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抗Human CCM2 抗体:
抗Rat (Rattus) CCM2 抗体:
抗Mouse (Murine) CCM2 抗体:
Human Polyclonal CCM2 Primary Antibody for ELISA, WB - ABIN251695
Zawistowski, Stalheim, Uhlik, Abell, Ancrile, Johnson, Marchuk: CCM1 and CCM2 protein interactions in cell signaling: implications for cerebral cavernous malformations pathogenesis. in Human molecular genetics 2005
Human Polyclonal CCM2 Primary Antibody for IHC, IHC (p) - ABIN4288902
Marchi, Corricelli, Trapani, Bravi, Pittaro, Delle Monache, Ferroni, Patergnani, Missiroli, Goitre, Trabalzini, Rimessi, Giorgi, Zavan, Cassoni, Dejana, Retta, Pinton: Defective autophagy is a key feature of cerebral cavernous malformations. in EMBO molecular medicine 2015
A novel missense mutation in CCM2 were detected in cerebral cavernous malformations patient. Several CCM2 gene polymorphisms in sporadic CCM patients were reported.
Data suggest that signaling via ANP (显示 NPPA 抗体)/ANPR (atrial natriuretic factor/ANP (显示 NPPA 抗体) receptor (显示 PPP5C 抗体)) in vascular endothelial cells activates PAK4 (p21-activated kinase 4 (显示 PAK4 抗体)) and CCM2 (cerebral cavernous malformation 2 protein), resulting in phosphorylation of MLC (myosin light chain), cytoskeletal reorganization, and cell spreading; kinase homology domain of ANPRA (guanylyl cyclase-A (显示 NPR1 抗体)) activates downstream targets of ANP (显示 NPPA 抗体)/ANPR signaling.
Studies suggest that the 3 proteins of the Cerebral Cavernous Malformations (CCM) complex KRIT1/CCM1 (显示 KRIT1 抗体), CCM2/malcavernin and CCM3/PDCD10 (显示 PDCD10 抗体) not only require one another for reciprocal stabilization, but also act as a platform for signal transduction.
a new mutation in MGC4607/CCM2 was identified in several family members with spinal and cutaneous angiomas.
both CCM2 and CCM3 (显示 PDCD10 抗体) are required for normal endothelial cell network formation.
Data find that several disease-associated missense mutations in CCM2 have the potential to interrupt the KRIT1 (显示 KRIT1 抗体)-CCM2 interaction by destabilizing the CCM2 PTB (显示 PTBP1 抗体) domain and that a KRIT1 (显示 KRIT1 抗体) mutation also disrupts this interaction
Prevalence, frequency and characterization of CCM1 (显示 KRIT1 抗体), CCM2 and CCM3 (显示 PDCD10 抗体) variants in cerebral cavernous malformation Spanish patients.
Cerebral cavernous malformation(CCM)s develop because of loss of heart of glass (HEG (显示 HEG1 抗体))-independent CCM2 signaling in murine transgenic endothelium of central nervous system after birth.
DNA sequencing and deletion/duplication testing of the CCM1 (显示 KRIT1 抗体), CCM2, and CCM3 (显示 PDCD10 抗体) genes in the proband revealed a CCM1 (显示 KRIT1 抗体) c.601CNG mutation.
CCM2 mutations are associated with cerebral cavernous malformation in some Japanese patients.
Loss of CCM2 is associated with Cerebral Cavernous Malformations.
CCM2 expression and it's role during ovary and testis development
CCM2:MEKK3 (显示 MAP3K3 抗体)-mediated regulation of Rho-ROCK signalling is required for maintenance of neurovascular integrity, a mechanism by which CCM2 loss leads to disease.
Down-modulation of STK25 (显示 STK25 抗体), but not STK24 (显示 STK24 抗体), rescued medulloblastoma cells from NGF (显示 NGFB 抗体)-induced TrkA (显示 NTRK1 抗体)-dependent cell death, suggesting that STK25 (显示 STK25 抗体) is part of the death-signaling pathway initiated by TrkA (显示 NTRK1 抗体) and CCM2.
The inducible deletion of Ccm2 in adult mice recapitulates the cerebral cavernous malformations-like brain lesions in humans.
Developmental timing of CCM2 loss influences cerebral cavernous malformations in mice.
Rac1/osmosensing scaffold for MEKK3 contributes via phospholipase C (显示 PLC 抗体)-gamma1 to activation of the osmoprotective transcription factor NFAT5 (显示 NFAT5 抗体).
Pdcd10 (显示 PDCD10 抗体) has a different role in cerebral cavernous malformation than Ccm2 and Krit1 (显示 KRIT1 抗体)
The KRIT1 (显示 KRIT1 抗体)-CCM2 interaction regulates endothelial junctional stability and vascular barrier function by suppressing activation of the RhoA (显示 RHOA 抗体)/ROCK signaling pathway.
CCM1 (显示 KRIT1 抗体) associates with CCM2, indicating that the genetic heterogeneity observed in familial cavernous malformation pathogenesis may reflect mutation of different molecular members of a coordinated signaling complex.
These findings suggest that CCM2L and CCM2 cooperate to regulate the activity of MEKK3 (显示 MAP3K3 抗体).
Zebrafish embryos with the recessive lethal mutations santa (san) and valentine (vtn (显示 VTN 抗体)) do not thicken, but do add the proper number of cells to the myocardium.
This gene encodes a scaffold protein that functions in the stress-activated p38 Mitogen-activated protein kinase (MAPK) signaling cascade. The protein interacts with SMAD specific E3 ubiquitin protein ligase 1 (also known as SMURF1) via a phosphotyrosine binding domain to promote RhoA degradation. The protein is required for normal cytoskeletal structure, cell-cell interactions, and lumen formation in endothelial cells. Mutations in this gene result in cerebral cavernous malformations. Multiple transcript variants encoding different isoforms have been found for this gene.
cerebral cavernous malformations 2 protein
, cerebral cavernous malformation 2
, cerebral cavernous malformation 2 homolog
, cerebral cavernous malformations protein 2 homolog
, osmosensing scaffold for MEKK3