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MAB8887 Anti-Collagen Type II Antibody, clone 6B3

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MAB8887
50 µg  
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Overview

Replacement Information

Key Specifications Table

Species ReactivityKey ApplicationsHostFormatAntibody Type
Ch, H, M, SalIF, IHC, WBMPurifiedMonoclonal Antibody
Description
Catalogue NumberMAB8887
Brand Family Chemicon®
Trade Name
  • Chemicon
DescriptionAnti-Collagen Type II Antibody, clone 6B3
References
Product Information
FormatPurified
HS Code3002 15 90
Control
  • Cartilage in lung or fetus
PresentationPurified immunoglobulin in 10 mM PBS, pH 7.4 with 0.2% BSA and 0.09% sodium azide.
Quality LevelMQ100
Applications
ApplicationAnti-Collagen Type II Antibody, clone 6B3 is an antibody against Collagen Type II for use in IF, IH & WB.
Key Applications
  • Immunofluorescence
  • Immunohistochemistry
  • Western Blotting
Application NotesWestern Blot (Mayne, 1994)

Immunohistochemistry (Formalin/Paraffin): 1-2 μg/mL, 30 minutes at room temperature. Staining of paraffin embedded tissues requires digestion of tissue sections with pepsin at 1mg/mL in Tris HCl, pH 2.0 for 15 minutes at RT or 10 minutes at 37ºC.

Immunofluorescence

ELISA

Optimal working dilutions must be determined by end user.
Biological Information
ImmunogenPurified type II collagen; obtained from adult chicken sternum by limited pepsinization.
Clone6B3
ConcentrationPlease refer to the Certificate of Analysis for the lot-specific concentration.
HostMouse
SpecificityIn Western blotting (but not ELISA), MAB8887 recognizes both a1(II) and a3(XI) chains which have identical primary structure. In Western blotting, MAB8887 reacts with the TCA fragment of lathyritic type II collagen after digestion with mammalian collagenase. It also reacts with pepsin-digested type II collagen. It will not react with intact Collagen II under traditional conditions.

Its epitope is localized in the triple helix of type II collagen. It shows no cross-reaction with type I or type III collagen. Immunoblotting of CNBr peptides of collagen II shows that MAB8887 reacts with CB11 (25kDa) fragment which is the site of immunogenic and arthritogenic epitopes along the intact type II molecule.

In pepsin solublized collagen II, MAB8887 reacts with a 95-97 kDa fragment, as well as, the native single chain of 120kDa. If propeptides are present, MAB8887 will detect a 200kDa fragment.
IsotypeIgG1
Species Reactivity
  • Chicken
  • Human
  • Mouse
  • Salamander
Antibody TypeMonoclonal Antibody
Entrez Gene Number
Entrez Gene SummaryThis gene encodes the alpha-1 chain of type II collagen, a fibrillar collagen found in cartilage and the vitreous humor of the eye. Mutations in this gene are associated with achondrogenesis, chondrodysplasia, early onset familial osteoarthritis, SED congenita, Langer-Saldino achondrogenesis, Kniest dysplasia, Stickler syndrome type I, and spondyloepimetaphyseal dysplasia Strudwick type. In addition, defects in processing chondrocalcin, a calcium binding protein that is the C-propeptide of this collagen molecule, are also associated with chondrodysplasia. There are two transcripts identified for this gene.
Gene Symbol
  • COL2A1
  • SEDC
  • COL11A3
  • ANFH
  • MGC131516
  • chondrocalcin
  • AOM
Purification MethodProtein G Purified
UniProt Number
UniProt SummaryFUNCTION: SwissProt: P02458 # 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.
SIZE: 1487 amino acids; 141785 Da
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. & 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: SwissProt: P02458 # Defects in COL2A1 are the cause of a variety of chondrodysplasia including hypochondrogenesis and osteoarthritis. & 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. & 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). & 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. & 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. & 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. & 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. & 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. & 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. & 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. & 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. & 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. & 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. & 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). & 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: SwissProt: P02458 ## Belongs to the fibrillar collagen family. & Contains 1 VWFC domain.
Molecular Weight120 kDa
Physicochemical Information
Dimensions
Materials Information
Toxicological Information
Safety Information according to GHS
Safety Information
Product Usage Statements
Usage Statement
  • Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Storage and Shipping Information
Storage ConditionsMaintain at 2–8°C in undiluted aliquots for up to 12 months
Packaging Information
Material Size50 µg
Transport Information
Supplemental Information
Specifications
Global Trade Item Number
Catalog Number GTIN
MAB8887 04053252398643

Documentation

Anti-Collagen Type II Antibody, clone 6B3 SDS

Title

Safety Data Sheet (SDS) 

