. It plays a critical role in mediating reciprocal interactions between the endothelium and surrounding matrix and mesenchyme. The protein also contributes to blood vessel maturation and stability, and may be involved in early development of the heart.[5] During pregnancy, angiopoietins act complementary to the VEGF system and contribute to endothelial cell survival and the remodeling of vessels. Few studies have examined the role of angiopoietins in human pregnancy complications like preeclampsia and intrauterine growth restriction (IUGR).

A knockout model of ANGPT1 was introduced in mice embryos. Results showed that embryos began to appear abnormal by day 11 and were dead by day 12.5 of pregnancy. The embryos showed prominent defects in endocardial and myocardial development as well as a less complex vascular network.

[6][7]