KRIT1 antibody (N-Term)

Catalog No. ABIN616004

This Rabbit Polyclonal antibody specifically detects KRIT1 in WB and IF. It exhibits reactivity toward Human.

Quick Overview for KRIT1 antibody (N-Term) (ABIN616004)

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)

Product Details anti-KRIT1 Antibody

Binding Specificity: AA 1-736, N-Term

Specificity: This antibody is anti-His depleated. It detects KRIT1 / CCM1.

Cross-Reactivity (Details): Species reactivity (tested):Human.

Purification: Protein A Chromatography

Immunogen: Highly pure (>95%) recombinant Human CCM-1 (Met1-Ser736) derived from E. coli fused to a C-teminal His-tag (6 x His) (Cat.-No AR26002PU-N)

Isotype: IgG

Application Details

Application Notes: Optimal working dilution should be determined by the investigator.

Restrictions: For Research Use only

Handling

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

Buffer: 5 mM PBS, pH 7.2

Handling Advice: Avoid repeated freezing and thawing.

Storage: 4 °C/-20 °C

Storage Comment: Prior to reconstitution store at 2-8 °C. Following reconstitution store undiluted at 2-8 °C for one month or (in aliquots) at -20 °C for longer.

Target Details for KRIT1

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

Alternative Name: KRIT1 / CCM1

Background: 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.Synonyms: Krev interaction trapped 1

Gene ID: 889

NCBI Accession: NP_004903

UniProt: O00522

Pathways: Cell RedoxHomeostasis