Anti-MSH2 Antibody Picoband®

DNA mismatch repair protein Msh2, also known as MutS protein homolog 2 or MSH2, is a protein that in humans is encoded by the MSH2 gene, which is located on chromosome 2. MSH2 is a tumor suppressor gene and more specifically a caretaker gene that codes for a DNA mismatch repair (MMR) protein, MSH2 which forms aheterodimer with MSH6 to make the human MutSα mismatch repair complex. It also dimerizes with MSH3 to form the MutSβ DNA repair complex. MSH2 is involved in many different forms of DNA repair, including transcription-coupled repair, homologous recombination, and base excision repair. It has been found that MSH2 may also be a coactivator of ESR1-dependent gene expression.

E.coli-derived human MSH2 recombinant protein (Position: Q337-N583) . Human MSH2 shares 94% and 93% amino acid (aa) sequence identity with mouse and rat MSH2, respectively.

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 ing 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. .

1. de Wind N, Dekker M, Berns A, Radman M, te Riele H (July 1995) . Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer. Cell 82 (2) : 321–30. 2. Mellon I, Rajpal DK, Koi M, Boland CR, Champe GN (April 1996) . Transcription-coupled repair deficiency and mutations in human mismatch repair genes. Science 272 (5261) : 557–60. 3. Wada-Hiraike, O., Yano, T., Nei, T., Matsumoto, Y., Nagasaka, K., Takizawa, S., Oishi, H., Arimoto, T., Nakagawa, S., Yasugi, T., Kato, S., Taketani, Y. The DNA mismatch repair gene hMSH2 is a potent coactivator of oestrogen receptor-alpha. Brit. J. Cancer 92: 2286-2291, 2005.

Store at -20°C for one year from date of receipt. After reconstitution, at 4°C for one month. It can also be aliquotted and stored frozen at -20°C for six months. Avoid repeated freeze-thaw cycles.