Fetal collagen protein; Collagen type III alpha 1 protein; Ehlers Danlos syndrome type IV; Collagen type III alpha protein; autosomal dominant protein; EDS4A protein

For Research Use Only. Not for use in diagnostic procedures.

Human

Collagen Type III protein was purified by affinity chromatography.

Sterile filtered liquid in 0.5M CH3COOH, with 0.01% NaN3.

Store at 4 degree C. Dilute only prior to immediate use.

Small volumes of COL3A1 native protein vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Purified native Human Collagen Type III protein

Cancer; Native Protein

User optimized

Western Blot analysis using Collagen Type III protein
Lane 1: Human Collagen III. Load: 100 ng per lane. Primary antibody: Collagen III antibody at 1:1000 ON at 4 deg C. Secondary antibody: Dylight (TM) 649 Goat anti-rabbit at 1:20, 000 for 30 min at RT. Block for 30 min at RT.

111,907 Da[Similar Products]

collagen, type III, alpha 1

collagen alpha-1(III) chain

Collagen alpha-1(III) chain

CO3A1_HUMAN

This gene encodes the pro-alpha1 chains of type III collagen, a fibrillar collagen that is found in extensible connective tissues such as skin, lung, uterus, intestine and the vascular system, frequently in association with type I collagen. Mutations in this gene are associated with Ehlers-Danlos syndrome types IV, and with aortic and arterial aneurysms. Two transcripts, resulting from the use of alternate polyadenylation signals, have been identified for this gene. [provided by R. Dalgleish, Feb 2008]

CO3A1: Collagen type III occurs in most soft connective tissues along with type I collagen. Defects in COL3A1 are a cause of Ehlers-Danlos syndrome type 3 (EDS3); also known as benign hypermobility syndrome. EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS3 is a form of Ehlers-Danlos syndrome characterized by marked joint hyperextensibility without skeletal deformity. Defects in COL3A1 are the cause of Ehlers-Danlos syndrome type 4 (EDS4). EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS4 is the most severe form of the disease. It is characterized by the joint and dermal manifestations as in other forms of the syndrome, characteristic facial features (acrogeria) in most patients, and by proneness to spontaneous rupture of bowel and large arteries. The vascular complications may affect all anatomical areas. Defects in COL3A1 are a cause of susceptibility to aortic aneurysm abdominal (AAA). AAA is a common multifactorial disorder characterized by permanent dilation of the abdominal aorta, usually due to degenerative changes in the aortic wall. Histologically, AAA is characterized by signs of chronic inflammation, destructive remodeling of the extracellular matrix, and depletion of vascular smooth muscle cells. Belongs to the fibrillar collagen family. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Extracellular matrix; Cell adhesion; Secreted, signal peptide; Secreted; Motility/polarity/chemotaxis

Chromosomal Location of Human Ortholog: 2q31

Cellular Component: extracellular matrix; extracellular space; endoplasmic reticulum lumen; extracellular region; collagen type III

Molecular Function: integrin binding; protein binding; platelet-derived growth factor binding; extracellular matrix structural constituent; metal ion binding; SMAD binding

Biological Process: skin development; integrin-mediated signaling pathway; platelet activation; receptor-mediated endocytosis; axon guidance; extracellular matrix organization and biogenesis; collagen fibril organization; wound healing; cell-matrix adhesion; heart development; negative regulation of immune response; positive regulation of Rho protein signal transduction; extracellular matrix disassembly; collagen catabolic process; response to radiation; gut development; response to mechanical stimulus; response to cytokine stimulus; transforming growth factor beta receptor signaling pathway; fibril organization and biogenesis; cerebral cortex development; peptide cross-linking; skeletal development; aging

Disease: Ehlers-danlos Syndrome, Type Iv, Autosomal Dominant; Ehlers-danlos Syndrome, Type Iii

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