ELISA/assay

Collagen Type I (COL1) ELISA Kit

MBS2022912

24-Strip-Wells

260 USD

ELISA Kit

Collagen Type I (COL1) ELISA Kit

[Collagen Type I (COL1)]

[Collagen, type I, alpha 2; Collagen alpha-2(I) chain; collagen alpha-2(I) chain; collagen, type I, alpha 2; Alpha-2 type I collagen]

[COL1]

[COL1A2; COL1A2; OI4]

CO1A2_HUMAN

Mouse

1,366

This assay has high sensitivity and excellent specificity for detection of CNTN6. No significant cross-reactivity or interference between CNTN6 and analogues was observed.

The stability of kit is determined by the loss rate of activity. The loss rate of this kit is less than 5% within the expiration date under appropriate storage condition. 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.

Typical Testing Data/Standard Curve (for reference only)

Samples: Human Serum, Plasma, Tissue Homogenates, Cell Lysates, Cell Culture Supernates And Other Biological Fluids. Assay Type: Quantitative Sandwich. Detection Range: 0.156-10ng/mL. Sensitivity: 0.059ng/mL.

Intra-assay Precision: Intra-assay Precision (Precision within an assay): 3 samples with low, middle and high level CNTN6 were tested 20 times on one plate, respectively. Intra-Assay: CV<10%. Inter-assay Precision: Inter-assay Precision (Precision between assays): 3 samples with low, middle and high level CNTN6 were tested on 3 different plates, 8 replicates in each plate. CV(%) = SD/meanX100. Inter-Assay: CV<12%

Metabolic pathway; Developmental science; Bone metabolism

Intended Uses: The kit is a sandwich enzyme immunoassay for in vitro quantitative measurement of CNTN6 in human serum, plasma, tissue homogenates, cell lysates, cell culture supernates and other biological fluids. Principle of the Assay: The microplate provided in this kit has been pre-coated with an antibody specific to CNTN6. Standards or samples are then added to the appropriate microplate wells with a biotin-conjugated antibody specific to CNTN6. 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 CNTN6, 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 CNTN6 in the samples is then determined by comparing the O.D. of the samples to the standard curve.

45708783

AAH42586.1

129,314 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); C-MYB Transcription Factor Network Pathway (138073); Collagen Biosynthesis And Modifying Enzymes Pathway (645289); Collagen Formation Pathway (645288); ECM-receptor Interaction Pathway (83068); ECM-receptor Interaction Pathway (479); Endothelins Pathway (137958)

This gene encodes the pro-alpha2 chain 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 VIIB, recessive Ehlers-Danlos syndrome Classical type, idiopathic osteoporosis, and atypical Marfan syndrome. Symptoms associated with mutations in this gene, however, tend to be less severe than mutations in the gene for the alpha1 chain of type I collagen (COL1A1) reflecting the different role of alpha2 chains in matrix integrity. Three transcripts, resulting from the use of alternate polyadenylation signals, have been identified for this gene. [provided by R. Dalgleish, Feb 2008]

COL1A2: Type I collagen is a member of group I collagen (fibrillar forming collagen). Defects in COL1A2 are the cause of Ehlers-Danlos syndrome type 7B (EDS7B). EDS is a connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. EDS7B is marked by bilateral congenital hip dislocation, hyperlaxity of the joints, and recurrent partial dislocations. Defects in COL1A2 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 COL1A2 are a cause of osteogenesis imperfecta type 2 (OI2); also known as osteogenesis imperfecta congenita (OIC) or lethal perinatal. 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 COL1A2 are the cause of Ehlers-Danlos syndrome autosomal recessive cardiac valvular form (EDSCV). A connective tissue disorder characterized by hyperextensible skin, atrophic cutaneous scars due to tissue fragility and joint hyperlaxity. In addition to joint laxity, skin hyperextensibility and friability, and abnormal scar formation, patients have mitral valve prolapse and insufficiency, mitral regurgitation, and aortic insufficiency. Defects in COL1A2 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 COL1A2 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. A chromosomal aberration involving COL1A2 may be a cause of lipoblastomas, which are benign tumors resulting from transformation of adipocytes, usually diagnosed in children. Translocation t(7;8)(p22;q13) with PLAG1. Belongs to the fibrillar collagen family. Protein type: Secreted, signal peptide; Secreted. Chromosomal Location of Human Ortholog: 7q22.1. Cellular Component: extracellular matrix; extracellular space; endoplasmic reticulum lumen; extracellular region; collagen type I. Molecular Function: protein binding, bridging; identical protein binding; protein binding; extracellular matrix structural constituent; platelet-derived growth factor binding; metal ion binding; SMAD binding. Biological Process: odontogenesis; extracellular matrix disassembly; platelet activation; blood vessel development; collagen catabolic process; receptor-mediated endocytosis; extracellular matrix organization and biogenesis; collagen fibril organization; skin morphogenesis; transforming growth factor beta receptor signaling pathway; regulation of blood pressure; blood coagulation; skeletal development; leukocyte migration; Rho protein signal transduction. Disease: Ehlers-danlos Syndrome, Type Vii, Autosomal Dominant; Osteogenesis Imperfecta, Type Ii; Ehlers-danlos Syndrome, Autosomal Recessive, Cardiac Valvular Form; Osteogenesis Imperfecta, Type Iii; Osteoporosis; Osteogenesis Imperfecta, Type Iv

24-Strip-Wells

260 USD

48-Strip-Wells

465

96-Strip-Wells

625

5x96-Strip-Wells

2530

10x96-Strip-Wells

4565