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PDCD10 encodes an evolutionarily conserved protein associated with cell apoptosis. Additionally we are shipping PDCD10 Antibodies (59) and PDCD10 Proteins (9) and many more products for this protein.
CCM3 restrains ANGPT2 (show UNC13B ELISA Kits)release from endothelial cells and maintains endot (show VAMP3 ELISA Kits)helial junctions. CCM3 depletion leads to increa (show ANGPT2 ELISA Kits)sed ANGPT2 release.
Data indicated that rs9853967 and rs11714980 polymorphisms in CCM3 and SERPINI1respectively could be associated with a protective role in cerebral cavernous malformations disease.
Inhibition of Notch (show NOTCH1 ELISA Kits) and activation of VEGF (show VEGFA ELISA Kits)/p38 (show CRK ELISA Kits) signaling were involved in miR (show MLXIP ELISA Kits)-425-5p/CCM3 mediated inhibition of angiogenesis by sodium arsenite.
Loss of endothelial programmed cell death 10 activates glioblastoma cells and promotes tumor growth.
Studies suggest that the 3 proteins of the Cerebral Cavernous Malformations (CCM) complex KRIT1/CCM1 (show KRIT1 ELISA Kits), CCM2/malcavernin (show CCM2 ELISA Kits) and CCM3/PDCD10 not only require one another for reciprocal stabilization, but also act as a platform for signal transduction.
Study highlights the potential role of CCM3 in regulating tight junction complex organization and brain endothelial barrier permeability through CCM3-ERK1/2 (show MAPK1/3 ELISA Kits)-cortactin (show CTTN ELISA Kits) cross-talk
A novel CCM3 missense mutation (c.422T>G) detected in 2 Greek brothers with cerebral cavernous malformations causes a loss of function in Pdcd10 protein due to its localization in the 8th helix. It affects Leu141. It may play a role in angiogenesis.
The proto-oncogene (show RAB1A ELISA Kits) PDCD10 is direct target of miR (show MLXIP ELISA Kits)-103 that can suppress Prostate cancer proliferation and migration by down-regulating the PDCD10.
We report for the first time that PDCD10 expression is downregulated in GBM, which is associated with the activation of Akt (show AKT1 ELISA Kits) signaling protein
miR (show MLXIP ELISA Kits)-181b was upregulated by hypoxia in retinoblastoma in an HIF-1a (show HIF1A ELISA Kits)-independent manner. Additionally, miR (show MLXIP ELISA Kits)-181b exerts its angiogenic function, at least in part, by inhibiting PDCD10 and GATA6 (show GATA6 ELISA Kits).
CCM3 suppresses UNC13B (show UNC13B ELISA Kits)- and vesicle-associated membrane protein 3 (VAMP3 (show VAMP3 ELISA Kits))-dependent exocytosis of angiopoietin 2 (ANGPT2 (show ANGPT2 ELISA Kits)) in brain endothelial cells. CCM3 deficiency in endothelial cells augments the exocytosis and secretion of ANGPT2 (show ANGPT2 ELISA Kits), which is associated with destabilized endothelial cell junctions, enlarged lumen formation and endothelial cell-pericyte dissociation.
CCM3 expression and it's role during ovary and testis development
Study shows that PDCD10 mutations result in vascular permeability mediated by ROCK activity and a particularly severe clinical phenotype of patients and mouse model for cerebral cavernous malformation disease.
Data show that sulindac sulfide and sulindac sulfone, which attenuate beta-catenin (show CTNNB1 ELISA Kits) transcription activity, reduce vascular malformations in endothelial programmed cell death 10 protein CCM3-deficient mice.
CCM3 has both cell autonomous and cell non-autonomous functions in neural progenitors and is specifically required in radial glia and newly born pyramidal neurons migrating through the subventricular zone
Although CCM3 stabilizes STK24, it counteracts STK24-mediated inhibition of exocytosis by recruiting STK24 away from the C2B domain through its Ca(2+)-sensitive interaction with UNC13D C2A domain.
Pdcd10 has a different role in cerebral cavernous malformation than Ccm2 (show CCM2 ELISA Kits) and Krit1 (show KRIT1 ELISA Kits)
Ccm3 has both neural cell autonomous and nonautonomous functions.
Stabilization of VEGFR2 (show KDR ELISA Kits) signaling by cerebral cavernous malformation 3 (also known as PDCD10) is critical for vascular development.
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.
programmed cell death 10
, TF-1 cell apoptosis-related protein 15
, apoptosis-related protein 15
, cerebral cavernous malformations 3 protein
, programmed cell death protein 10