ELISA/assay

Mouse Collagen alpha-1 (I) chain, COL1A1 ELISA Kit

MBS945699

48-Strip-Wells

510 USD

ELISA Kit

Mouse Collagen alpha-1 (I) chain, COL1A1 ELISA Kit

collagen, type I, alpha 1

Mouse Collagen alpha-1 (I) chain (COL1A1) ELISA kit; OI4; alpha 1 type I collagen; collagen alpha 1 chain type I; collagen of skin; tendon and bone; alpha-1 chain; pro-alpha-1 collagen type 1; collagen; type I; alpha 1

collagen alpha-1(I) chain; Collagen alpha-1(I) chain; collagen alpha-1(I) chain; collagen alpha-1(I) chain; alpha-1 type 1 collagen; alpha-1 type I collagen; procollagen, type I, alpha 1; collagen, type I, alpha 1; Alpha-1 type I collagen

COL1A1

Col1a1; Col1a1; Cola1; Mov13; Cola-1; Mov-13; Col1a-1; Cola1

CO1A1_MOUSE

Mouse

1453

This assay has high sensitivity and excellent specificity for detection of mouse COL1A1. No significant cross-reactivity or interference between mouse COL1A1 and analogues was observed.

Unopened test kits should be stored at 2 to 8 degree C upon receipt. Please refer to pdf manual for further storage instructions.

Samples: Serum, plasma, tissue homogenates. Assay Type: Sandwich. Detection Range: 0.312 ng/ml -20 ng/ml. Sensitivity: The minimum detectable dose of mouse COL1A1 is typically less than 0.078 nng/ml. The sensitivity of this assay, or Lower Limit of Detection (LLD) was defined as the lowest protein concentration that could be differentiated from zero. It was determined the mean O.D value of 20 replicates of the zero standard added by their three standard deviations.

Intra-assay Precision: Intra-assay Precision (Precision within an assay): CV%<8%. Three samples of known concentration were tested twenty times on one plate to assess. Inter-assay Precision: Inter-assay Precision (Precision between assays): CV%<10%. Three samples of known concentration were tested in twenty assays to assess.

Principle of the assay: This assay employs the quantitative sandwich enzyme immunoassay technique. Antibody specific for COL1A1 has been pre-coated onto a microplate. Standards and samples are pipetted into the wells and any COL1A1 present is bound by the immobilized antibody. After removing any unbound substances, a biotin-conjugated antibody specific for COL1A1 is added to the wells. After washing, avidin conjugated Horseradish Peroxidase (HRP) is added to the wells. Following a wash to remove any unbound avidin-enzyme reagent, a substrate solution is added to the wells and color develops in proportion to the amount of COL1A1 bound in the initial step. The color development is stopped and the intensity of the color is measured.

34328108

NP_031768.2

NM_007742.3

P11087

138,032 Da

Amoebiasis Pathway (167330); Amoebiasis Pathway (167191); Axon Guidance Pathway (575211); Cell Surface Interactions At The Vascular Wall Pathway (575507); Developmental Biology Pathway (575210); ECM-receptor Interaction Pathway (83265); ECM-receptor Interaction Pathway (479); Focal Adhesion Pathway (198353); Focal Adhesion Pathway (83264); Focal Adhesion Pathway (478)

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. [provided by RefSeq, Sep 2015]

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: Secreted, signal peptide; Extracellular matrix; Secreted. Cellular Component: extracellular matrix; Golgi apparatus; proteinaceous extracellular matrix; extracellular space; collagen; endoplasmic reticulum; cytoplasm; collagen type I; extracellular region; secretory granule. Molecular Function: identical protein binding; protein binding; extracellular matrix structural constituent; platelet-derived growth factor binding; metal ion binding. Biological Process: skin development; blood vessel development; intramembranous ossification; collagen fibril organization; skin morphogenesis; wound healing; embryonic skeletal development; positive regulation of transcription, DNA-dependent; protein transport; sensory perception of sound; visual perception; skeletal morphogenesis; collagen biosynthetic process; skeletal development; endochondral ossification; positive regulation of cell migration

48-Strip-Wells

510 USD

96-Strip-Wells

725

5x96-Strip-Wells

2565

10x96-Strip-Wells

4800