| 產(chǎn)品編號(hào) | bs-2975R |
| 英文名稱 | Rabbit Anti-Noggin antibody |
| 中文名稱 | 指(趾)關(guān)節(jié)粘連NOG蛋白抗體 |
| 別 名 | NOG; SYM 1; SYM1; Symphalangism 1 (proximal); Synostoses (multiple) syndrome 1; SYNS 1; SYNS1; NOGG_HUMAN. |
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Specific References (5) | bs-2975R has been referenced in 5 publications.
[IF=8.724] Yong Tang. et al. Phosphorylation inhibition of protein-tyrosine phosphatase 1B tyrosine-152 induces bone regeneration coupled with angiogenesis for bone tissue engineering. Bioact Mater. 2021 Jul;6:2039 IF,IHC ; Mouse.
[IF=3.405] Dawson LE et al. Induction of Myogenic Differentiation Improves Chemosensitivity of Chemoresistant Cells in Soft-Tissue Sarcoma Cell Lines. Sarcoma. 2020 Mar 26;2020:8647981. FC ; human.
[IF=2.58] Song, Liang-Li, et al. "Expression Characteristics of BMP2, BMPR-IA and Noggin in Different Stages of Hair Follicle in Yak Skin." General and Comparative Endocrinology (2017). WB ; Other Species.
[IF=2.413] Shouhui Wang. et al. The changes of bone vessels and their role in bone loss in tail-suspended rats. Acta Astronaut. 2021 Dec;189:368 IF ; rat.
[IF=2.107] Sun X et al. Expression and distribution of bone morphogenetic protein 4 and its antagonist Noggin in the skin of Kazakh sheep (Ovis aries) with a white and brown coat color. Acta Histochem
. 2020 May;122(4):151539. WB,IHC ; sheep.
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| 研究領(lǐng)域 | 細(xì)胞生物 發(fā)育生物學(xué) 信號(hào)轉(zhuǎn)導(dǎo) 干細(xì)胞 |
| 抗體來源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | Human,Mouse,Rat (predicted: Rabbit,Pig,Sheep,Cow,Chicken,Dog,Horse) |
| 產(chǎn)品應(yīng)用 | IHC-P=1:100-500,IHC-F=1:100-500,Flow-Cyt=1ug/Test,IF=1:100-500
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 理論分子量 | 23kDa |
| 細(xì)胞定位 | 分泌型蛋白 |
| 性 狀 | Liquid |
| 濃 度 | 1mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human Noggin: 28-130/232 |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 緩 沖 液 | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
| 保存條件 | Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles. |
| 注意事項(xiàng) | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
| PubMed | PubMed |
| 產(chǎn)品介紹 |
Noggin is a secreted protein involved at multiple stages of vertebrate embryonic development including neural induction and is known to exert its effects by inhibiting the bone morphogenetic protein (BMP)-signaling pathway. It binds several BMPs with very high (picomolar) affinities, with a marked preference for BMP2 and BMP4 over BMP7. By binding tightly to BMPs, Noggin prevents BMPs from binding their receptors. Noggin binds the bone morphogenetic proteins (BMP) such as BMP-4 and BMP-7, and inhibits BMP signaling by blocking the molecular interfaces of the binding epitopes for both type I and type II receptors. Interaction of BMP and its antagonist Noggin governs various developmental and cellular processes, including embryonic dorsal-ventral axis, induction of neural tissue, formation of joints in the skeletal system and neurogenesis in the adult brain. Noggin plays a key role in neural induction by inhibiting BMP4, along with other TGF-β signaling inhibitors such as chordin and follistatin. Mouse knockout experiments have demonstrated that noggin also plays a crucial role in bone development, joint formation, and neural tube fusion. Function: Essential for cartilage morphogenesis and joint formation. Inhibitor of bone morphogenetic proteins (BMP) signaling which is required for growth and patterning of the neural tube and somite Subunit: Homodimer. Subcellular Location: Secreted. DISEASE: Defects in NOG are a cause of symphalangism proximal syndrome (SYM1) [MIM:185800]. SYM1 is characterized by the hereditary absence of the proximal interphalangeal (PIP) joints (Cushing symphalangism). Severity of PIP joint involvement diminishes towards the radial side. Distal interphalangeal joints are less frequently involved and metacarpophalangeal joints are rarely affected whereas carpal bone malformation and fusion are common. In the lower extremities, tarsal bone coalition is common. Conducive hearing loss is seen and is due to fusion of the stapes to the petrous part of the temporal bone. Defects in NOG are the cause of multiple synostoses syndrome type 1 (SYNS1) [MIM:186500]; also known as synostoses, multiple, with brachydactyly/symphalangism-brachydactyly syndrome. SYNS1 is characterized by tubular-shaped (hemicylindrical) nose with lack of alar flare, otosclerotic deafness, and multiple progressive joint fusions commencing in the hand. The joint fusions are progressive, commencing in the fifth proximal interphalangeal joint in early childhood (or at birth in some individuals) and progressing in an ulnar-to-radial and proximal-to-distal direction. With increasing age, ankylosis of other joints, including the cervical vertebrae, hips, and humeroradial joints, develop. Defects in NOG are the cause of tarsal-carpal coalition syndrome (TCC) [MIM:186570]. TCC is an autosomal dominant disorder characterized by fusion of the carpals, tarsals and phalanges, short first metacarpals causing brachydactyly, and humeroradial fusion. TCC is allelic to SYM1, and different mutations in NOG can result in either TCC or SYM1 in different families. Defects in NOG are a cause of stapes ankylosis with broad thumb and toes (SABTS) [MIM:184460]; also known as Teunissen-Cremers syndrome. SABTS is a congenital autosomal dominant disorder that includes hyperopia, a hemicylindrical nose, broad thumbs, great toes, and other minor skeletal anomalies but lacked carpal and tarsal fusion and symphalangism. Defects in NOG are the cause of brachydactyly type B2 (BDB2) [MIM:611377]. BDB2 is a subtype of brachydactyly characterized by hypoplasia/aplasia of distal phalanges in combination with distal symphalangism, fusion of carpal/tarsal bones, and partial cutaneous syndactyly. Similarity: Belongs to the noggin family. SWISS: Q13253 Gene ID: 9241 Database links: UniProtKB/Swiss-Prot: Q13253.1 |
| 產(chǎn)品圖片 |
Tissue/cell: rat kidney tissue; 4% Paraformaldehyde-fixed and paraffin-embedded;
Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min;
Incubation: Anti-Noggin Polyclonal Antibody, Unconjugated(bs-2975R) 1:500, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining
Blank control（black line）:Hela.
Primary Antibody (green line): Rabbit Anti-Noggin antibody (bs-2975R)
Dilution:1ug/Test;
Secondary Antibody : Goat anti-rabbit IgG-AF488
Dilution: 0.5ug/Test.
Negative control（white blue line）: PBS
Isotype control（orange line）: Normal Rabbit IgG
Protocol
The cells were fixed with 4% PFA (10min at room temperature)and then permeabilized with 90% ice-cold methanol for 20 min at -20℃.The cells were then incubated in 5%BSA to block non-specific protein-protein interactions for 30 min at room temperature .Cells stained with Primary Antibody for 30 min at room temperature. The secondary antibody used for 40 min at room temperature. Acquisition of 20,000 events was performed.
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