COL2A1 antibody, Rabbit A' Bovine Collagen II Antibody, Rabbit Polyclonal Antibody

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Rabbit A' Bovine Collagen II Antibody, Rabbit Polyclonal Antibody

Catalog Number: 18-511-244590

Buy COL2A1 antibody -

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Related Product Names:

- COL2A1 antibody; COL2A1; Rabbit A' Bovine Collagen II
- Rabbit A' Bovine Collagen II; Alpha-1 type II collagen; Collagen alpha-1(II) chain

- Gene Information - Information in yellow represents specific gene information and does not necessarily represent specific product details. For more information please contact sales@genwaybio.com.

Gene Name: COL2A1	Gene Name Synonym: N/A
Gi #: N/A	NCBI Acc #: NP_001835.3	Swiss Prot Acc #: P02458
Length (aa): N/A	Mol. Weight (Da): 141785	Chrom Location: N/A

Host Animal: Rabbit

Immunogen: Collagen Type II extracted and purified from bovine cartilage

Specificity: Collagen Type II

Specificity: Cross-reactivity: (RIA) Bovine Collagen Type II 100% Bovine Collagen Type IX <0.1% Bovine Collagen Type XI <3.0%

Type of Product: Polyclonal Antibodies to Collagens and Extracellular Matrix Proteins

Concentration: . Titer: 1:100 (RIA)

Buffer: Not applicable.

Applications Notes : Suitable for use in IFA, RIA, ELISA (tested). For immunostaining of extra or intracellular components in light microscopy. For the quantitation of Collagen Type II in biological fluids or in culture supernatants. In indirect IFA with fluorescent anti-rabbit IgG conjugate, use at the following dilution: 1:40 on frozen bovine articular cartilage. Each laboratory should determine an optimum working titer for use in its particular application. Other applications have not been tested but use in such assays should not necessarily be excluded.

Source/Host: Rabbit

Purity/Purification: Ion exchange chromatography (DEAE-Trisacryl).

Clonality: Polyclonal

Format: Purified, Lyophilized. Reconstitute with 0.5ml deionized water.

Storage: Lyophilized Store (up to 24 months) at 2-8 C. Long term store at -20 C. Reconstituted: Aliquot and store at -20 C for up to 6 months. Avoid multiple freeze/thaw cycles.

Shipping: Products may be shipped on ice pack or dry ice.

TESTING: (secondary reagents and protocols )

Not Available

COL2A1 ANTIBODY TARGET DESCRIPTION:

Synonym Names for COL2A1 antibody: COL2A1; Rabbit A' Bovine Collagen II; Alpha-1 type II collagen; Collagen alpha-1(II) chain

Rabbit A' Bovine Collagen II. Rabbit Antibody to Bovine Collagen Type II

Function: Type II collagen is specific for cartilaginous tissues. It is essential for the normal embryonic development of the skeleton, for linear growth and for the ability of cartilage to resist compressive forces.

Subunit: Homotrimers of alpha 1(II) chains.

Subcellular Location: Secreted, extracellular space, extracellular matrix (By similarity).

Tissue Specificity: High expression of isoform 2 in juvenile chondrocyte and low in fetal chondrocyte.

Ptm: Prolines at the third position of the tripeptide repeating unit (G-X-Y) are hydroxylated in some or all of the chains.

Ptm: The N-telopeptide is covalently linked to the helical COL2 region of alpha 1(IX), alpha 2(IX) and alpha 3(IX) chain. The C-telopeptide is covalently linked to an another site in the helical region of alpha 3(IX) COL2.

Disease: Defects in COL2A1 are the cause of a variety of chondrodysplasia including hypochondrogenesis and osteoarthritis.

Disease: Defects in COL2A1 are the cause of spondyloepiphyseal dysplasia congenital type (SEDC) [MIM:183900]. This disorder is characterized by disproportionate short stature and pleiotropic involvement of the skeletal and ocular systems.

Disease: Defects in COL2A1 are the cause of Strudwick type spondyloepimetaphyseal dysplasia (SEMD) [MIM:184250]. SEMD is characterized by disproportionate short stature, pectus carinatum, and scoliosis, as well as dappled metaphyses (which is not seen in SEDC).

Disease: Defects in COL2A1 are the cause of achondrogenesis hypochondrogenesis type 2 (ACG2) [MIM:200610]. ACG2 is a disease characterized by the absence of ossification in the vertebral column, sacrum and pubic bones.

Disease: Defects in COL2A1 are the cause of Legg-Calve-Perthes disease (LCPD) [MIM:150600]; also known as Legg-Perthes disease or Perthes disease. LCPD is characterized by loss of circulation to the femoral head, resulting in avascular necrosis in a growing child. Clinical pictures of the disease vary, depending on the phase of disease progression through ischemia, revascularization, fracture and collapse, and repair and remodeling of the bone.

Disease: Defects in COL2A1 are the cause of Kniest syndrome (KS) [MIM:156550]; also known as Kniest dysplasia or metatropic dwarfism type II. KS is a moderately severe chondrodysplasia phenotype that results from mutations in the COL2A1 gene. Characteristics of the disorder include a short trunk and extremities, mid-face hypoplasia, cleft palate, myopia, retinal detachment, and hearing loss.

