Anti-Collagen II antibody [5B2.5] (ab3092)

Overview

• Product nameAnti-Collagen II antibody [5B2.5]See all Collagen II primary antibodies ...
• Description
  Mouse monoclonal [5B2.5] to Collagen II
• SpecificityThis antibody is highly specific to type II collagen and shows no cross-reaction with types I, III, IV, V, VI, IX, X, or XI. In Western blotting, this antibody reacts with the TCA fragment of lathyritic type II collagen after digestion with mammalian collagenase. It does not react with pepsin-digested type II collagen.
• Tested applicationsIHC-Fr, IHC-P, WB, ICC/IF more details
• Species reactivity
  Reacts with: Mouse, Human, Pig
  Predicted to work with: Chicken
• Immunogen

  A purified preparation of lathyritic type II collagen from embryonic chicken sternum.

• EpitopeGGFDEK, slightly preceding the lysine residue involved in crosslinking. Two terminal glycine residues consitute a key structural element of the epitope. The epitope is lost after digestion of lathyritic type II collagen with recombinant stromelysin.
• Positive controlCartilage.

Properties

• FormLiquid
• Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
• Storage buffer10mM PBS, pH7.4, 0.2%BSA, 0.09% sodium azide
• Concentration information loading...
• PurityProtein A purified
• Clonality Monoclonal
• Clone number5B2.5
• IsotypeIgG2a
• Light chain typekappa
• Research Areas
  • Stem Cells
  • Mesenchymal Stem Cells
  • Chondrogenesis

  • Signal Transduction
  • Cytoskeleton / ECM
  • Extracellular Matrix
  • ECM Proteins
  • Collagen

  • Signal Transduction
  • Cytoskeleton / ECM
  • Extracellular Matrix
  • Structures
  • Bone

Applications

Target

• FunctionType 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.
• Tissue specificityIsoform 2 is highly expressed in juvenile chondrocyte and low in fetal chondrocyte.
• Involvement in diseaseDefects 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 spondyloepimetaphyseal dysplasia Strudwick type (SEMD-STR) [MIM:184250]. A bone disease characterized by disproportionate short stature from birth, with a very short trunk and shortened limbs, and skeletal abnormalities including lordosis, scoliosis, flattened vertebrae, pectus carinatum, coxa vara, clubfoot, and abnormal epiphyses or metaphyses. A distinctive radiographic feature is irregular sclerotic changes, described as dappled in the metaphyses of the long bones.
  Defects in COL2A1 are the cause of achondrogenesis type 2 (ACG2) [MIM:200610]; also known as achondrogenesis-hypochondrogenesis type II. 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 dysplasia (KD) [MIM:156550]; also known as Kniest syndrome or metatropic dwarfism type II. KD 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 known as 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 (OACD) [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 Stickler syndrome type 1 (STL1) [MIM:108300]; also known as vitreous type 1, or membranous vitreous type. STL1 is an autosomal dominant form of Stickler syndrome, an inherited disorder that associates ocular signs with more or less complete forms of Pierre Robin sequence, bone disorders and sensorineural deafness. Ocular disorders may include juvenile cataract, myopia, strabismus, vitreoretinal or chorioretinal degeneration, retinal detachment, and chronic uveitis. Robin sequence includes an opening in the roof of the mouth (a cleft palate), a large tongue (macroglossia), and a small lower jaw (micrognathia). Bones are affected by slight platyspondylisis and large, often defective epiphyses. Juvenile joint laxity is followed by early signs of arthrosis. The degree of hearing loss varies among affected individuals and may become more severe over time. Syndrome expressivity is variable.
  Defects in COL2A1 are the cause of Stickler syndrome type 1 non-syndromic ocular (STL1O) [MIM:609508]. STL1O is an autosomal dominant form of Stickler syndrome characterized by the ocular signs typically seen in STL1 such as cataract, myopia, retinal detachment. STL1 systemic features of premature osteoarthritis, cleft palate, hearing impairment, and craniofacial abnormalities are either absent or very mild in STL1O patients.
  Defects in COL2A1 are a cause of rhegmatogenous retinal detachment autosomal dominant (DRRD) [MIM:609508]. Rhegmatogenous retinal detachment most frequently results from a break or tear in the retina that allows fluid from the vitreous humor to enter the potential space beneath the retina. It is often associated with pathologic myopia and in most cases leads to visual impairment or blindness if untreated.
• Sequence similaritiesBelongs to the fibrillar collagen family.
  Contains 1 fibrillar collagen NC1 domain.
  Contains 1 VWFC domain.
• Post-translational
  modificationsProline residues at the third position of the tripeptide repeating unit (G-X-Y) are hydroxylated in some or all of the chains. Proline residues at the second position of the tripeptide repeating unit (G-X-Y) are hydroxylated in some 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.
• Cellular localizationSecreted > extracellular space > extracellular matrix.

Target information above from: UniProt accession P02458 The UniProt Consortium
The Universal Protein Resource (UniProt) in 2010
Nucleic Acids Res. 38:D142-D148 (2010) .

Information by UniProt
• Database links
  • Entrez Gene: 395069 Chicken
  • Entrez Gene: 1280 Human
  • Entrez Gene: 12824 Mouse
  • Entrez Gene: 397323 Pig
  • Omim: 120140 Human
  • SwissProt: P02458 Human
  • SwissProt: P28481 Mouse
  • Unigene: 408182 Human

  • Unigene: 2423 Mouse

  see all

• Alternative names
  Alpha 1 type II collagen antibodyAlpha-1 type II collagen antibodyAOM antibody

  Cartilage collagen antibodyChondrocalcin antibodyCO2A1_HUMAN antibodyCOL11A3 antibodyCOL2A1 antibodyCOL2A1 protein antibodyCollagen alpha 1(II) chain precursor antibodyCollagen II alpha 1 polypeptide antibodyCollagen type II alpha 1 (primary osteoarthritis spondyloepiphyseal dysplasia congenital) antibodyMGC131516 antibodySEDC antibody

  see all

Anti-Collagen II antibody [5B2.5] images

• 

  Immunohistochemistry (Frozen sections) - Collagen II antibody [5B2.5] (ab3092)Image courtesy of Leanne Partington by Abreview.
  ab3092 staining Collagen II in porcine trachea by Immunohistochemistry (Frozen sections).
  
  Tissue was fixed in acetone. Samples were then blocked using 1% BSA/ 10% goat serum for 2 hours at room temperature and then incubated with ab3092 at a 1/100 dilution for 18 hours at 4°C. The secondary used was an Alexa-Fluor 488 goat anti-mouse IgG (H+L) monoclonal, used at a 1/200 dilution.

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• 

  Immunohistochemistry (Frozen sections) - Collagen II antibody [5B2.5] (ab3092)Image from Meech R et al, Development. 2005 May;132(9):2135-46. Epub 2005 Mar 30, Fig 2. DOI 10.1242/dev.01811
  ab3092 staining Collagen II in murine developing limbs by Immunohistochemistry (Frozen sections).
  
  Barx2 (red) and collagen II (green) protein expression during limb development. Barx2 and collagen II are co-expressed in the developing articular cartilage of carpal joints in newborn mice.
• 

  Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Collagen II antibody [5B2.5] (ab3092)Image courtesy of an anonymous Abreview.
  ab3092 staining Collagen II in decalcified rabbit femur sections by Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections).
  
  Sections were fixed in formaldehyde and a heat mediated antigen retrieval step was performed. Samples were then permeabilized using methanol and incubated with ab3092 at a 1/100 dilution for 1 hour. The secondary used was an undiluted HRP conjugated goat anti-mouse polyclonal.

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