ELISA/assay

Bovine Collagen Type I Alpha 2 ELISA Kit

MBS741393

48-Strip-Wells

470 USD

ELISA Kit

Bovine Collagen Type I Alpha 2 ELISA Kit

Collagen Type I Alpha 2

collagen alpha-2(I) chain; Collagen alpha-2(I) chain; collagen alpha-2(I) chain; collagen alpha-2(I) chain; type I procollagen; alpha 2(I)-collagen; alpha-2 type I collagen; collagen I, alpha-2 polypeptide; collagen of skin, tendon and bone, alpha-2 chain; collagen, type I, alpha 2; Alpha-2 type I collagen

COL1a2

COL1A2; COL1A2; OI4

CO1A2_HUMAN

Bovine

This assay has high sensitivity and excellent specificity for detection of CoL-1alpha2. No significant cross-reactivity or interference between CoL-1alpha2 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between CoL-1alpha2 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 1.0 ng/mL.

Intended Uses: This CoL-1alpha2 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Bovine CoL-1alpha2. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Cell Biology

Principle of the assay: CoL-1alpha2 ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-CoL-1alpha2 antibody and an CoL-1alpha2-HRP conjugate. The assay sample and buffer are incubated together with CoL-1alpha2-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 CoL-1alpha2 concentration since CoL-1alpha2 from samples and CoL-1alpha2-HRP conjugate compete for the anti-CoL-1alpha2 antibody binding site. Since the number of sites is limited, as more sites are occupied by CoL-1alpha2 from the sample, fewer sites are left to bind CoL-1alpha2-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The CoL-1alpha2 concentration in each sample is interpolated from this standard curve.

48762934

NP_000080.2

NM_000089.3

129,314 Da

Amoebiasis Pathway (167324); Amoebiasis Pathway (167191); Assembly Of Collagen Fibrils And Other Multimeric Structures Pathway (730306); Binding And Uptake Of Ligands By Scavenger Receptors Pathway (771599); C-MYB Transcription Factor Network Pathway (138073); Collagen Biosynthesis And Modifying Enzymes Pathway (645289); Collagen Formation Pathway (645288); ECM-receptor Interaction Pathway (83068); ECM-receptor Interaction Pathway (479); Endothelins Pathway (137958)

This gene encodes the pro-alpha2 chain of type I collagen whose triple helix comprises two alpha1 chains and one alpha2 chain. Type I is a fibril-forming collagen found in most connective tissues and is abundant in bone, cornea, dermis and tendon. Mutations in this gene are associated with osteogenesis imperfecta types I-IV, Ehlers-Danlos syndrome type VIIB, recessive Ehlers-Danlos syndrome Classical type, idiopathic osteoporosis, and atypical Marfan syndrome. Symptoms associated with mutations in this gene, however, tend to be less severe than mutations in the gene for the alpha1 chain of type I collagen (COL1A1) reflecting the different role of alpha2 chains in matrix integrity. Three transcripts, resulting from the use of alternate polyadenylation signals, have been identified for this gene. [provided by R. Dalgleish, Feb 2008]

COL1A2: Type I collagen is a member of group I collagen (fibrillar forming collagen). Defects in COL1A2 are the cause of Ehlers-Danlos syndrome type 7B (EDS7B). EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS7B is marked by bilateral congenital hip dislocation, hyperlaxity of the joints, and recurrent partial dislocations. Defects in COL1A2 are a cause of osteogenesis imperfecta type 1 (OI1). A dominantly inherited connective tissue disorder characterized by bone fragility and blue sclerae. Osteogenesis imperfecta type 1 is non-deforming with normal height or mild short stature, and no dentinogenesis imperfecta. Defects in COL1A2 are a cause of osteogenesis imperfecta type 2 (OI2); also known as osteogenesis imperfecta congenita (OIC) or lethal perinatal. A connective tissue disorder characterized by bone fragility, with many perinatal fractures, severe bowing of long bones, undermineralization, and death in the perinatal period due to respiratory insufficiency. Defects in COL1A2 are the cause of Ehlers-Danlos syndrome autosomal recessive cardiac valvular form (EDSCV). A connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. In addition to joint laxity, skin hyperextensibility and friability, and abnormal scar formation, patients have mitral valve prolapse and insufficiency, mitral regurgitation, and aortic insufficiency. Defects in COL1A2 are a cause of osteogenesis imperfecta type 3 (OI3). A connective tissue disorder characterized by progressively deforming bones, very short stature, a triangular face, severe scoliosis, grayish sclera, and dentinogenesis imperfecta. Defects in COL1A2 are a cause of osteogenesis imperfecta type 4 (OI4); also known as osteogenesis imperfecta with normal sclerae. A connective tissue disorder characterized by moderately short stature, mild to moderate scoliosis, grayish or white sclera and dentinogenesis imperfecta. A chromosomal aberration involving COL1A2 may be a cause of lipoblastomas, which are benign tumors resulting from transformation of adipocytes, usually diagnosed in children. Translocation t(7;8)(p22;q13) with PLAG1. Belongs to the fibrillar collagen family. Protein type: Secreted, signal peptide; Secreted. Chromosomal Location of Human Ortholog: 7q22.1. Cellular Component: extracellular matrix; extracellular space; endoplasmic reticulum lumen; extracellular region; collagen type I. Molecular Function: protein binding, bridging; identical protein binding; protein binding; metal ion binding; extracellular matrix structural constituent; platelet-derived growth factor binding; SMAD binding. Biological Process: platelet activation; receptor-mediated endocytosis; blood vessel development; extracellular matrix organization and biogenesis; collagen fibril organization; skin morphogenesis; Rho protein signal transduction; odontogenesis; collagen catabolic process; extracellular matrix disassembly; regulation of blood pressure; transforming growth factor beta receptor signaling pathway; blood coagulation; leukocyte migration; skeletal development. Disease: Ehlers-danlos Syndrome, Type Vii, Autosomal Dominant; Osteogenesis Imperfecta, Type Ii; Ehlers-danlos Syndrome, Autosomal Recessive, Cardiac Valvular Form; Osteogenesis Imperfecta, Type Iii; Osteoporosis; Osteogenesis Imperfecta, Type Iv

48-Strip-Wells

470 USD

96-Strip-Wells

675