ELISA/assay

Human Collagen Type IV ELISA Kit

MBS725110

48-Strip-Wells

470 USD

ELISA Kit

Human Collagen Type IV ELISA Kit

Collagen Type IV

Human Collagen Type IV (Col IV); Human Collagen Type IV ELISA Kit; Collagen Type IV; Collagen Type IV (Human)

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

Col IV

COL4A1; COL4A1; ICH; HANAC; POREN1; arresten

CO4A1_HUMAN

Human

This assay has high sensitivity and excellent specificity for detection of CoL-4. No significant cross-reactivity or interference between CoL-4 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between CoL-4 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: Sandwich. Sensitivity: 1.0 ng/mL.

Human ELISA Kit

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

P02462

160,615 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]

Function: 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. Ref.12 Ref.17 Ref.18 Ref.19Arresten, comprising the C-terminal NC1 domain, inhibits angiogenesis and tumor formation. The C-terminal half is found to possess the anti-angiogenic activity. Specifically inhibits endothelial cell proliferation, migration and tube formation. Inhibits expression of hypoxia-inducible factor 1alpha and ERK1/2 and p38 MAPK activation. Ligand for alpha1/beta1 integrin. Ref.12 Ref.17 Ref.18 Ref.19. Subunit structure: There are six type IV collagen isoforms, alpha 1(IV)-alpha 6(IV), each of which can form a triple helix structure with 2 other chains to generate type IV collagen network. Subcellular location: Secreted extracellular space extracellular matrix basement membrane. Tissue specificity: Highly expressed in placenta. Ref.12 Ref.17. Domain: Alpha chains of type IV collagen have a non-collagenous domain (NC1) at their C-terminus, frequent interruptions of the G-X-Y repeats in the long central triple-helical domain (which may cause flexibility in the triple helix), and a short N-terminal triple-helical 7S domain. Post-translational modification: Lysines at the third position of the tripeptide repeating unit (G-X-Y) are hydroxylated in all cases and bind carbohydrates.Prolines at the third position of the tripeptide repeating unit (G-X-Y) are hydroxylated in some or all of the chains.Type IV collagens contain numerous cysteine residues which are involved in inter- and intramolecular disulfide bonding. 12 of these, located in the NC1 domain, are conserved in all known type IV collagens.The trimeric structure of the NC1 domains is stabilized by covalent bonds between Lys and Met residues.Proteolytic processing produces the C-terminal NC1 peptide, arresten. Involvement in disease: Brain small vessel disease with hemorrhage (BSVDH) [MIM:607595]: Brain small vessel diseases underlie 20 to 30 percent of ischemic strokes and a larger proportion of intracerebral hemorrhages. Inheritance is autosomal dominant.Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.23 Ref.24 Ref.27 Ref.30 Ref.31Hereditary angiopathy with nephropathy aneurysms and muscle cramps (HANAC) [MIM:611773]: 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.Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.25 Ref.29Porencephaly 1 (POREN1) [MIM:175780]: A neurologic disorder characterized by a fluid-filled cysts or cavities within the cerebral hemispheres, neurologic manifestations, facial paresis, and visual defects. Affected individuals typically have hemiplegia, seizures, and intellectual disability. Porencephaly type 1 is usually unilateral and results from focal destructive lesions such as fetal vascular occlusion or birth trauma.Note: The disease is caused by mutations affecting the gene represented in this entry. Ref.21 Ref.22 Ref.28. Sequence similarities: Belongs to the type IV collagen family.Contains 1 collagen IV NC1 (C-terminal non-collagenous) domain.

48-Strip-Wells

470 USD

96-Strip-Wells

675