PDCD10

This gene encodes an evolutionarily conserved protein associated with cell apoptosis. The protein interacts with the serine/threonine protein kinase MST4 to modulate the extracellular signal-regulated kinase (ERK) pathway. It also interacts with and is phosphoryated by serine/threonine kinase 25, and is thought to function in a signaling pathway essential for vascular developent. Mutations in this gene are one cause of cerebral cavernous malformations, which are vascular malformations that cause seizures and cerebral hemorrhages. Multiple alternatively spliced variants, encoding the same protein, have been identified. [provided by RefSeq]

Full Name

programmed cell death 10

Function

Promotes cell proliferation. Modulates apoptotic pathways. Increases mitogen-activated protein kinase activity and STK26 activity (PubMed:27807006).
Important for cell migration, and for normal structure and assembly of the Golgi complex (PubMed:27807006).
Important for KDR/VEGFR2 signaling. Increases the stability of KDR/VEGFR2 and prevents its breakdown. Required for normal cardiovascular development. Required for normal angiogenesis, vasculogenesis and hematopoiesis during embryonic development (By similarity).

Biological Process

AngiogenesisIEA:UniProtKB-KW
Cellular response to leukemia inhibitory factorIEA:Ensembl
Endothelium development1 PublicationIC:ComplexPortal
Establishment of Golgi localizationManual Assertion Based On ExperimentIMP:UniProtKB
Golgi reassemblyManual Assertion Based On ExperimentIMP:UniProtKB
Intrinsic apoptotic signaling pathway in response to hydrogen peroxideManual Assertion Based On ExperimentIGI:UniProtKB
Negative regulation of apoptotic processManual Assertion Based On ExperimentIDA:UniProtKB
Negative regulation of blood vessel endothelial cell proliferation involved in sprouting angiogenesisManual Assertion Based On ExperimentIMP:UniProtKB
Negative regulation of cell migration involved in sprouting angiogenesisManual Assertion Based On ExperimentIMP:UniProtKB
Negative regulation of gene expressionManual Assertion Based On ExperimentIMP:UniProtKB
Positive regulation of cell migrationManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of cell population proliferationManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of gene expressionManual Assertion Based On ExperimentIMP:UniProtKB
Positive regulation of intracellular protein transportManual Assertion Based On ExperimentIMP:UniProtKB
Positive regulation of MAP kinase activityManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of Notch signaling pathwayManual Assertion Based On ExperimentIMP:UniProtKB
Positive regulation of peptidyl-serine phosphorylationManual Assertion Based On ExperimentIMP:UniProtKB
Positive regulation of protein serine/threonine kinase activityManual Assertion Based On ExperimentIMP:UniProtKB
Positive regulation of stress-activated MAPK cascadeManual Assertion Based On ExperimentIDA:UniProtKB
Protein stabilizationManual Assertion Based On ExperimentIMP:UniProtKB
Regulation of angiogenesis1 PublicationIC:ComplexPortal
Regulation of Golgi organizationManual Assertion Based On ExperimentIBA:GO_Central
Response to hydrogen peroxideManual Assertion Based On ExperimentIDA:UniProtKB
Wound healing, spreading of cellsManual Assertion Based On ExperimentIMP:UniProtKB

Cellular Location

Cytoplasm
Golgi apparatus membrane
Cell membrane
Partially co-localizes with endogenous PXN at the leading edges of migrating cells.

Involvement in disease

Cerebral cavernous malformations 3 (CCM3):
A form of cerebral cavernous malformations, a congenital vascular anomaly of the central nervous system that can result in hemorrhagic stroke, seizures, recurrent headaches, and focal neurologic deficits. The lesions are characterized by grossly enlarged blood vessels consisting of a single layer of endothelium and without any intervening neural tissue, ranging in diameter from a few millimeters to several centimeters. CCM3 inheritance is autosomal dominant.