DNA Mismatch Repair Protein Msh2 (MSH2) Antibody

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383.5€ (100 µl)

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935106861
info@markelab.com
name
DNA Mismatch Repair Protein Msh2 (MSH2) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx011203
tested applications
ELISA, WB, IHC, IF/ICC

Description

MSH2 was identified as a locus frequently mutated in hereditary nonpolyposis colon cancer (HNPCC). When cloned, it was discovered to be a human homolog of the E. coli mismatch repair gene mutS, consistent with the characteristic alterations in microsatellite sequences (RER+ phenotype) found in HNPCC.

Documents del producto

Instrucciones
Data sheet
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Product specifications

Category
Primary Antibodies
Immunogen Target
DNA Mismatch Repair Protein Msh2 (MSH2)
Host
Mouse
Reactivity
Human, Monkey
Recommended Dilution
ELISA: 1/10000, WB: 1/500 - 1/2000, IHC: 1/200 - 1/1000, IF/ICC: 1/200 - 1/1000. Optimal dilutions/concentrations should be determined by the end user.
Clonality
Monoclonal
Conjugation
Unconjugated
Isotype
IgG1
Purification
Unpurified ascites.
Size 1
100 µl
Form
Liquid
Tested Applications
ELISA, WB, IHC, IF/ICC
Buffer
Ascitic fluid containing 0.03% sodium azide.
Availability
Shipped within 5-10 working days.
Storage
Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
P43246
Gene ID
4436
NCBI Accession
NP_000242.1, NM_000251.2
OMIM
114500
Background
Antibody anti-MSH2
Status
RUO
Note
Concentration: Not determined. -

Descripción

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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. 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.

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MSH2 antibody

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. 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.

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