Recombinant Anti-Collagen II antibody [EPR12268] (ab188570)
Key features and details
- Produced recombinantly (animal-free) for high batch-to-batch consistency and long term security of supply
- Rabbit monoclonal [EPR12268] to Collagen II
- Suitable for: WB
- Reacts with: Rat, Human
Related conjugates and formulations
Overview
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Product name
Anti-Collagen II antibody [EPR12268]
See all Collagen II primary antibodies -
Description
Rabbit monoclonal [EPR12268] to Collagen II -
Host species
Rabbit -
Tested applications
Suitable for: WBmore details
Unsuitable for: ICC/IF -
Species reactivity
Reacts with: Rat, Human -
Immunogen
Synthetic peptide. This information is proprietary to Abcam and/or its suppliers.
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General notes
This product is a recombinant monoclonal antibody, which offers several advantages including:
- - High batch-to-batch consistency and reproducibility
- - Improved sensitivity and specificity
- - Long-term security of supply
- - Animal-free production
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
We are constantly working hard to ensure we provide our customers with best in class antibodies. As a result of this work we are pleased to now offer this antibody in purified format. We are in the process of updating our datasheets. The purified format is designated 'PUR' on our product labels. If you have any questions regarding this update, please contact our Scientific Support team.
Properties
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Form
Liquid -
Storage instructions
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle. -
Storage buffer
pH: 7.2
Preservative: 0.01% Sodium azide
Constituents: 59% PBS, 40% Glycerol (glycerin, glycerine), 0.05% BSA -
Concentration information loading...
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Purity
Protein A purified -
Clonality
Monoclonal -
Clone number
EPR12268 -
Isotype
IgG -
Research areas
Associated products
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Alternative Versions
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Isotype control
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Related Products
Applications
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab188570 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Application | Abreviews | Notes |
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WB |
1/1000 - 1/10000. Predicted molecular weight: 141 kDa.
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Notes |
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WB
1/1000 - 1/10000. Predicted molecular weight: 141 kDa. |
Target
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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. -
Tissue specificity
Isoform 2 is highly expressed in juvenile chondrocyte and low in fetal chondrocyte. -
Involvement in 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.
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 similarities
Belongs 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 localization
Secreted > extracellular space > extracellular matrix. - Information by UniProt
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Database links
- Entrez Gene: 1280 Human
- Entrez Gene: 25412 Rat
- Omim: 120140 Human
- SwissProt: P02458 Human
- SwissProt: P05539 Rat
- Unigene: 408182 Human
- Unigene: 10124 Rat
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Alternative names
- Alpha 1 type II collagen antibody
- Alpha-1 type II collagen antibody
- AOM antibody
see all
Images
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All lanes : Anti-Collagen II antibody [EPR12268] (ab188570) at 1/5000 dilution (purified)
Lane 1 : Rat cartilage lysate at 20 µg
Lane 2 : Human cartilage lysate at 15 µg
Secondary
All lanes : Goat Anti-Rabbit IgG H&L (HRP) (ab97051) at 1/20000 dilution
Predicted band size: 141 kDa
Additional bands at: 36 kDa (possible isoform)Blocking and diluting buffer: 5% NFDM/TBST
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Anti-Collagen II antibody [EPR12268] (ab188570) at 1/1000 dilution (purified) + Human Collagen II recombinant protein at 0.01 µg
Secondary
Goat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/1000 dilution
Predicted band size: 141 kDa
Additional bands at: 36 kDa (possible isoform)
Datasheets and documents
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SDS download
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Datasheet download
Certificate of Compliance
References (63)
ab188570 has been referenced in 63 publications.
- Miao Y et al. Contribution of ferroptosis and GPX4's dual functions to osteoarthritis progression. EBioMedicine 76:103847 (2022). PubMed: 35101656
- Luobu Z et al. CircSCAPER contributes to IL-1β-induced osteoarthritis in vitro via miR-140-3p/EZH2 axis. Bone Joint Res 11:61-72 (2022). PubMed: 35103493
- Zhou X et al. Melatonin Prevents Cartilage Degradation in Early-Stage Osteoarthritis Through Activation of miR-146a/NRF2/HO-1 Axis. J Bone Miner Res 37:1056-1072 (2022). PubMed: 35147250
- Du X et al. Circular RNA hsa_circ_0083756 promotes intervertebral disc degeneration by sponging miR-558 and regulating TREM1 expression. Cell Prolif 55:e13205 (2022). PubMed: 35187741
- Yu Z et al. Circular RNA circ_0020014 contributes to osteoarthritis progression via miR-613/ADAMTS5 axis. Bosn J Basic Med Sci 22:716-727 (2022). PubMed: 35225755