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PDCD10 encodes an evolutionarily conserved protein associated with cell apoptosis. Additionally we are shipping PDCD10 Proteins (9) and many more products for this protein.
Showing 10 out of 57 products:
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 Antibodies) and activation of VEGF (show VEGFA Antibodies)/p38 (show CRK Antibodies) signaling were involved in miR (show MLXIP Antibodies)-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 Antibodies), CCM2/malcavernin (show CCM2 Antibodies) 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 Antibodies)-cortactin (show CTTN Antibodies) 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 Antibodies) PDCD10 is direct target of miR (show MLXIP Antibodies)-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 Antibodies) signaling protein
miR (show MLXIP Antibodies)-181b was upregulated by hypoxia in retinoblastoma in an HIF-1a (show HIF1A Antibodies)-independent manner. Additionally, miR (show MLXIP Antibodies)-181b exerts its angiogenic function, at least in part, by inhibiting PDCD10 and GATA6 (show GATA6 Antibodies).
Results broaden our knowledge on the mechanisms by which CCM3 deficiency results in disease and open new avenues of research into both CCM3 and senescence biology.
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 (show SQRDL Antibodies) and sulindac sulfone, which attenuate beta-catenin (show CTNNB1 Antibodies) 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 Antibodies) and Krit1 (show KRIT1 Antibodies)
Ccm3 has both neural cell autonomous and nonautonomous functions.
Stabilization of VEGFR2 (show KDR Antibodies) 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