Somatic hypermutation in MutS homologue (MSH)3-, MSH6-, and MSH3/MSH6-deficient mice reveals a role for the MSH2-MSH6 heterodimer in modulating the base substitution pattern

Journal of Experimental Medicine

Volumn 191, Issue 3, 2000, Pages 579-584

  Wiesendanger, Margrit ^a   Kneitz, Burkhard ^a   Edelmann, Winfried ^a   Scharff, Matthew D ^a  

^a ALBERT EINSTEIN COLLEGE OF MEDICINE   (United States)

Author keywords

DNA mismatch repair; Germinal center; Immunoglobulin genes; Msh3; Msh6

Indexed keywords

IMMUNOGLOBULIN;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BASE MISPAIRING; CONTROLLED STUDY; DNA REPAIR; DNA REPLICATION; GERMINAL CENTER; HUMORAL IMMUNITY; IMMUNE RESPONSE; MOUSE; MUTATION RATE; NONHUMAN; NUCLEIC ACID BASE SUBSTITUTION; PEYER PATCH; PRIORITY JOURNAL; SOMATIC MUTATION;

ADENOSINE TRIPHOSPHATASES; ANIMALS; B-LYMPHOCYTES; BACTERIAL PROTEINS; BASE PAIR MISMATCH; DIMERIZATION; DNA REPAIR; DNA-BINDING PROTEINS; ESCHERICHIA COLI PROTEINS; MICE; MULTIDRUG RESISTANCE-ASSOCIATED PROTEINS; MUTATION; MUTS DNA MISMATCH-BINDING PROTEIN; MUTS HOMOLOG 2 PROTEIN; PROTO-ONCOGENE PROTEINS; SPLEEN;

EID: 0034614916     PISSN: 00221007     EISSN: None     Source Type: Journal    
DOI: 10.1084/jem.191.3.579     Document Type: Article

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