Anti-Collagen II 抗体 (ab34712)
Key features and details
- Rabbit polyclonal to Collagen II
- Suitable for: ELISA, IP, ICC/IF, IHC-P, WB
- Reacts with: Mouse, Rat, Sheep, Chicken, Cow, Dog, Human, Pig
- Isotype: IgG
製品の概要
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製品名
Anti-Collagen II antibody
Collagen II 一次抗体 製品一覧 -
製品の詳細
Rabbit polyclonal to Collagen II -
由来種
Rabbit -
特異性
Some class specific anti-collagens may be specific for three-dimensional epitopes which may result in diminished reactivity with denatured collagen or formalin-fixed, paraffin embedded tissues. This antibody reacts with most mammalian Type II collagens and has expected cross-reactivity with Type IV and VI and negligible cross reactivity to Type I, III and V collagens. Non-specific cross reaction of anti-collagen antibodies with other human serum proteins or non-collagen extracellular matrix proteins has not been tested.
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アプリケーション
適用あり: ELISA, IP, ICC/IF, IHC-P, WBmore details -
種交差性
交差種: Mouse, Rat, Sheep, Chicken, Cow, Dog, Human, Pig
交差が予測される動物種: Mammals -
免疫原
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ポジティブ・コントロール
- IHC-P: Human bronchiolar cartilage; Human Mesenchymal stem cells; Human HEMC-SS spheroids.
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特記事項
The Life Science industry has been in the grips of a reproducibility crisis for a number of years. Abcam is leading the way in addressing this with our range of recombinant monoclonal antibodies and knockout edited cell lines for gold-standard validation. Please check that this product meets your needs before purchasing.
If you have any questions, special requirements or concerns, please send us an inquiry and/or contact our Support team ahead of purchase. Recommended alternatives for this product can be found below, along with publications, customer reviews and Q&As
製品の特性
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製品の状態
Liquid -
保存方法
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Add glycerol to a final volume of 50% for extra stability and aliquot. Store at -20°C or -80°C. Avoid freeze / thaw cycle. -
バッファー
Preservative: 0.01% Sodium azide
Constituents: 0.88% Sodium chloride, 0.424% Tripotassium orthophosphate -
Concentration information loading...
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精製度
Immunogen affinity purified -
特記事項(精製)
Collagen II Antibody has been prepared by immunoaffinity chromatography using immobilized antigens followed by extensive cross-adsorption against other collagens. -
ポリ/モノ
ポリクローナル -
アイソタイプ
IgG -
研究分野
関連製品
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Compatible Secondaries
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Isotype control
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Related Products
アプリケーション
The Abpromise guarantee
Abpromise保証は、 次のテスト済みアプリケーションにおけるab34712の使用に適用されます
アプリケーションノートには、推奨の開始希釈率がありますが、適切な希釈率につきましてはご検討ください。
アプリケーション | Abreviews | 特記事項 |
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ELISA | (1) |
1/5000 - 1/50000.
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IP |
1/100.
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ICC/IF | (3) |
Use at an assay dependent concentration.
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IHC-P | (8) |
1/50 - 1/400.
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WB |
1/1000 - 1/10000. Predicted molecular weight: 141 kDa.
This product is not recommended for use under denaturing conditions in WB, IP, and ELISA. We would suggest testing it under native conditions. |
特記事項 |
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ELISA
1/5000 - 1/50000. |
IP
1/100. |
ICC/IF
Use at an assay dependent concentration. |
IHC-P
1/50 - 1/400. |
WB
1/1000 - 1/10000. Predicted molecular weight: 141 kDa. This product is not recommended for use under denaturing conditions in WB, IP, and ELISA. We would suggest testing it under native conditions. |
ターゲット情報
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機能
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. -
組織特異性
Isoform 2 is highly expressed in juvenile chondrocyte and low in fetal chondrocyte. -
関連疾患
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. -
配列類似性
Belongs to the fibrillar collagen family.
Contains 1 fibrillar collagen NC1 domain.
Contains 1 VWFC domain. -
翻訳後修飾
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. -
細胞内局在
Secreted > extracellular space > extracellular matrix. - Information by UniProt
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参照データベース
- Entrez Gene: 395069 Chicken
- Entrez Gene: 407142 Cow
- Entrez Gene: 1280 Human
- Entrez Gene: 12824 Mouse
- Entrez Gene: 25412 Rat
- Omim: 120140 Human
- SwissProt: P02460 Chicken
- SwissProt: P02459 Cow
see all -
別名
- Alpha 1 type II collagen antibody
- Alpha-1 type II collagen antibody
- AOM antibody
see all
画像
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ab34712 (1:400, 45 min RT) showed moderate staining in FFPE human bronchiolar cartilage. Slides were steamed in 0.01 M sodium citrate buffer, pH 6.0 at 99-100°C - 20 minutes for antigen retrieval.
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Formalin-fixed, paraffin-embedded human Mesenchymal stem cells stained for collagen II using ab34712 at 1/100 dilution i immunohistochemical analysis.
Healthy donor-derived MSCs were injected into the center of nano-fiber plugs and cultured in MSCGM for the specified period. The samples were assessed immunohistochemically for the expression of type-II collagen on Days 7 and 28. Scale bars, 50 μm.
プロトコール
データシートおよび資料
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SDS download
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Datasheet download
参考文献 (766)
ab34712 は 766 報の論文で使用されています。
- Jiang D et al. microRNA-105-5p protects against chondrocyte injury, extracellular matrix degradation, and osteoarthritis progression by targeting SPARCL1. Histol Histopathol 39:483-496 (2024). PubMed: 37534667
- Hao Y et al. FOXO3-Activated HOTTIP Sequesters miR-615-3p away from COL2A1 to Mitigate Intervertebral Disc Degeneration. Am J Pathol 194:280-295 (2024). PubMed: 37981220
- Kong K et al. Mechanical overloading leads to chondrocyte degeneration and senescence via Zmpste24-mediated nuclear membrane instability. iScience 26:108119 (2023). PubMed: 37965144
- Kim Y et al. Enhanced Intervertebral Disc Repair via Genetically Engineered Mesenchymal Stem Cells with Tetracycline Regulatory System. Int J Mol Sci 24:N/A (2023). PubMed: 38003216
- Kim JR et al. A causative role for periarticular skeletal muscle weakness in the progression of joint damage and pain in OA. Sci Rep 13:21349 (2023). PubMed: 38049482