Msh2 (NM_008628) Mouse Tagged ORF Clone Lentiviral Particle

CAT#: MR211249L3V

  • LentiORF®

Lenti ORF particles, Msh2 (Myc-DDK-tagged) - Mouse mutS homolog 2 (E. coli) (Msh2), 200ul, >10^7 TU/mL

ORF Plasmid: DDK tGFP



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CNY 14,440.00


货期*
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规格
    • 200 ul

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Specifications

Product Data
Product Name Msh2 (NM_008628) Mouse Tagged ORF Clone Lentiviral Particle
Synonyms AI788990
Vector pLenti-C-Myc-DDK-P2A-Puro
ACCN NM_008628
ORF Size 2808 bp
Sequence Data
The ORF insert of this clone is exactly the same as(MR211249).
OTI Disclaimer The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info
OTI Annotation This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene.
Reference Data
RefSeq NM_008628.2, NP_032654.1
RefSeq Size 3056 bp
RefSeq ORF 2808 bp
Locus ID 17685
Gene Summary 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. Recruits DNA helicase MCM9 to chromatin which unwinds the mismatch containg DNA strand. 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.[UniProtKB/Swiss-Prot Function]
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