On the molecular mechanism of somatic hypermutation of rearranged immunoglobulin genes

Andrew Franklin; Robert V. Blanden

doi:10.1111/j.1440-1711.2004.01289.x

On the molecular mechanism of somatic hypermutation of rearranged immunoglobulin genes

Andrew Franklin^*, Robert V. Blanden

^*Corresponding author for this work

Research output: Contribution to journal › Review article › peer-review

7 Citations (Scopus)

Abstract

Somatic hypermutation (SHM) diversifies the genes that encode immunoglobulin variable regions in antigen-activated germinal centre B lymphocytes. Available evidence strongly suggests that DNA deamination potentiates phase I SHM and subsequently triggers phase II SHM. A concise review of this evidence is followed by a detailed critique of two possible models which suggest that polymerase-η potentiates phase II SHM via either its DNA-dependent or its RNA-dependent DNA synthetic activity. Quantitative analysis, in the context of extant data that define the features of SHM, favours the RNA-dependent mechanism.

Original language	English
Pages (from-to)	557-567
Number of pages	11
Journal	Immunology and Cell Biology
Volume	82
Issue number	6
DOIs	https://doi.org/10.1111/j.1440-1711.2004.01289.x
Publication status	Published - Dec 2004

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10.1111/j.1440-1711.2004.01289.x

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title = "On the molecular mechanism of somatic hypermutation of rearranged immunoglobulin genes",

abstract = "Somatic hypermutation (SHM) diversifies the genes that encode immunoglobulin variable regions in antigen-activated germinal centre B lymphocytes. Available evidence strongly suggests that DNA deamination potentiates phase I SHM and subsequently triggers phase II SHM. A concise review of this evidence is followed by a detailed critique of two possible models which suggest that polymerase-η potentiates phase II SHM via either its DNA-dependent or its RNA-dependent DNA synthetic activity. Quantitative analysis, in the context of extant data that define the features of SHM, favours the RNA-dependent mechanism.",

keywords = "Affinity maturation, DNA deamination, Molecular mechanism, RNA-dependent DNA synthesis, Somatic hypermutation",

author = "Andrew Franklin and Blanden, {Robert V.}",

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AU - Franklin, Andrew

AU - Blanden, Robert V.

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AB - Somatic hypermutation (SHM) diversifies the genes that encode immunoglobulin variable regions in antigen-activated germinal centre B lymphocytes. Available evidence strongly suggests that DNA deamination potentiates phase I SHM and subsequently triggers phase II SHM. A concise review of this evidence is followed by a detailed critique of two possible models which suggest that polymerase-η potentiates phase II SHM via either its DNA-dependent or its RNA-dependent DNA synthetic activity. Quantitative analysis, in the context of extant data that define the features of SHM, favours the RNA-dependent mechanism.

KW - Affinity maturation

KW - DNA deamination

KW - Molecular mechanism

KW - RNA-dependent DNA synthesis

KW - Somatic hypermutation

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U2 - 10.1111/j.1440-1711.2004.01289.x

DO - 10.1111/j.1440-1711.2004.01289.x

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VL - 82

SP - 557

EP - 567

JO - Immunology and Cell Biology

JF - Immunology and Cell Biology

IS - 6

ER -

On the molecular mechanism of somatic hypermutation of rearranged immunoglobulin genes

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