ELISA/assay

Mouse arresten ELISA Kit

MBS7202946

48-Strip-Wells

440 USD

ELISA Kit

Mouse arresten ELISA Kit

[arresten]

[arresten, partial; 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]

[COL4A1; COL4A1; ICH; HANAC; POREN1; arresten]

CO4A1_HUMAN

Mouse

This assay has high sensitivity and excellent specificity for detection of ARMC6. No significant cross-reactivity or interference between ARMC6 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between ARMC6 and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C.

Typical Testing Data/Standard Curve (for reference only)

Samples: Serum, Plasma, Cell Culture Supernatants, Body Fluid And Tissue Homogenate. Assay Type: Quantitative Competitive. Sensitivity: 0.1 ng/mL.

Signal Transduction

Intended Uses: This ARMC6 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human ARMC6. This ELISA kit for research use only, not for therapeutic or diagnostic applications!. Principle of the Assay: ARMC6 ELISA kit applies the competitive enzyme immunoassay technique utilizing an anti-ARMC6 antibody and an ARMC6-HRP conjugate. The assay sample and buffer are incubated together with ARMC6-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 ARMC6 concentration since ARMC6 from samples and ARMC6-HRP conjugate compete for the anti-ARMC6 antibody binding site. Since the number of sites is limited, as more sites are occupied by ARMC6 from the sample, fewer sites are left to bind ARMC6-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The ARMC6 concentration in each sample is interpolated from this standard curve.

31096018

AAP43112.1

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: Extracellular matrix; Secreted, signal peptide; Secreted. 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; collagen catabolic process; receptor-mediated endocytosis; axon guidance; extracellular matrix disassembly; 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

440 USD

96-Strip-Wells

640

5x96-Strip-Wells

2895

10x96-Strip-Wells

5415