Human Collagen Type IV (COL4) ELISA Kit | COL4 elisa kit
Human Collagen Type IV (COL4) ELISA Kit
To minimize extra influence on the performance, operation procedures and lab conditions, especially room temperature, air humidity, incubator temperature should be strictly controlled. It is also strongly suggested that the whole assay is performed by the same operator from the beginning to the end.
Principle of the Assay: The microplate provided in this kit has been pre-coated with an antibody specific to COL4. Standards or samples are then added to the appropriate microplate wells with a biotin-conjugated antibody specific to COL4. Next, Avidin conjugated to Horseradish Peroxidase (HRP) is added to each microplate well and incubated. After TMB substrate solution is added, only those wells that contain COL4, biotin-conjugated antibody and enzyme-conjugated Avidin will exhibit a change in color. The enzyme-substrate reaction is terminated by the addition of sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450nm +/- 10nm. The concentration of COL4 in the samples is then determined by comparing the O.D. of the samples to the standard curve.
NCBI and Uniprot Product Information
NCBI Description
This gene encodes one of the six subunits of type IV collagen, the major structural component of basement membranes. Mutations in this gene are associated with X-linked Alport syndrome, also known as hereditary nephritis. 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. Alternatively spliced transcript variants have been identified for this gene. [provided by RefSeq, Aug 2010]
Uniprot Description
COL4A5: 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 COL4A5 are the cause of Alport syndrome X- linked (APSX). APSX is characterized by progressive glomerulonephritis, renal failure, sensorineural deafness, specific eye abnormalities (lenticonous and macular flecks), and glomerular basement membrane defects. The disorder shows considerable heterogeneity in that families differ in the age of end-stage renal disease and the occurrence of deafness. Deletions covering the N-terminal regions of COL4A5 and COL4A6, which are localized in a head-to-head manner, are found in the chromosome Xq22.3 centromeric deletion syndrome. This results in a phenotype with features of diffuse leiomyomatosis and Alport syndrome (DL-ATS). Belongs to the type IV collagen family. 2 isoforms of the human protein are produced by alternative splicing.
Protein type: Secreted, signal peptide; Extracellular matrix; Motility/polarity/chemotaxis; Secreted
Chromosomal Location of Human Ortholog: Xq22
Cellular Component: endoplasmic reticulum lumen; collagen type IV; extracellular region; basal lamina; neuromuscular junction
Molecular Function: extracellular matrix structural constituent
Biological Process: extracellular matrix disassembly; collagen catabolic process; axon guidance; extracellular matrix organization and biogenesis; neuromuscular junction development
Disease: Alport Syndrome, X-linked