Anti-Collagen Type II Antibody, clone 6B3 Certificates of Analysis

TitleLot Number
MOUSE ANTI-CHICKEN COLLAGEN TYPE II 2915272
MOUSE ANTI-CHICKEN COLLAGEN TYPE II MONOCLONAL ANTIBODY - 2122421 2122421
MOUSE ANTI-CHICKEN COLLAGEN TYPE II MONOCLONAL ANTIBODY - 2370664 2370664
MOUSE ANTI-CHICKEN COLLAGEN TYPE II MONOCLONAL ANTIBODY - 2382098 2382098
MOUSE ANTI-CHICKEN COLLAGEN TYPE II MONOCLONAL ANTIBODY - 2390370 2390370
MOUSE ANTI-CHICKEN COLLAGEN TYPE II MONOCLONAL ANTIBODY - 2397072 2397072
MOUSE ANTI-CHICKEN COLLAGEN TYPE II MONOCLONAL ANTIBODY - 2459047 2459047
MOUSE ANTI-CHICKEN COLLAGEN TYPE II - 3160123 3160123
MOUSE ANTI-CHICKEN COLLAGEN TYPE II - 3215502 3215502
MOUSE ANTI-CHICKEN COLLAGEN TYPE II - 3232344 3232344

References

Reference overviewApplicationPub Med ID
Mesenchymal stem cells in rabbit meniscus and bone marrow exhibit a similar feature but a heterogeneous multi-differentiation potential: superiority of meniscus as a cell source for meniscus repair.
Ding, Z; Huang, H
BMC musculoskeletal disorders  16  65  2015

Show Abstract
25887689 25887689
Using the avian mutant talpid2 as a disease model for understanding the oral-facial phenotypes of oral-facial-digital syndrome.
Schock, EN; Chang, CF; Struve, JN; Chang, YT; Chang, J; Delany, ME; Brugmann, SA
Disease models & mechanisms  8  855-66  2015

Show Abstract
Immunoblotting (Western)26044959 26044959
Low-density lipoprotein receptor-related protein 5 governs Wnt-mediated osteoarthritic cartilage destruction.
Shin, Y; Huh, YH; Kim, K; Kim, S; Park, KH; Koh, JT; Chun, JS; Ryu, JH
Arthritis research & therapy  16  R37  2014

Show Abstract
24479426 24479426
Prostaglandin E2 (PGE2) exerts biphasic effects on human tendon stem cells.
Zhang, J; Wang, JH
PloS one  9  e87706  2014

Show Abstract
24504456 24504456
Increased mandibular condylar growth in mice with estrogen receptor beta deficiency.
Kamiya, Y; Chen, J; Xu, M; Utreja, A; Choi, T; Drissi, H; Wadhwa, S
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research  28  1127-34  2013

Show Abstract
23197372 23197372
Repair of a chondral defect using a cell free scaffold in a young patient--a case report of successful scaffold transformation and colonisation.
Schüettler, KF; Struewer, J; Rominger, MB; Rexin, P; Efe, T
BMC surgery  13  11  2013

Show Abstract
23590134 23590134
Structural and functional analysis of intra-articular interzone tissue in axolotl salamanders.
Cosden-Decker, RS; Bickett, MM; Lattermann, C; MacLeod, JN
Osteoarthritis and cartilage / OARS, Osteoarthritis Research Society  20  1347-56  2012

Show Abstract
Immunohistochemistry22800772 22800772
Basic fibroblast growth factor supports expansion of mouse compact bone-derived mesenchymal stem cells (MSCs) and regeneration of bone from MSC in vivo.
Eiki Yamachika,Hidetsugu Tsujigiwa,Masakazu Matsubara,Yasuhisa Hirata,Kenichiro Kita,Kiyofumi Takabatake,Nobuyoshi Mizukawa,Yoshihiro Kaneda,Hitoshi Nagatsuka,Seiji Iida
Journal of molecular histology  43  2012

Show Abstract
22203245 22203245
Articular Cartilage Regeneration With Autologous Peripheral Blood Progenitor Cells and Hyaluronic Acid After Arthroscopic Subchondral Drilling: A Report of 5 Cases With Histology.
Saw KY, Anz A, Merican S, Tay YG, Ragavanaidu K, Jee CS, McGuire DA
Arthroscopy  2011

Show Abstract
21334844 21334844
Uniaxial mechanical strain modulates the differentiation of neural crest stem cells into smooth muscle lineage on micropatterned surfaces.
Li, X; Chu, J; Wang, A; Zhu, Y; Chu, WK; Yang, L; Li, S
PloS one  6  e26029  2011

Show Abstract Full Text Article
22016804 22016804

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Categories

Life Science Research > Antibodies and Assays > Primary Antibodies