MutS Homolog 2, Colon Cancer, Nonpolyposis Type 1 (E. Coli) (MSH2) antibody
|Synonyms||FCC1, COCA1, HNPCC, LCFS2, HNPCC1, AI788990|
Alternatives Western Blotting (WB), Immunohistochemistry (Formalin-fixed Paraffin-embedded Sections) (IHC (ffpe)), Immunohistochemistry (Frozen Sections) (IHC (fro))
|8 references available|
|Quantity||0.1 mg (0.5 mg/ml)|
|Price||Product not available in this region.|
|Immunogen||Recombinant Human MSH2 Protein|
|Description||The repair of mismatched DNA is essential to maintaining the integrity of genetic information over time. In bacteria the DNA repair process is accomplished by the MutL, MutH, and MutS proteins. The MutS protein initially recognizes and binds to mismatched DNA. Following this, MutH, an endonuclease, and MutL form a complex with MutS and carry out an excision repair mechanism. When bacteria are deficient in one of these enzymes a mutator phenotype arises characterized by genetic instability. The important role played by DNA repair enzymes is emphasized by the fact that they are highly conserved from bacteria to yeast to mammals. In yeast the proteins are called MutS homolog 2 (MSH2), MutL homolog (MLH1), and PMS1 which is also a homolog of MutL. MSH2 is involved in the initial recognition of mismatched nucleotides during the replication mismatch repair process. It is thought that after MSH2 binds to a mismatched DNA duplex it is joined by a heterodimer of MLH1 and PMS1 which together help facilitate the later steps in mismatch repair. The human homologs of DNA mismatch repair enzymes MLH1, PMS2, and MSH2 have recently been cloned. G219-1129 recognizes human MSH-2. A recombinant full-length human MSH2 protein was used as immunogen.|
1. Since applications vary, each investigator should titrate the reagent to obtain optimal results.
2. Please refer to us for technical protocols.
3. Caution: Sodium azide yields highly toxic hydrazoic acid under acidic conditions. Dilute azide compounds in running water before discarding to avoid accumulation of potentially explosive deposits in plumbing.
|Molecular Weight||102 kDa|
Related Products: ABIN968533
|Application Notes||For IHC, intestine is suggested as a positive control. Staining is typically seen in the crypts of Lieberkuhn, similar to that described by others. Staining is primarily nuclear, but may also be observed in the cytoplasm.|
|Purification||Purified from tissue culture supernatant or ascites by affinity chromatography.|
|Buffer||Aqueous buffered solution.|
|Preservative||0.09% Sodium azide.|
|Storage||Store undiluted at 4°C.|
|Research Area||Cancer, DNA/RNA|
|Restrictions||For Research Use only|
Kramer, Kramer, Williamson et al.: "Cloning and nucleotide sequence of DNA mismatch repair gene PMS1 from Saccharomyces cerevisiae: homology of PMS1 to procaryotic MutL and HexB." in: Journal of bacteriology, Vol. 171, Issue 10, pp. 5339-46, 1989 (PubMed).
Su, Modrich: "Escherichia coli mutS-encoded protein binds to mismatched DNA base pairs." in: Proceedings of the National Academy of Sciences of the United States of America, Vol. 83, Issue 14, pp. 5057-61, 1986 (PubMed).
Wilson, Ewel, Duguid et al.: "Differential cellular expression of the human MSH2 repair enzyme in small and large intestine." in: Cancer research, Vol. 55, Issue 22, pp. 5146-50, 1995 (PubMed).
Prolla, Pang, Alani et al.: "MLH1, PMS1, and MSH2 interactions during the initiation of DNA mismatch repair in yeast." in: Science (New York, N.Y.), Vol. 265, Issue 5175, pp. 1091-3, 1994 (PubMed).
Fishel, Lescoe, Rao et al.: "The human mutator gene homolog MSH2 and its association with hereditary nonpolyposis colon cancer." in: Cell, Vol. 75, Issue 5, pp. 1027-38, 1994 (PubMed).
Leach, Nicolaides, Papadopoulos et al.: "Mutations of a mutS homolog in hereditary nonpolyposis colorectal cancer." in: Cell, Vol. 75, Issue 6, pp. 1215-25, 1994 (PubMed).
Prolla, Christie, Liskay: "Dual requirement in yeast DNA mismatch repair for MLH1 and PMS1, two homologs of the bacterial mutL gene." in: Molecular and cellular biology, Vol. 14, Issue 1, pp. 407-15, 1994 (PubMed).
Cleaver: "It was a very good year for DNA repair." in: Cell, Vol. 76, Issue 1, pp. 1-4, 1994 (PubMed).