ELISA/assay

Human Collagen Type I ELISA Kit

MBS727467

48-Strip-Wells

470 USD

ELISA Kit

Human Collagen Type I ELISA Kit

Collagen Type I

Human Collagen Type I ELISA Kit; Collagen Type I; Collagen Type I (Human)

collagen, type I, alpha 1, isoform CRA_a; Collagen alpha-1(I) chain; collagen alpha-1(I) chain; collagen alpha-1(I) chain; alpha-1 type I collagen; pro-alpha-1 collagen type 1; collagen alpha 1 chain type I; collagen alpha-1(I) chain preproprotein; collagen of skin, tendon and bone, alpha-1 chain; collagen, type I, alpha 1; Alpha-1 type I collagen

Col I

COL1A1; COL1A1; OI4

CO1A1_HUMAN

Human

This assay has high sensitivity and excellent specificity for detection of CoL-1. No significant cross-reactivity or interference between CoL-1 and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between CoL-1 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-1 ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human CoL-1. This ELISA kit for research use only, not for therapeutic or diagnostic applications!. Principle of the Assay: CoL-1 ELISA kit applies the quantitative sandwich enzyme immunoassay technique. The microtiter plate has been pre-coated with a monoclonal antibody specific for CoL-1. Standards or samples are then added to the microtiter plate wells and CoL-1 if present, will bind to the antibody pre-coated wells. In order to quantitatively determine the amount of CoL-1 present in the sample, a standardized preparation of horseradish peroxidase (HRP)-conjugated polyclonal antibody, specific for CoL-1 are added to each well to "sandwich" the CoL-1 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-1 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-1 concentration in each sample is interpolated from this standard curve.

119615037

EAW94631

P02452

138,941 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); Collagen Biosynthesis And Modifying Enzymes Pathway (645289); Collagen Formation Pathway (645288); ECM-receptor Interaction Pathway (83068); ECM-receptor Interaction Pathway (479); Extracellular Matrix Organization Pathway (576262); Focal Adhesion Pathway (198795)

This gene encodes the pro-alpha1 chains 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 VIIA, Ehlers-Danlos syndrome Classical type, Caffey Disease and idiopathic osteoporosis. Reciprocal translocations between chromosomes 17 and 22, where this gene and the gene for platelet-derived growth factor beta are located, are associated with a particular type of skin tumor called dermatofibrosarcoma protuberans, resulting from unregulated expression of the growth factor. Two transcripts, resulting from the use of alternate polyadenylation signals, have been identified for this gene. [provided by R. Dalgleish, Feb 2008]

COL1A1: Type I collagen is a member of group I collagen (fibrillar forming collagen). Defects in COL1A1 are the cause of Caffey disease (CAFFD); also known as infantile cortical hyperostosis. Caffey disease is characterized by an infantile episode of massive subperiosteal new bone formation that typically involves the diaphyses of the long bones, mandible, and clavicles. The involved bones may also appear inflamed, with painful swelling and systemic fever often accompanying the illness. The bone changes usually begin before 5 months of age and resolve before 2 years of age. Defects in COL1A1 are a cause of Ehlers-Danlos syndrome type 1 (EDS1); also known as Ehlers-Danlos syndrome gravis. EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS1 is the severe form of classic Ehlers-Danlos syndrome. Defects in COL1A1 are the cause of Ehlers-Danlos syndrome type 7A (EDS7A); also known as autosomal dominant Ehlers-Danlos syndrome type VII. EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS7A is marked by bilateral congenital hip dislocation, hyperlaxity of the joints, and recurrent partial dislocations. Defects in COL1A1 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 COL1A1 are a cause of osteogenesis imperfecta type 2 (OI2); also known as osteogenesis imperfecta congenita. 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 COL1A1 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 COL1A1 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. Genetic variations in COL1A1 are a cause of susceptibility to osteoporosis (OSTEOP); also known as involutional or senile osteoporosis or postmenopausal osteoporosis. Osteoporosis is characterized by reduced bone mass, disruption of bone microarchitecture without alteration in the composition of bone. Osteoporotic bones are more at risk of fracture. A chromosomal aberration involving COL1A1 is found in dermatofibrosarcoma protuberans. Translocation t(17;22)(q22;q13) with PDGF. Belongs to the fibrillar collagen family. Protein type: Extracellular matrix; Secreted; Secreted, signal peptide. Chromosomal Location of Human Ortholog: 17q21.33. Cellular Component: Golgi apparatus; extracellular matrix; extracellular space; endoplasmic reticulum lumen; extracellular region; collagen type I; secretory granule. Molecular Function: identical protein binding; protein binding; platelet-derived growth factor binding; metal ion binding; extracellular matrix structural constituent. Biological Process: response to peptide hormone stimulus; extracellular matrix organization and biogenesis; intramembranous ossification; collagen fibril organization; response to cAMP; embryonic skeletal development; positive regulation of transcription, DNA-dependent; response to estradiol stimulus; response to corticosteroid stimulus; extracellular matrix disassembly; protein transport; sensory perception of sound; visual perception; collagen biosynthetic process; skeletal development; endochondral ossification; response to drug; blood vessel development; receptor-mediated endocytosis; platelet activation; skin morphogenesis; osteoblast differentiation; collagen catabolic process; response to hyperoxia; response to hydrogen peroxide; blood coagulation; leukocyte migration; positive regulation of cell migration. Disease: Osteogenesis Imperfecta, Type I; Ehlers-danlos Syndrome, Type Vii, Autosomal Dominant; Osteogenesis Imperfecta, Type Ii; Ehlers-danlos Syndrome, Type I; Osteogenesis Imperfecta, Type Iii; Osteoporosis; Caffey Disease; Osteogenesis Imperfecta, Type Iv

48-Strip-Wells

470 USD

96-Strip-Wells

675