Human Collagen Type III Alpha 1 ELISA Kit | COL3a1 elisa kit

Human Collagen Type III Alpha 1 ELISA Kit

Cat. Num. AAA726642

• Gene Names: COL3A1; EDS4A
• Reactivity: Human
• Synonyms: Collagen Type III Alpha 1; Human Collagen Type III Alpha 1 ELISA Kit; COL3a1 elisa kit

• Reactivity: Human
• Specificity: This assay has high sensitivity and excellent specificity for detection of COL3a1. No significant cross-reactivity or interference between COL3a1 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between COL3a1 and all the analogues, therefore, cross reaction may still exist in some cases.

• Samples: Serum, plasma, cell culture supernatants, body fluid and tissue homogenate
• Assay Type: Quantitative Competitive or Sandwich
• Sensitivity: 1.0 ng/mL
• Preparation and Storage: Store all reagents at 2-8 degree C.

Typical Testing Data/Standard Curve (for reference only)

Related Product Information for COL3a1 elisa kit

Intended Uses: This COL3a1 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human COL3a1. This ELISA kit for research use only, not for therapeutic or test applications!

Principle of the Assay: COL3a1 ELISA kit applies the competitive enzyme immunoassay technique utilizing an anti-COL3a1 antibody and an COL3a1-HRP conjugate. The assay sample and buffer are incubated together with COL3a1-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the COL3a1 concentration since COL3a1 from samples and COL3a1-HRP conjugate compete for the anti-COL3a1 antibody binding site. Since the number of sites is limited, as more sites are occupied by COL3a1 from the sample, fewer sites are left to bind COL3a1-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The COL3a1 concentration in each sample is interpolated from this standard curve.

Product Categories/Family for COL3a1 elisa kit

Cell Biology

NCBI and Uniprot Product Information

• NCBI GI #: 119631316
• NCBI GeneID: 1281
• Molecular Weight: 111,907 Da
• NCBI Official Full Name: collagen, type III, alpha 1 (Ehlers-Danlos syndrome type IV, autosomal dominant), isoform CRA_b
• NCBI Official Synonym Full Names: collagen, type III, alpha 1
• NCBI Official Symbol: COL3A1
• NCBI Official Synonym Symbols: EDS4A
• NCBI Protein Information: collagen alpha-1(III) chain; collagen alpha-1(III) chain; collagen, fetal; alpha1 (III) collagen; Ehlers-Danlos syndrome type IV, autosomal dominant
• UniProt Protein Name: Collagen alpha-1(III) chain
• Protein Family: Collagen
• UniProt Gene Name: COL3A1
• UniProt Entry Name: CO3A1_HUMAN

NCBI Description

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]

Uniprot Description

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; Motility/polarity/chemotaxis; Secreted, signal peptide; Secreted

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; extracellular matrix structural constituent; platelet-derived growth factor binding; metal ion binding; SMAD binding

Biological Process: integrin-mediated signaling pathway; skin development; receptor-mediated endocytosis; platelet activation; axon guidance; extracellular matrix organization and biogenesis; collagen fibril organization; wound healing; heart development; cell-matrix adhesion; negative regulation of immune response; positive regulation of Rho protein signal transduction; collagen catabolic process; extracellular matrix disassembly; 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