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Collagen Type I 蛋白

This Native Collagen Type I protein is expressed in Human.
产品编号 ABIN7849679
发货至: 中国
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Quick Overview for Collagen Type I 蛋白 (ABIN7849679)

抗原

See all Collagen Type I (COL1) 蛋白
Collagen Type I (COL1) (Collagen, Type I (COL1))

蛋白类型

Native

宿主

  • 3
  • 2
  • 1
  • 1

资源

  • 2
  • 2
  • 1
  • 1
Human

应用范围

ELISA
  • 原理

    Type I Collagen Protein
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  • 应用备注

    Optimal working dilution should be determined by the investigator.

    限制

    仅限研究用
  • 状态

    Liquid

    缓冲液

    500 mM CH3COOH without preservative.

    储存液

    Without preservative

    储存条件

    4 °C,-20 °C,-80 °C

    储存方法

    Ship at 4°C.Upon receipt, aliquot and store at -20°C or -80°C for long term. Avoid repeated freeze and thaw cycles.
  • 抗原

    Collagen Type I (COL1) (Collagen, Type I (COL1))

    别名

    Type I Collagen

    背景

    Synonyms: Collagen alpha-2 (I) chain, Alpha-2 type I collage, COL1A2

    Description: Purified human type I collagen protein.

    Background: Type I collagen is the most abundant collagen of the human body which forms large, eosinophilic fibers known as collagen fibers. It is present in scar tissue, the end product when tissue heals by repair, as well as tendons, the endomysium of myofibrils, the organic part of bone, the dermis, the dentin and organ capsules. Collagen type I is the primary component of the extracellular matrix (ECM). Repression of collagen type I gene (COL1A2) transcription by the pro-inflammatory cytokine interferon gamma (IFN-γ) in vascular smooth muscle cells (VSMCs) is a key step during atherogenesis that leads to the destabilization of the atherosclerotic plaque. Weng X et al data indicate that a repressor complex that contains RFX5, HDAC2, Sin3B, and G9a is responsible for IFN-γ induced COL1A2 repression in VSMCs. Targeting individual component of this complex will likely yield potential therapeutic solutions against atherosclerosis. The abundant amount of relatively young collagen type I in cerebral aneurysms (CAs) suggests that there is an ongoing collagen remodeling in aneurysms, which is significantly more rapid in patients with risk factors. Etminan N et al findings challenge the concept that CAs are present for decades and that they undergo only sporadic episodes of structural change.

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