Home
>
Product
>
Antibody
>
Rabbit Anti-MSH3/FITC Conjugated antibody
background:
Component of the post-replicative DNA mismatch repair system (MMR). Heterodimerizes with MSH2 to form MutS beta which binds to DNA mismatches thereby initiating DNA repair. When bound, the MutS beta heterodimer bends the DNA helix and shields approximately 20 base pairs. MutS beta recognizes large insertion-deletion loops (IDL) up to 13 nucleotides long. 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.
Function:
Component of the post-replicative DNA mismatch repair system (MMR). Heterodimerizes with MSH2 to form MutS beta which binds to DNA mismatches thereby initiating DNA repair. When bound, the MutS beta heterodimer bends the DNA helix and shields approximately 20 base pairs. MutS beta recognizes large insertion-deletion loops (IDL) up to 13 nucleotides long. 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.
Subunit:
Heterodimer consisting of MSH2-MSH3 (MutS beta). Forms a ternary complex with MutL alpha (MLH1-PMS1). Interacts with EXO1.
Post-translational modifications:
Phosphorylated upon DNA damage, probably by ATM or ATR.
DISEASE:
Defects in MSH3 are a cause of susceptibility to endometrial cancer (ENDMC)
Similarity:
Belongs to the DNA mismatch repair MutS family. MSH3 subfamily.
Database links:
Entrez Gene: 4437 Human
Omim: 600887 Human
SwissProt: P20585 Human
Unigene: 280987 Human
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
Involvement in disease;Defects in MSH3 are a cause of susceptibility to endometrial cancer
|
|