Rat Procollagen I N-Terminal Propeptide (PINP) ELISA Kit | PINP elisa kit

Rat Procollagen I N-Terminal Propeptide (PINP) Instant ELISA Kit

Cat. Num. AAA2708189

• Gene Names: Col1a1; COLIA1
• Reactivity: Rat
• Applications: ELISA
• Synonyms: Procollagen I N-Terminal Propeptide (PINP); Rat Procollagen I N-Terminal Propeptide (PINP) Instant ELISA Kit; Procollagen I N-Terminal Propeptide; P1NP; N-Propeptide Of Type I Procollagen; Procollagen I Amino Terminal Propeptide; PINP elisa kit

• Reactivity: Rat
• Specificity: This assay has high sensitivity and excellent specificity for detection of Instant Procollagen I N-Terminal Propeptide (PINP).; No significant cross-reactivity or interference between Instant Procollagen I N-Terminal Propeptide (PINP) and analogues was observed.
• Sequence Length: 1453

• Applicable Applications for PINP elisa kit: ELISA (EIA)
• Assay Type: Double-antibody Sandwich
• Samples: Serum, plasma, tissue homogenates, cell lysates, cell culture supernates and other biological fluids
• Detection Range: 246.9-20000pg/mL
• Sensitivity: The minimum detectable dose of this kit is typically less than 92.4pg/mL
• Precision: Intra-assay Precision (Precision within an assay): 3 samples with low, middle and high level Instant Procollagen I N-Terminal Propeptide (PINP) were tested 20 times on one plate, respectively.; Inter-assay Precision (Precision between assays): 3 samples with low, middle and high level Instant Procollagen I N-Terminal Propeptide (PINP) were tested on 3 different plates, 8 replicates in each plate.; CV(%) = SD/meanX100; Intra-Assay: CV<10%; Inter-Assay: CV<12%
• Test Principle: The test principle applied in this kit is enzyme immunoassay. The microtiter plate provided in this kit has been pre-coated with an antibody specific to Instant Procollagen I N-Terminal Propeptide (PINP). Standards or samples and HRP-labeled detection antibody specific to Instant Procollagen I N-Terminal Propeptide (PINP) (Detection Reagent A) are then added to the appropriate microtiter plate wells. Next, TMB substrate solution is added, only those wells that contain Instant Procollagen I N-Terminal Propeptide (PINP), and HRP-labeled detection antibody 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 Instant Procollagen I N-Terminal Propeptide (PINP) in the samples is then determined by comparing the O.D. of the samples to the standard curve.
• Preparation and Storage: 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)

NCBI and Uniprot Product Information

• NCBI GI #: 158711704
• NCBI GeneID: 29393
• NCBI Accession #: NP_445756.1
• NCBI GenBank Nucleotide #: NP_445756.1
• UniProt Accession #: P02454
• NCBI Official Full Name: collagen alpha-1(I) chain
• NCBI Official Synonym Full Names: collagen type I alpha 1 chain
• NCBI Official Symbol: Col1a1
• NCBI Official Synonym Symbols: COLIA1
• NCBI Protein Information: collagen alpha-1(I) chain
• UniProt Protein Name: Collagen alpha-1(I) chain
• UniProt Gene Name: Col1a1
• UniProt Entry Name: CO1A1_RAT

NCBI Description

extracellular matrix collagen protein [RGD, Feb 2006]

Uniprot Description

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; Secreted, signal peptide; Extracellular matrix

Cellular Component: collagen; collagen type I; cytoplasm; endoplasmic reticulum; extracellular matrix; extracellular region; extracellular space; Golgi apparatus; proteinaceous extracellular matrix; secretory granule

Molecular Function: extracellular matrix structural constituent; identical protein binding; metal ion binding; platelet-derived growth factor binding; protein binding

Biological Process: blood vessel development; collagen biosynthetic process; collagen fibril organization; embryonic skeletal development; endochondral ossification; intramembranous ossification; ossification; osteoblast differentiation; positive regulation of cell migration; positive regulation of transcription, DNA-dependent; protein transport; response to cAMP; response to corticosteroid stimulus; response to drug; response to estradiol stimulus; response to hydrogen peroxide; response to hyperoxia; response to mechanical stimulus; response to nutrient; response to nutrient levels; response to peptide hormone stimulus; response to steroid hormone stimulus; sensory perception of sound; skeletal development; skeletal morphogenesis; skin development; skin morphogenesis; visual perception; wound healing