product summary
Loading...
company name :
MyBioSource
product type :
ELISA/assay
product name :
Rat Cross Linked N-Telopeptide Of Type I Collagen (NTXI) ELISA Kit
catalog :
MBS263860
quantity :
48-Strip-Wells
price :
290 USD
more info or order :
product information
catalog number :
MBS263860
products type :
ELISA Kit
products full name :
Rat Cross Linked N-Telopeptide Of Type I Collagen (NTXI) ELISA Kit
products short name :
Cross Linked N-Telopeptide Of Type I Collagen (NTXI)
other names :
Collagen alpha-2(I) chain; Collagen alpha-2(I) chain; collagen alpha-2(I) chain; collagen alpha-2(I) chain; type I procollagen; alpha 2(I)-collagen; alpha-2 type I collagen; collagen I, alpha-2 polypeptide; collagen of skin, tendon and bone, alpha-2 chain; collagen, type I, alpha 2; Alpha-2 type I collagen
products gene name :
NTXI
other gene names :
COL1A2; COL1A2; OI4
uniprot entry name :
CO1A2_HUMAN
reactivity :
Rat
sequence length :
1366
specificity :
No cross-reaction with other factors.
storage stability :
Store all reagents at 2-8 degree C.
other info1 :
Samples: Rat serum, plasma or cell culture supernatant and organizations in the natural and recombinant NTXI concentration. Assay Type: Sandwich. Detection Range: 200 ng/ml-3.12 ng/ml. Sensitivity: 0.6 ng/ml.
other info2 :
Intra-assay Precision: <= 8%. Inter-assay Precision: <= 12%
products description :
Principle of the Assay This experiment use double-sandwich elisa technique and the ELISA Kit provided is typical. The pre-coated antibody is Rat NTXI monoclonal antibody and the detecting antibody is polyclonal antibody with biotin labeled. Samples and biotin labeling antibody are added into ELISA plate wells and washed out with PBS or TBS. Then Avidin-peroxidase conjugates are added to ELISA wells in order; Use TMB substrate for coloring after reactant thoroughly washed out by PBS or TBS. TMB turns into blue in peroxidase catalytic and finally turns into yellow under the action of acid. The color depth and the testing factors in samples are positively correlated.
ncbi gi num :
296439507
ncbi acc num :
P08123.7
ncbi mol weight :
129,314 Da
ncbi pathways :
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)
ncbi summary :
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]
uniprot summary :
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; metal ion binding; platelet-derived growth factor binding; SMAD binding. Biological Process: platelet activation; receptor-mediated endocytosis; blood vessel development; extracellular matrix organization and biogenesis; collagen fibril organization; skin morphogenesis; Rho protein signal transduction; odontogenesis; extracellular matrix disassembly; collagen catabolic process; transforming growth factor beta receptor signaling pathway; regulation of blood pressure; blood coagulation; skeletal development; leukocyte migration. 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
size1 :
48-Strip-Wells
price1 :
290 USD
size2 :
96-Strip-Wells
price2 :
450
more info or order :
company information
MyBioSource
P.O. Box 153308
San Diego, CA 92195-3308
sales@mybiosource.com
https://www.mybiosource.com
1-888-627-0165
headquarters: USA
MyBioSource, LLC was orginally founded in Vancouver by three enthusiastic scientists who are passionate about providing the world with the best reagents available. Together, they form a company with a big vision known as MyBioSource. MyBioSource is now located in San Diego, California, USA.

"MyBioSource's number 1 vision is to be the world's number 1 quality reagents provider."

Our goal is to provide researchers, scientists and customers alike with a one-stop-shop for all of their reagents needs, whether it is monoclonal antibody, polyclonal antibody, recombinant protein, peptide, etc...

"MyBioSource offers the best products at unbeatable prices."

Please spend a few minutes to browse our online catalogs and see the wide range of products available. We ship our products through our shipping/distribution facility in San Diego, California, USA.

Would you like to receive email and e-newsletter from MyBioSource about new products, special offers and events? Please click here to join our Mailing List!