Overview

  • Product nameAnti-Collagen II [5B2.5] antibodySee 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, Chicken, Human, Pig
  • Immunogen

    Tissue, cells or virus corresponding to Chicken Collagen II. 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 control
    • Cartilage.

Properties

Applications

Our Abpromise guarantee covers the use of ab3092 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Notes
IHC-Fr Use at an assay dependent concentration.

Use at an assay dependent dilution.

IHC-P 1/100. PubMed: 19757060
WB Use a concentration of 1 - 2 µg/ml.
ICC/IF Use at an assay dependent concentration.

Use at an assay dependent concentration.

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
    modifications
    Proline 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
  • Alternative names
    • Alpha 1 type II collagen antibody
    • Alpha-1 type II collagen antibody
    • AOM antibody
    • Cartilage collagen antibody
    • Chondrocalcin antibody
    • CO2A1_HUMAN antibody
    • COL11A3 antibody
    • COL2A1 antibody
    • COL2A1 protein antibody
    • Collagen alpha 1(II) chain precursor antibody
    • Collagen II alpha 1 polypeptide antibody
    • Collagen type II alpha 1 (primary osteoarthritis spondyloepiphyseal dysplasia congenital) antibody
    • MGC131516 antibody
    • SEDC antibody
    see all

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

  • 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.

    See 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.

    See Abreview

  • 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.

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

This product has been referenced in:
  • Guillaume O  et al. Shape-memory porous alginate scaffolds for regeneration of the annulus fibrosus: Effect of TGF-ß3 supplementation and oxygen culture conditions. Acta Biomater 10:1985-95 (2014). Read more (PubMed: 24380722) »
  • Esquivies L  et al. Designer nodal/BMP2 chimeras mimic nodal signaling, promote chondrogenesis, and reveal a BMP2-like structure. J Biol Chem 289:1788-97 (2014). IHC-P ; Chicken . Read more (PubMed: 24311780) »

See all 8 Publications for this product

Product Wall

Application Western blot
Sample Human Cell lysate - whole cell (hMSCs diferentiated to chondrocytes)
Loading amount 50 µg
Specification hMSCs diferentiated to chondrocytes
Treatment beta mercaptoethanol for 5min
Gel Running Conditions Reduced Denaturing (any KD gel)
Blocking step Milk as blocking agent for 1 hour(s) and 0 minute(s) · Concentration: 5% · Temperature: 24°C
Username

Abcam user community

Verified customer

Submitted Mar 26 2013



Unfortunately we have not tested this antibody in zebrafish and therefore we do not know whether it is likely to work. I have compared the immunogen of ab3092 (A purified preparation of lathyritic type II collagen from embryonic chicken stern...

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Application Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections)
Sample Pig Tissue sections (Articular Cartilage)
Specification Articular Cartilage
Fixative 10% NBF
Antigen retrieval step Heat mediated - Buffer/Enzyme Used: Tris/EDTA pH 9.0 or Sodium Citrate pH 6.0
Permeabilization No
Blocking step Serum as blocking agent for 45 minute(s) · Concentration: 1% · Temperature: RT°C
Username

Krista Sider

Verified customer

Submitted Jan 15 2013

Thank you for contacting us.

The information about mammalian collagenase has been added from publication I previously sent. We ourselves do not hold any information regarding mammalian collagenase. The information has been added on the datashe...

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Thank you for contacting us.

Please forward the attached publication to customer. They themselves will be able to find solution for this.

I hope this information is helpful to you. Please do not hesitate to contact us if you need any ...

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Thank you your patience.

I am sorry this product did not perform as stated on the datasheet and for the inconvenience this has caused. As requested, I have issued a free of charge replacement with the order number xxx with ab34712. This will b...

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Yes, I can sent you ab34712 and you would be eligible also for the testing discount for trying it in pig.

I will need to arrange the free of charge replacement shipment via Cedarlane, but can sent you the discount code already now:
DISCOUN...

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Thank you for your phone call. The testing discount information is below as well as the detailed instructions.
As for ab3092, could you please send me the lot number so that I can check that I have the correct Cedarlane order. Also, please let me ...

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Thank you for contacting us.

We unfortunaltey do not sell mammalian collagenase enzyme. Please try Sigma Aldrich website for this.

I hope this information is helpful to you. Please do not hesitate to contact us if you need any more ad...

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Vielen Dank für Ihre Antwort.

Leider haben wir den ab3092 noch nicht gegen Rind getestet. Wir wissen daher nicht, obe er mit Rinkcrossreagiert. Ich kann Ihnen jedoch gerne auch ein Testangebot machen sowie für denab23446 (der ab2344...

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