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KRIT1 抗体

This anti-KRIT1 antibody is a 兔 多克隆 antibody detecting KRIT1 in WB 和 IF. Suitable for 人.
产品编号 ABIN1589846
发货至: 中国

Quick Overview for KRIT1 抗体 (ABIN1589846)

抗原

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

适用

  • 24
  • 20
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宿主

  • 35
  • 4

克隆类型

  • 35
  • 4
多克隆

标记

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This KRIT1 antibody is un-conjugated

应用范围

  • 32
  • 17
  • 13
  • 13
  • 3
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  • 1
  • 1
Western Blotting (WB), Immunofluorescence (IF)
  • 原理

    CCM-1 antibody

    特异性

    Recombinant human CCM1

    产品特性

    Chromosomal location: 7q21.2

    纯化方法

    Protein A purified

    免疫原

    Recombinant human CCM1 (ABIN7539340)

    亚型

    IgG
  • 应用备注

    Western Blot: Use 1-5 μg/mL

    限制

    仅限研究用
  • 状态

    Lyophilized

    溶解方式

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

    缓冲液

    0.5X PBS, pH 7.2

    注意事项

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

    储存条件

    4 °C,-20 °C

    储存方法

    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.

    有效期

    24 months
  • 抗原

    KRIT1 (KRIT1, Ankyrin Repeat Containing (KRIT1))

    别名

    CCM-1

    背景

    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.

    基因ID

    889, 3

    NCBI登录号

    NM_004912, NP_004903

    UniProt

    O00522

    途径

    Cell RedoxHomeostasis
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