Disease: Defects in COL2A1 are a cause of primary avascular necrosis of femoral head (ANFH) [MIM:608805]; also called ischemic necrosis of the femoral head or osteonecrosis of the femoral head. ANFH causes disability that often requires surgical intervention. Most cases are sporadic, but families in which there is an autosomal dominant inheritance of the disease have been identified. It has been estimated that 300,000 to 600,000 people in the United States have ANFH. Approximately 15,000 new cases of this common and disabling disorder are reported annually. The age at the onset is earlier than that for osteoarthritis. The diagnosis is typically made when patients are between the ages of 30 and 60 years. The clinical manifestations, such as pain on exertion, a limping gait, and a discrepancy in leg length, cause considerable disability. Moreover, nearly 10 percent of the 500,000 total-hip arthroplasties performed each year in the United States involve patients with ANFH. As a result, this disease creates a substantial socioeconomic cost as well as a burden for patients and their families.

Disease: Defects in COL2A1 are the cause of osteoarthritis with mild chondrodysplasia [MIM:604864]. Osteoarthritis is a common disease that produces joint pain and stiffness together with radiologic evidence of progressive degeneration of joint cartilage. Some forms of osteoarthritis are secondary to events such as trauma, infections, metabolic disorders, or congenital or heritable conditions that deform the epiphyses or related structures. In most patients, however, there is no readily identifiable cause of osteoarthritis. Inheritance in a Mendelian dominant manner has been demonstrated in some families with primary generalized osteoarthritis. Reports demonstrate coinheritance of primary generalized osteoarthritis with specific alleles of the gene COL2A1, the precursor of the major protein of cartilage.

Disease: Defects in COL2A1 are the cause of platyspondylic lethal skeletal dysplasia Torrance type (PLSD-T) [MIM:151210]. Platyspondylic lethal skeletal dysplasias (PLSDs) are a heterogeneous group of chondrodysplasias characterized by severe platyspondyly and limb shortening. PLSD-T is characterized by varying platyspondyly, short ribs with anterior cupping, hypoplasia of the lower ilia with broad ischial and pubic bones, and shortening of the tubular bones with splayed and cupped metaphyses. Histology of the growth plate typically shows focal hypercellularity with slightly enlarged chondrocytes in the resting cartilage and relatively well-preserved columnar formation and ossification at the chondro-osseous junction. PLSD-T is generally a perinatally lethal disease, but a few long-term survivors have been reported.

Disease: Defects in COL2A1 are the cause of multiple epiphyseal dysplasia with myopia and conductive deafness (EDMMD) [MIM:132450]. Multiple epiphyseal dysplasia is a generalized skeletal dysplasia associated with significant morbidity. Joint pain, joint deformity, waddling gait, and short stature are the main clinical signs and symptoms. EDMMD is an autosomal dominant disorder characterized by epiphyseal dysplasia associated with progressive myopia, retinal thinning, crenated cataracts, conductive deafness.

Disease: Defects in COL2A1 are the cause of spondyloperipheral dysplasia (SPD) [MIM:271700]. SPD patients manifest short stature, midface hypoplasia, sensorineural hearing loss, spondyloepiphyseal dysplasia, platyspondyly and brachydactyly.

Disease: Defects in COL2A1 are the cause of Wagner syndrome type II (WS-II); a disease characterized by early-onset cataracts, lattice degeneration of the retina, and retinal detachment without involvement of monocular tissues.

Disease: Defects in COL2A1 are the cause of Stickler syndrome type 1 (STL1) [MIM:108300]; also known as vitreous type 1, or membranous vitreous type. STL1 is an autosomal dominant disorder characterized by progressive myopia beginning in the first decade of life, vitreo-retinal degeneration, retinal detachment, cleft palate, midfacial hypoplasia, osteoarthritis, and sensorineural hearing loss.

Disease: Defects in COL2A1 are a cause of autosomal dominant rhegmatogenous retinal detachment (DRRD) [MIM:609508]. RDD most frequently results from retinal tearing at the time of posterior vitreous detachment. Non-syndromic RRD can be inherited in a clearly dominant fashion, although in most of these cases, the genetic locus for the disorder is unknown. However, RRD is also a common feature of the type II collagenopathies (disorders due to mutations in the gene COL2A1) and some recent examples of mutations in this gene suggest that COL2A1 should be considered a candidate gene for dominant RRD (DRRD).

Disease: Of special interest are three different variants that replace arginine codons at positions 275, 719 and 989 in the triple-helical domain with codons for cysteine, an amino acid not normally found in the triple-helical domain of type II collagen from any species. They are of special interest, because they are the only amino acid substitutions in the triple-helical domain that replaces a Y-position amino acid and cause a disease phenotype. Also, they are recurrent in that they have been found in more than one unrelated individual.

Similarity: Belongs to the fibrillar collagen family.

Similarity: Contains 1 VWFC domain.

OMIM: 108300; phenotype. [NCBI / EBI]
120140; gene+phenotype. [NCBI / EBI]
132450; phenotype. [NCBI / EBI]
150600; phenotype. [NCBI / EBI]
151210; phenotype. [NCBI / EBI]
156550; phenotype. [NCBI / EBI]
183900; phenotype. [NCBI / EBI]
184250; phenotype. [NCBI / EBI]
200610; phenotype. [NCBI / EBI]
271700; phenotype. [NCBI / EBI]
604864; phenotype. [NCBI / EBI]
608805; phenotype. [NCBI / EBI]
609508; phenotype. [NCBI / EBI]

Pathways:
KEGG pathway: Cell Communication 01430
KEGG pathway: ECM-receptor interaction 04512
KEGG pathway: Focal adhesion 04510

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Precautions: COL2A1 antibody is for in vitro research use only. Not for use in diagnostics or therapeutic procedures.

Important Notes: During shipment, small volumes of COL2A1 antibody vial. For products with volumes of 200 µL or less, we recommend gently tapping the vial on a hard surface or briefly centrifuging the vial in a tabletop centrifuge to dislodge any liquid in the container’s cap. Actual concentration, volume and quantity will be printed on the vial's label. Please refer to the vials label for this information.

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