| 產(chǎn)品編號(hào) | bs-23630R-Gold |
| 英文名稱 | Rabbit Anti-MSH2/Gold Conjugated antibody |
| 中文名稱 | 膠體金標(biāo)記的錯(cuò)配修復(fù)蛋白2抗體 |
| 別 名 | MSH-2; BAT26; DNA mismatch repair protein Msh2; FCC1; COCA1; HNPCC; LCFS2; HNPCC1; BAT26; COCA 1; COCA1; DNA mismatch repair protein Msh2; FCC 1; FCC1; hMSH2; HNPCC 1; HNPCC; HNPCC1; LCFS2; MSH 2; Msh2; MSH2_HUMAN; MutS homolog 2; MutS homolog 2 colon cancer nonpolyposis type 1; MutS protein homolog 2. |
| 規(guī)格價(jià)格 | 100ul/2980元 購買 大包裝/詢價(jià) |
| 說 明 書 | 100ul（10nm 15nm 35nm） |
| 研究領(lǐng)域 | 腫瘤 細(xì)胞生物 表觀遺傳學(xué) |
| 抗體來源 | Rabbit |
| 克隆類型 | Polyclonal |
| 交叉反應(yīng) | (predicted: Human, Mouse, Rat, Dog, Pig, Cow, Horse, Rabbit, Sheep, ) |
| 產(chǎn)品應(yīng)用 | IEM=1:20-200 ICA=1:20-200 ChIP=1:20-200
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
| 分 子 量 | 104kDa |
| 性 狀 | Lyophilized or Liquid |
| 濃 度 | 0.4mg/ml |
| 免 疫 原 | KLH conjugated synthetic peptide derived from human MSH2 |
| 亞 型 | IgG |
| 純化方法 | affinity purified by Protein A |
| 儲(chǔ) 存 液 | 0.02M TBS(pH8.2) with 1% BSA, 0.03% Proclin300. |
| 保存條件 | Store at 2-8 oC for 3-6 months. Avoid repeated freeze/thaw cycles. |
| 產(chǎn)品介紹 |
background: Component of the post-replicative DNA mismatch repair system (MMR). Forms two different heterodimers: MutS alpha (MSH2-MSH6 heterodimer) and MutS beta (MSH2-MSH3 heterodimer) which binds to DNA mismatches thereby initiating DNA repair. When bound, heterodimers bend the DNA helix and shields approximately 20 base pairs. MutS alpha recognizes single base mismatches and dinucleotide insertion-deletion loops (IDL) in the DNA. MutS beta recognizes larger insertion-deletion loops up to 13 nucleotides long. After mismatch binding, MutS alpha or beta forms a ternary complex with the MutL alpha heterodimer, which is thought to be responsible for directing the downstream MMR events, including strand discrimination, excision, and resynthesis. ATP binding and hydrolysis play a pivotal role in mismatch repair functions. The ATPase activity associated with MutS alpha regulates binding similar to a molecular switch: mismatched DNA provokes ADP-->ATP exchange, resulting in a discernible conformational transition that converts MutS alpha into a sliding clamp capable of hydrolysis-independent diffusion along the DNA backbone. This transition is crucial for mismatch repair. MutS alpha may also play a role in DNA homologous recombination repair. In melanocytes may modulate both UV-B-induced cell cycle regulation and apoptosis. Function: Component of the post-replicative DNA mismatch repair system (MMR). Forms two different heterodimers: MutS alpha (MSH2-MSH6 heterodimer) and MutS beta (MSH2-MSH3 heterodimer) which binds to DNA mismatches thereby initiating DNA repair. When bound, heterodimers bend the DNA helix and shields approximately 20 base pairs. MutS alpha recognizes single base mismatches and dinucleotide insertion-deletion loops (IDL) in the DNA. MutS beta recognizes larger insertion-deletion loops up to 13 nucleotides long. After mismatch binding, MutS alpha or beta forms a ternary complex with the MutL alpha heterodimer, which is thought to be responsible for directing the downstream MMR events, including strand discrimination, excision, and resynthesis. ATP binding and hydrolysis play a pivotal role in mismatch repair functions. The ATPase activity associated with MutS alpha regulates binding similar to a molecular switch: mismatched DNA provokes ADP-->ATP exchange, resulting in a discernible conformational transition that converts MutS alpha into a sliding clamp capable of hydrolysis-independent diffusion along the DNA backbone. This transition is crucial for mismatch repair. MutS alpha may also play