Aliases for APELA Gene
External Ids for APELA Gene
Previous GeneCards Identifiers for APELA Gene
This gene encodes a peptide hormone that binds to the Apelin receptor. The encoded protein is required for heart development in zebrafish and has been shown to maintain self-renewal of human embryonic stem cells through activation of the PI3K/AKT pathway. Experiments in human and mouse cell lines point to additional roles for the encoded protein in angiogenesis and regulation of vascular tone. [provided by RefSeq, Jul 2016]
GeneCards Summary for APELA Gene
APELA (Apelin Receptor Early Endogenous Ligand) is a Protein Coding gene. Diseases associated with APELA include Thyroid Cancer, Nonmedullary, 1 and Vaginal Mullerian Papilloma. Gene Ontology (GO) annotations related to this gene include hormone activity and apelin receptor binding.
UniProtKB/Swiss-Prot Summary for APELA Gene
Endogenous ligand for the apelin receptor (APLNR) (PubMed:25639753, PubMed:28137936). Hormone required for mesendodermal differentiation, blood vessels formation and heart morphogenesis during early development and for adult cardiovascular homeostasis (PubMed:25639753, PubMed:28137936). Drives internalization of APLNR. Acts as a motogen by promoting mesendodermal cell migration during gastrulation by binding and activating APLNR. Acts as an early embryonic regulator of cellular movement with a role in migration and development of cardiac progenitor cells. May act as a chemoattractant for the activation of angioblast migration toward the embryonic midline, i.e. the position of the future vessel formation, during vasculogenesis. Positively regulates sinus venosus (SV)-derived endothelial cells migration into the developing heart to promote coronary blood vessel sprouting. Plays a role in placental vascular development; promotes placental trophoblast invasion and spiral artery remodeling in the uterus. Involved in the regulation of maternal cardiovascular homeostasis to prevent gestational hypertension and for potent cardioprotective functions during heart failure. Mediates myocardial contractility in an ERK1/2-dependent manner (By similarity).