KRIT1 antibody

Catalog No. ABIN1589846

Product Details anti-KRIT1 Antibody

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

Reactivity: Human

Host: Rabbit

Clonality: Polyclonal

Conjugate: This KRIT1 antibody is un-conjugated

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

Purpose: CCM-1 antibody

Specificity: Recombinant human CCM1

Characteristics: Chromosomal location: 7q21.2

Purification: Protein A purified

Immunogen: Recombinant human CCM1 (ABIN7539340)

Isotype: IgG

Application Details

Application Notes: Western Blot: Use 1-5 μg/mL

Restrictions: For Research Use only

Handling

Format: Lyophilized

Reconstitution: 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

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

Storage: 4 °C,-20 °C

Storage Comment: 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.

Expiry Date: 24 months

Target Details for KRIT1

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

Alternative Name: CCM-1 (KRIT1 Products)

Background: 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.

Gene ID: 889, 3

NCBI Accession: NM_004912, NP_004903

UniProt: O00522

Pathways: Cell RedoxHomeostasis