a role in DNA homologous recombination repair. In melanocytes may modulate both UV-B-induced cell cycle regulation and apoptosis. Subunit: Heterodimer consisting of MSH2-MSH6 (MutS alpha) or MSH2-MSH3 (MutS beta). Both heterodimer form a ternary complex with MutL alpha (MLH1-PMS1). Interacts with EXO1. Part of the BRCA1-associated genome surveillance complex (BASC), which contains BRCA1, MSH2, MSH6, MLH1, ATM, BLM, PMS2 and the RAD50-MRE11-NBS1 protein complex. This association could be a dynamic process changing throughout the cell cycle and within subnuclear domains. Interacts with ATR. Interacts with SLX4/BTBD12; this interaction is direct and links MutS beta to SLX4, a subunit of different structure-specific endonucleases. Interacts with SMARCAD1. Subcellular Location: Nucleus. Tissue Specificity: Ubiquitously expressed. Post-translational modifications: Phosphorylated by PRKCZ, which may prevent MutS alpha degradation by the ubiquitin-proteasome pathway. Phosphorylated upon DNA damage, probably by ATM or ATR. DISEASE: Hereditary non-polyposis colorectal cancer 1 (HNPCC1) [MIM:120435]: An autosomal dominant disease associated with marked increase in cancer susceptibility. It is characterized by a familial predisposition to early-onset colorectal carcinoma (CRC) and extra-colonic tumors of the gastrointestinal, urological and female reproductive tracts. HNPCC is reported to be the most common form of inherited colorectal cancer in the Western world. Clinically, HNPCC is often divided into two subgroups. Type I is characterized by hereditary predisposition to colorectal cancer, a young age of onset, and carcinoma observed in the proximal colon. Type II is characterized by increased risk for cancers in certain tissues such as the uterus, ovary, breast, stomach, small intestine, skin, and larynx in addition to the colon. Diagnosis of classical HNPCC is based on the Amsterdam criteria: 3 or more relatives affected by colorectal cancer, one a first degree relative of the other two; 2 or more generation affected; 1 or more colorectal cancers presenting before 50 years of age; exclusion of hereditary polyposis syndromes. The term 'suspected HNPCC' or 'incomplete HNPCC' can be used to describe families who do not or only partially fulfill the Amsterdam criteria, but in whom a genetic basis for colon cancer is strongly suspected. Note=The disease is caused by mutations affecting the gene represented in this entry. Muir-Torre syndrome (MRTES) [MIM:158320]: Rare autosomal dominant disorder characterized by sebaceous neoplasms and visceral malignancy. Note=The disease is caused by mutations affecting the gene represented in this entry. Endometrial cancer (ENDMC) [MIM:608089]: A malignancy of endometrium, the mucous lining of the uterus. Most endometrial cancers are adenocarcinomas, cancers that begin in cells that make and release mucus and other fluids. Note=Disease susceptibility is associated with variations affecting the gene represented in this entry. Similarity: Belongs to the DNA mismatch repair MutS family. Database links: Entrez Gene: 4436 Human Entrez Gene: 17685 Mouse Omim: 120435 Human SwissProt: P43246 Human SwissProt: P43247 Mouse Unigene: 597656 Human Unigene: 4619 Mouse Unigene: 471165 Mouse Unigene: 3174 Rat Important Note: This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. MSH2是核苷酸錯(cuò)配修復(fù)酶之一，其突變和多種腫瘤的發(fā)生有關(guān)，主要用于：先天性結(jié)腸癌、散發(fā)性結(jié)腸癌及一些消化系統(tǒng)腫瘤方面的研究。DNA錯(cuò)配修復(fù)系統(tǒng)是指由特異修復(fù)DNA堿基錯(cuò)配的酶組成，保證DNA遺傳物質(zhì)的高保真性。它由MLH1、MSH2、PMS1、PMS2、MSH6和MSH3基因組成。如果上述基因發(fā)生突變或失活，會(huì)使細(xì)胞錯(cuò)配修復(fù)功能缺陷，產(chǎn)生遺傳不穩(wěn)定性，導(dǎo)致腫瘤易感。MSH2基因突變發(fā)生在散發(fā)性結(jié)腸癌中。 hMSH-2和hMLH1都與腫瘤的發(fā)生有關(guān)。 |
