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MSH6 (基因名), DNA mismatch repair protein Msh6 (蛋白名), MSH6_HUMAN.
产品名称:

Human MSH6/ DNA mismatch repair protein Msh6 Recombinant Protein
DNA错配修复蛋白Msh6

货号:

R2360h

商标:
EIAab®
监管等级:
别名:

G/T mismatch-binding protein, MutS protein homolog 6, MutS-alpha 160 kDa subunit, GTBP, p160, hMSH6, GTBP

序列号:
P52701
来源:
E.coli
种属:
Human
标签:
His
纯度:
>90% by SDS-PAGE
浓度:
Reconstitution Dependent
形态:
Liquid
内毒素水平:
Please contact protein@eiaab.com The technician for more information.
应用:
存储缓冲液:
50mM NaH2PO4, 500mM NaCl Buffer with 500mM Imidazole, 10%glycerol(PH8.0)
存储:
Store at -20°C. (Avoid repeated freezing and thawing.)
研究领域:
Cancer
Human MSH6 Protein
规格 & 价格: cart
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Human MSH6 Protein
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产品说明书
说明书: 下载说明书
MSDS: MSDS
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R&D 技术数据
更多信息,请参阅手册,或联系我们的技术支持: tech@eiaab.com.
基因位点
Cytogenetic band: 2p16.3 by HGNC 2p16.3 by Entrez Gene 2p16.3 by Ensembl
MSH6 Gene in genomic location: bands according to Ensembl, locations according to GeneLoc (and/or Entrez Gene and/or Ensembl if different)
基因位点
通用注释


亚单元:
Heterodimer consisting of MSH2-MSH6 (MutS alpha). Forms 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 herpes simplex virus 1 protein UL12 (PubMed:21957315).


功能:
Component of the post-replicative DNA mismatch repair system (MMR). Heterodimerizes with MSH2 to form MutS alpha, which binds to DNA mismatches thereby initiating DNA repair. When bound, MutS alpha bends the DNA helix and shields approximately 20 base pairs, and recognizes single base mismatches and dinucleotide insertion-deletion loops (IDL) in the DNA. After mismatch binding, 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. Recruited on chromatin in G1 and early S phase via its PWWP domain that specifically binds trimethylated 'Lys-36' of histone H3 (H3K36me3): early recruitment to chromatin to be replicated allowing a quick identification of mismatch repair to initiate the DNA mismatch repair reaction.


亚细胞位置:
Nucleus Chromosome Associates with H3K36me3 via its PWWP domain.


该产品尚未在任何出版物中被引用。

[1].
"Mutation analysis of the MLH1, MSH2 and MSH6 genes in patients with double primary cancers of the colorectum and the endometrium: a population-based study in northern Sweden."

[2].
"MSH6 germline mutations are rare in colorectal cancer families."

[3].
"Mutations of GTBP in genetically unstable cells."

[4].
"Screening for germline mutations of MLH1, MSH2, MSH6 and PMS2 genes in Slovenian colorectal cancer patients: implications for a population specific detection strategy of Lynch syndrome."

[5].
"Cancer risk in MLH1, MSH2 and MSH6 mutation carriers; different risk profiles may influence clinical management."

[6].
"Meta-analysis of MSH6 gene mutation frequency in colorectal and endometrial cancers."

[7].
"Association of MUTYH and MSH6 germline mutations in colorectal cancer patients."

[8].
"Classification of ambiguous mutations in DNA mismatch repair genes identified in a population-based study of colorectal cancer."

[9].
"Detection of mismatch repair gene germline mutation carrier among Chinese population with colorectal cancer."

[10].
"Germline MSH6 mutations are more prevalent in endometrial cancer patient cohorts than hereditary non polyposis colorectal cancer cohorts."
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