Collagen alpha-1(III) chain

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

Human cells

Greater than 95% as determined by reducing SDS-PAGE.

Supplied as a 0.2 muM filtered solution of 20mM HAc-NaAc, 150mM NaCl, pH 4.5.

Lyophilized protein should be stored at -20 degree C, though stable at room temperature for 3 weeks. Reconstituted protein solution can be stored at 2-8 degree C for 2-7 days. Aliquots of reconstituted samples are stable at -20 degree C for 3 months.

Small volumes of COL3A1 recombinant 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.

Recombinant Mouse COL3A1 Protein is produced by our mammalian expression system and the target gene encoding Gln155-Gly1219 is expressed with a 6His tag at the C-terminus.

ELISA (EIA),Western Blot (WB), SDS-PAGE, Mass Spectrometry (MS)

138,943 Da

collagen, type III, alpha 1

collagen alpha-1(III) chain

Collagen alpha-1(III) chain

CO3A1_MOUSE

This gene encodes the alpha-1 subunit of the fibril-forming type III collagen found in bone, cartilage, dentin, tendon, bone marrow stroma and other connective tissue. The encoded protein forms homotrimeric type III procollagen that undergoes proteolytic processing during fibril formation. A majority of mice lacking the encoded protein die within two days of birth but about 5% of the animals survive to *****hood. The surviving mice exhibit severe cortical malformation and experience significantly shorter lifespan. The mutant mouse named "tight skin 2" exhibiting systemic sclerosis phenotype was found to harbor a missense point mutation in this gene. A pseudogene of this gene has been defined on chromosome 8. [provided by RefSeq, Nov 2015]

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

Cellular Component: collagen; collagen type III; extracellular matrix; extracellular space; proteinaceous extracellular matrix

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

Biological Process: blood vessel development; cell-matrix adhesion; cerebral cortex development; collagen fibril organization; fibril organization and biogenesis; gut development; heart development; integrin-mediated signaling pathway; negative regulation of immune response; peptide cross-linking; positive regulation of Rho protein signal transduction; response to cytokine stimulus; response to radiation; skin development; transforming growth factor beta receptor signaling pathway; wound healing

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