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KRIT1 antibody

The Rabbit Polyclonal anti-KRIT1 antibody has been validated for WB and IF. It is suitable to detect KRIT1 in samples from Human.
Catalog No. ABIN1589846

Quick Overview for KRIT1 antibody (ABIN1589846)

Target

See all KRIT1 Antibodies
KRIT1 (KRIT1, Ankyrin Repeat Containing (KRIT1))

Reactivity

  • 24
  • 20
  • 5
Human

Host

  • 35
  • 4
Rabbit

Clonality

  • 35
  • 4
Polyclonal

Conjugate

  • 16
  • 3
  • 3
  • 3
  • 2
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
  • 1
This KRIT1 antibody is un-conjugated

Application

  • 32
  • 17
  • 13
  • 13
  • 3
  • 3
  • 3
  • 1
  • 1
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 Notes

    Western Blot: Use 1-5 μg/mL

    Restrictions

    For Research Use only
  • 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

    KRIT1 (KRIT1, Ankyrin Repeat Containing (KRIT1))

    Alternative Name

    CCM-1

    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
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