KRIT1 Antikörper

Produktnummer ABIN1589846

Produktdetails anti-KRIT1 Antikörper

Target: KRIT1 (KRIT1, Ankyrin Repeat Containing (KRIT1))

Reaktivität: Human

Wirt: Kaninchen

Klonalität: Polyklonal

Konjugat: Dieser KRIT1 Antikörper ist unkonjugiert

Applikation: Western Blotting (WB), Immunofluorescence (IF)

Verwendungszweck: CCM-1 antibody

Spezifität: Recombinant human CCM1

Produktmerkmale: Chromosomal location: 7q21.2

Aufreinigung: Protein A purified

Immunogen: Recombinant human CCM1 (ABIN7539340)

Isotyp: IgG

Anwendungsinformationen

Applikationshinweise: Western Blot: Use 1-5 μg/mL

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Lyophilized

Rekonstitution: Centrifuge vial prior to opening. Reconstitute in sterile water to a concentration of 0.1-1.0 mg/mL.

Buffer: 0.5X PBS, pH 7.2

Handhabung: Centrifuge vial prior to opening. Avoid repeated freeze-thaw cycles.

Lagerung: 4 °C,-20 °C

Informationen zur Lagerung: The lyophilized antibody is stable for at least 2 years at -20°C. After sterile reconstitution the antibody is stable at 2-8°C for up to 6 months. Frozen aliquots are stable for at least 6 months when stored at -20°C. Addition of a carrier protein or 50% glycerol is recommended for frozen aliquots.

Haltbarkeit: 24 months

Details zu KRIT1

Target: KRIT1 (KRIT1, Ankyrin Repeat Containing (KRIT1))

Andere Bezeichnung: CCM-1 (KRIT1 Produkte)

Hintergrund: CCM-1, Cerebral cavernous malformations protein 1, KRIT1, KRIT1, ankyrin repeat containing, CAM,Cerebral cavernous malformations (CCM) are frequent vascular abnormalities caused by mutations in one of the CCM genes. CCM-1 (also known as KRIT1) stabilizes endothelial junctions and is essential for vascular morphogenesis in mouse embryos. However, cellular functions of CCM-1 during the early steps of the CCM pathogenesis remain unknown. It was shown that CCM-1 represents an antiangiogenic protein to keep the human endothelium quiescent. CCM-1 inhibits endothelial proliferation, apoptosis, migration, lumen formation, and sprouting angiogenesis in primary human endothelial cells. CCM-1 strongly induces DLL4-NOTCH signaling, which promotes AKT phosphorylation but reduces phosphorylation of the mitogen-activated protein kinase ERK. Consistently, blocking of NOTCH activity alleviates CCM-1 effects. ERK phosphorylation is increased in human CCM lesions. Transplantation of CCM-1-silenced human endothelial cells into SCID mice recapitulates hallmarks of the CCM pathology and serves as a unique CCM model system.

Gen-ID: 889, 3

NCBI Accession: NM_004912, NP_004903

UniProt: O00522

Pathways: Cell RedoxHomeostasis