Emerging links between hypermutation of antibody genes and DNA polymerases.

Abstract:

Substantial antibody variability is created when nucleotide substitutions are introduced into immunoglobulin variable genes by a controlled process of hypermutation. Evidence points to a mechanism involving DNA repair events at sites of targeted breaks. In vertebrate cells, there are many recently identified DNA polymerases that inaccurately copy templates. Some of these are candidates for enzymes that introduce base changes during hypermutation. Recent research has focused on possible roles for DNA polymerases zeta (POLZ), eta (POLH), iota (POLI), and mu (POLM) in the process.

Polymerases:

Topics:

Health/Disease, Nucleotide Analogs / Template Lesions, Fidelity, Enzyme Substrate Interactions

Status:

new topics/pols set partial results complete validated

Results:

Polymerase Reference Property Result Context
Human Pol eta Gearhart PJ2001 Template lesions Bypasses Reaction: Nucleotide incorporation; Substrate: n/a; DNA lesion: 8-hydroxyguanine
Human Pol eta Gearhart PJ2001 Template lesions Bypasses Reaction: Nucleotide incorporation; Substrate: n/a; DNA lesion: UV-induced Pyrimidine Dimer
Human Pol eta Gearhart PJ2001 Overall Error Rate 0.03 errors/bp Technique: Sequencing
Human Pol eta Gearhart PJ2001 Associated condition hypermutation and/or XERODERMA PIGMENTOSUM
Human Pol iota Gearhart PJ2001 Overall Error Rate 0.3 errors/bp Technique: Sequencing
Human Pol iota Gearhart PJ2001 Associated condition hypermutation
Human Pol mu Gearhart PJ2001 Associated condition hypermutation
Human Pol zeta Gearhart PJ2001 Overall Error Rate 0.0005 errors/bp Technique: Sequencing
Human Pol zeta Gearhart PJ2001 Associated condition Somatic Hypermutation

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