Programmed Cell Death 10 Proteins (PDCD10)

Human Programmed Cell Death 10 (PDCD10) interaction partners

1. CCM3 restrains ANGPT2 release from endothelial cells and maintains endot (show VAMP3 Proteins)helial junctions. CCM3 depletion leads to increa (show ANGPT2 Proteins)sed ANGPT2 release.

2. Data indicated that rs9853967 and rs11714980 polymorphisms in CCM3 and SERPINI1respectively could be associated with a protective role in cerebral cavernous malformations disease.

3. Inhibition of Notch (show NOTCH1 Proteins) and activation of VEGF (show VEGFA Proteins)/p38 (show CRK Proteins) signaling were involved in miR (show MLXIP Proteins)-425-5p/CCM3 mediated inhibition of angiogenesis by sodium arsenite.

4. Loss of endothelial programmed cell death 10 activates glioblastoma cells and promotes tumor growth.

5. Studies suggest that the 3 proteins of the Cerebral Cavernous Malformations (CCM) complex KRIT1/CCM1 (show KRIT1 Proteins), CCM2/malcavernin (show CCM2 Proteins) and CCM3/PDCD10 not only require one another for reciprocal stabilization, but also act as a platform for signal transduction.

6. Study highlights the potential role of CCM3 in regulating tight junction complex organization and brain endothelial barrier permeability through CCM3-ERK1/2-cortactin (show CTTN Proteins) cross-talk

7. 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.

8. The proto-oncogene (show RAB1A Proteins) PDCD10 is direct target of miR (show MLXIP Proteins)-103 that can suppress Prostate cancer proliferation and migration by down-regulating the PDCD10.

9. We report for the first time that PDCD10 expression is downregulated in GBM, which is associated with the activation of Akt (show AKT1 Proteins) signaling protein

10. miR (show MLXIP Proteins)-181b was upregulated by hypoxia in retinoblastoma in an HIF-1a (show HIF1A Proteins)-independent manner. Additionally, miR (show MLXIP Proteins)-181b exerts its angiogenic function, at least in part, by inhibiting PDCD10 and GATA6 (show GATA6 Proteins).

Mouse (Murine) Programmed Cell Death 10 (PDCD10) interaction partners

1. CCM3 suppresses UNC13B- and vesicle-associated membrane protein 3 (VAMP3 (show VAMP3 Proteins))-dependent exocytosis of angiopoietin 2 (ANGPT2 (show ANGPT2 Proteins)) in brain endothelial cells. CCM3 deficiency in endothelial cells augments the exocytosis and secretion of ANGPT2 (show ANGPT2 Proteins), which is associated with destabilized endothelial cell junctions, enlarged lumen formation and endothelial cell-pericyte dissociation.

2. CCM3 expression and it's role during ovary and testis development

3. 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.

4. Data show that sulindac sulfide (show SQRDL Proteins) and sulindac sulfone, which attenuate beta-catenin (show CTNNB1 Proteins) transcription activity, reduce vascular malformations in endothelial programmed cell death 10 protein CCM3-deficient mice.

5. 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

6. 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.

7. Pdcd10 has a different role in cerebral cavernous malformation than Ccm2 (show CCM2 Proteins) and Krit1 (show KRIT1 Proteins)

8. Ccm3 has both neural cell autonomous and nonautonomous functions.

9. Stabilization of VEGFR2 (show KDR Proteins) signaling by cerebral cavernous malformation 3 (also known as PDCD10) is critical for vascular development.