Pdcd10 cDNA ORF clone, Mus musculus(house mouse)

Connexin 43 gap junctions contribute to brain endothelial barrier hyperpermeability in familial cerebral cavernous malformations type III by modulating tight junction structure.
Johnson AM, Roach JP, Hu A, Stamatovic SM, Zochowski MR, Keep RF, Andjelkovic AV
FASEB journal : official publication of the Federation of American Societies for Experimental Biology(2018 Jan)

Combined HMG-COA reductase and prenylation inhibition in treatment of CCM.
Nishimura S, Mishra-Gorur K, Park J, Surovtseva YV, Sebti SM, Levchenko A, Louvi A, Gunel M
Proceedings of the National Academy of Sciences of the United States of America114(21)5503-5508(2017 May)

Endothelial exocytosis of angiopoietin-2 resulting from CCM3 deficiency contributes to cerebral cavernous malformation.
Jenny Zhou H, Qin L, Zhang H, Tang W, Ji W, He Y, Liang X, Wang Z, Yuan Q, Vortmeyer A, Toomre D, Fuh G, Yan M, Kluger MS, Wu D, Min W
Nature medicine22(9)1033-1042(2016 09)

KLF4 is a key determinant in the development and progression of cerebral cavernous malformations.
Cuttano R, Rudini N, Bravi L, Corada M, Giampietro C, Papa E, Morini MF, Maddaluno L, Baeyens N, Adams RH, Jain MK, Owens GK, Schwartz M, Lampugnani MG, Dejana E
EMBO molecular medicine8(1)6-24(2016 Jan)

Defective autophagy is a key feature of cerebral cavernous malformations.
Marchi S, Corricelli M, Trapani E, Bravi L, Pittaro A, Delle Monache S, Ferroni L, Patergnani S, Missiroli S, Goitre L, Trabalzini L, Rimessi A, Giorgi C, Zavan B, Cassoni P, Dejana E, Retta SF, Pinton P
EMBO molecular medicine7(11)1403-17(2015 Nov)

CCM3 suppresses UNC13B- and vesicle-associated membrane protein 3 (VAMP3)-dependent exocytosis of angiopoietin 2 (ANGPT2) in brain endothelial cells. CCM3 deficiency in endothelial cells augments the exocytosis and secretion of ANGPT2, which is associated with destabilized endothelial cell junctions, enlarged lumen formation and endothelial cell-pericyte dissociation.
Title: Endothelial exocytosis of angiopoietin-2 resulting from CCM3 deficiency contributes to cerebral cavernous malformation.

CCM3 expression and it's role during ovary and testis development
Title: Expression of CCM2 and CCM3 during mouse gonadogenesis.

Data show that sulindac sulfide and sulindac sulfone, which attenuate beta-catenin transcription activity, reduce vascular malformations in endothelial programmed cell death 10 protein CCM3-deficient mice.
Title: Sulindac metabolites decrease cerebrovascular malformations in CCM3-knockout mice.

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.
Title: Exceptional aggressiveness of cerebral cavernous malformation disease associated with PDCD10 mutations.

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
Title: Ccm3, a gene associated with cerebral cavernous malformations, is required for neuronal migration.