Collagen Type I Protein

Catalog No. ABIN7849679

This Native Collagen Type I protein is expressed in Human.

Quick Overview for Collagen Type I Protein (ABIN7849679)

Target: Collagen Type I (COL1) (Collagen, Type I (COL1))

Protein Type: Native

Origin: Human

Source: Human

Application: ELISA

Product Details

Purpose: Type I Collagen Protein

Application Details

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

Restrictions: For Research Use only

Handling

Format: Liquid

Buffer: 500 mM CH3COOH without preservative.

Preservative: Without preservative

Storage: 4 °C,-20 °C,-80 °C

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

Target Details

Target: Collagen Type I (COL1) (Collagen, Type I (COL1))

Alternative Name: Type I Collagen

Background:

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.