(Q96224610)

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SAMHD1-mediated dNTP degradation is required for efficient DNA repair during antibody class switch recombination

scientific article published on 08 June 2020

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12 June 2020

SAMHD1-mediated dNTP degradation is required for efficient DNA repair during antibody class switch recombination (English)

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12 June 2020

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12 June 2020

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12 June 2020

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12 June 2020

author name string

Jiangliang Xu

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12 June 2020

Hodaka Fujii

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12 June 2020

Mikiyo Nakata

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12 June 2020

Maki Kobayashi

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12 June 2020

Ji-Yang Wang

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12 June 2020

Nasim A Begum

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12 June 2020

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8 June 2020

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12 June 2020

The EMBO Journal

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12 June 2020

e102931

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12 June 2020

HIV-1 restriction factor SAMHD1 is a deoxynucleoside triphosphate triphosphohydrolase

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Staggered AID-dependent DNA double strand breaks are the predominant DNA lesions targeted to S mu in Ig class switch recombination

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Differential regulation of S-region hypermutation and class-switch recombination by noncanonical functions of uracil DNA glycosylase

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Decrease in topoisomerase I is responsible for activation-induced cytidine deaminase (AID)-dependent somatic hypermutation

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Genomic instability resulting from Blm deficiency compromises development, maintenance, and function of the B cell lineage

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Nuclease activity of the human SAMHD1 protein implicated in the Aicardi-Goutieres syndrome and HIV-1 restriction.

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SAMHD1 is the dendritic- and myeloid-cell-specific HIV-1 restriction factor counteracted by Vpx

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Structural insight into dGTP-dependent activation of tetrameric SAMHD1 deoxynucleoside triphosphate triphosphohydrolase

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SAMHD1 is mutated recurrently in chronic lymphocytic leukemia and is involved in response to DNA damage.

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AID is required for germinal center-derived lymphomagenesis

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Chromatin enrichment for proteomics

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Dna2 nuclease deficiency results in large and complex DNA insertions at chromosomal breaks

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Inactivation of Pol θ and C-NHEJ eliminates off-target integration of exogenous DNA.

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SAMHD1 restricts HIV-1 infection in resting CD4(+) T cells.

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Low dNTP levels are necessary but may not be sufficient for lentiviral restriction by SAMHD1.

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Histone3 lysine4 trimethylation regulated by the facilitates chromatin transcription complex is critical for DNA cleavage in class switch recombination

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SAMHD1 enhances immunoglobulin hypermutation by promoting transversion mutation.

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Constitutive expression of AID leads to tumorigenesis

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Classical non-homologous end-joining pathway utilizes nascent RNA for error-free double-strand break repair of transcribed genes

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APE1 is dispensable for S-region cleavage but required for its repair in class switch recombination

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Essential Roles for Polymerase θ-Mediated End Joining in the Repair of Chromosome Breaks

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DNA damage response signaling does not trigger redistribution of SAMHD1 to nuclear foci

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Single-Stranded Nucleic Acids Bind to the Tetramer Interface of SAMHD1 and Prevent Formation of the Catalytic Homotetramer

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Aicardi-Goutieres syndrome gene and HIV-1 restriction factor SAMHD1 is a dGTP-regulated deoxynucleotide triphosphohydrolase

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IgH class switching and translocations use a robust non-classical end-joining pathway

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RNA Helicase DDX1 Converts RNA G-Quadruplex Structures into R-Loops to Promote IgH Class Switch Recombination.

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1 reference

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DNA double-strand break response factors influence end-joining features of IgH class switch and general translocation junctions.

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