Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Select your species
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 (Montrer NPPA Kits ELISA)/ANPR (atrial natriuretic factor/ANP (Montrer NPPA Kits ELISA) receptor (Montrer PPP5C Kits ELISA)) in vascular endothelial cells activates PAK4 (p21-activated kinase 4 (Montrer PAK4 Kits ELISA)) 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 (Montrer NPR1 Kits ELISA)) activates downstream targets of ANP (Montrer NPPA Kits ELISA)/ANPR signaling.
Studies suggest that the 3 proteins of the Cerebral Cavernous Malformations (CCM) complex KRIT1/CCM1 (Montrer KRIT1 Kits ELISA), CCM2/malcavernin and CCM3/PDCD10 (Montrer PDCD10 Kits ELISA) 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 (Montrer PDCD10 Kits ELISA) 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 (Montrer KRIT1 Kits ELISA)-CCM2 interaction by destabilizing the CCM2 PTB (Montrer PTBP1 Kits ELISA) domain and that a KRIT1 (Montrer KRIT1 Kits ELISA) mutation also disrupts this interaction
Prevalence, frequency and characterization of CCM1 (Montrer KRIT1 Kits ELISA), CCM2 and CCM3 (Montrer PDCD10 Kits ELISA) variants in cerebral cavernous malformation Spanish patients.
Cerebral cavernous malformation(CCM)s develop because of loss of heart of glass (HEG)-independent CCM2 signaling in murine transgenic endothelium of central nervous system after birth.
DNA sequencing and deletion/duplication testing of the CCM1 (Montrer KRIT1 Kits ELISA), CCM2, and CCM3 (Montrer PDCD10 Kits ELISA) genes in the proband revealed a CCM1 (Montrer KRIT1 Kits ELISA) 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 (Montrer MAP3K3 Kits ELISA)-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 (Montrer STK25 Kits ELISA), but not STK24 (Montrer STK24 Kits ELISA), rescued medulloblastoma cells from NGF (Montrer NGFB Kits ELISA)-induced TrkA (Montrer NTRK1 Kits ELISA)-dependent cell death, suggesting that STK25 (Montrer STK25 Kits ELISA) is part of the death-signaling pathway initiated by TrkA (Montrer NTRK1 Kits ELISA) 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 (Montrer PLC Kits ELISA)-gamma1 to activation of the osmoprotective transcription factor NFAT5 (Montrer NFAT5 Kits ELISA).
Pdcd10 (Montrer PDCD10 Kits ELISA) has a different role in cerebral cavernous malformation than Ccm2 and Krit1 (Montrer KRIT1 Kits ELISA)
The KRIT1 (Montrer KRIT1 Kits ELISA)-CCM2 interaction regulates endothelial junctional stability and vascular barrier function by suppressing activation of the RhoA (Montrer RHOA Kits ELISA)/ROCK signaling pathway.
CCM1 (Montrer KRIT1 Kits ELISA) 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.
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