ELISA/assay

Mouse Collagen Type IV ELISA Kit

MBS722690

48-Strip-Wells

470 USD

ELISA Kit

Mouse Collagen Type IV ELISA Kit

Collagen Type IV

collagen, type IV, alpha 1, isoform CRA_a; Collagen alpha-1(IV) chain; collagen alpha-1(IV) chain; collagen alpha-1(IV) chain; COL4A1 NC1 domain; collagen IV, alpha-1 polypeptide; collagen of basement membrane, alpha-1 chain; collagen, type IV, alpha 1

CIV

COL4A1; COL4A1; ICH; HANAC; POREN1; arresten

CO4A1_HUMAN

Mouse

Store all reagents at 2-8 degree C.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Sandwich

Intended Uses: This CoL-4 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Mouse CoL-4. This ELISA kit for research use only, not for therapeutic or diagnostic applications. !Intended Uses: This CoL-4 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Mouse CoL-4. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Cell Biology

Principle of the Assay: CoL-4 ELISA kit applies the quantitative sandwich enzyme immunoassay technique. The microtiter plate has been pre-coated with a monoclonal antibody specific for CoL-4. Standards or samples are then added to the microtiter plate wells and CoL-4 if present, will bind to the antibody pre-coated wells. In order to quantitatively determine the amount of CoL-4 present in the sample, a standardized preparation of horseradish peroxidase (HRP)-conjugated polyclonal antibody, specific for CoL-4 are added to each well to "sandwich" the CoL-4 immobilized on the plate. The microtiter plate undergoes incubation, and then the wells are thoroughly washed to remove all unbound components. Next, substrate solutions are added to each well. The enzyme (HRP) and substrate are allowed to react over a short incubation period. Only those wells that contain CoL-4 and enzyme-conjugated antibody will exhibit a change in color. The enzyme-substrate reaction is terminated by addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The CoL-4 concentration in each sample is interpolated from this standard curve.

119629513

EAX09108.1

127,981 Da

Amoebiasis Pathway (167324); Amoebiasis Pathway (167191); Assembly Of Collagen Fibrils And Other Multimeric Structures Pathway (730306); Axon Guidance Pathway (105688); Binding And Uptake Of Ligands By Scavenger Receptors Pathway (771599); Collagen Biosynthesis And Modifying Enzymes Pathway (645289); Collagen Formation Pathway (645288); Developmental Biology Pathway (477129); ECM-receptor Interaction Pathway (83068); ECM-receptor Interaction Pathway (479)

This gene encodes the major type IV alpha collagen chain of basement membranes. Like the other members of the type IV collagen gene family, this gene is organized in a head-to-head conformation with another type IV collagen gene so that each gene pair shares a common promoter. [provided by RefSeq, Jul 2008]

COL4A1: Type IV collagen is the major structural component of glomerular basement membranes (GBM), forming a chicken-wire meshwork together with laminins, proteoglycans and entactin/nidogen. Defects in COL4A1 are a cause of brain small vessel disease with hemorrhage (BSVDH). Brain small vessel diseases underlie 20 to 30 percent of ischemic strokes and a larger proportion of intracerebral hemorrhages. Inheritance is autosomal dominant. Defects in COL4A1 are the cause of hereditary angiopathy with nephropathy aneurysms and muscle cramps (HANAC). The clinical renal manifestations include hematuria and bilateral large cysts. Histologic analysis revealed complex basement membrane defects in kidney and skin. The systemic angiopathy appears to affect both small vessels and large arteries. Defects in COL4A1 are a cause of familial porencephaly (POREN1). Porencephaly is a term used for any cavitation or cerebrospinal fluid-filled cyst in the brain. Porencephaly type 1 is usually unilateral and results from focal destructive lesions such as fetal vascular occlusion or birth trauma. Type 2, or schizencephalic porencephaly, is usually symmetric and represents a primary defect or arrest in the development of the cerebral ventricles. Belongs to the type IV collagen family. 2 isoforms of the human protein are produced by alternative splicing. Protein type: Secreted, signal peptide; Secreted; Extracellular matrix. Chromosomal Location of Human Ortholog: 13q34. Cellular Component: extracellular matrix; endoplasmic reticulum lumen; collagen type IV; extracellular region; basement membrane. Molecular Function: protein binding; platelet-derived growth factor binding; extracellular matrix structural constituent; extracellular matrix constituent conferring elasticity. Biological Process: patterning of blood vessels; extracellular matrix disassembly; collagen catabolic process; receptor-mediated endocytosis; axon guidance; extracellular matrix organization and biogenesis; epithelial cell differentiation; blood vessel morphogenesis; brain development; neuromuscular junction development. Disease: Porencephaly 1; Brain Small Vessel Disease With Or Without Ocular Anomalies; Angiopathy, Hereditary, With Nephropathy, Aneurysms, And Muscle Cramps; Hemorrhage, Intracerebral, Susceptibility To; Retinal Arteries, Tortuosity Of

48-Strip-Wells

470 USD

96-Strip-Wells

675