<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu D</submitter><funding>National Cancer Institute</funding><funding>NCI NIH HHS</funding><funding>National Institute of General Medical Sciences</funding><funding>NIGMS NIH HHS</funding><pagination>227-243</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9632267</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>57(3)</volume><pubmed_abstract>The most common human lymphoid chromosomal translocations involve concurrent failures of the recombination activating gene (RAG) complex and Activation-Induced Deaminase (AID). These are two enzymes that are normally expressed for purposes of the two site-specific DNA recombination processes: V(D)J recombination and class switch recombination (CSR). First, though it is rare, a low level of expression of AID can introduce long-lived T:G mismatch lesions at 20-600 bp fragile zones. Second, the V(D)J recombination process can occasionally fail to rejoin coding ends, and this failure may permit an opportunity for Artemis:DNA-dependent kinase catalytic subunit (DNA-PKcs) to convert the T:G mismatch sites at the fragile zones into double-strand breaks. The 20-600 bp fragile zones must be, at lea</pubmed_abstract><journal>Critical reviews in biochemistry and molecular biology</journal><pubmed_title>The mechanisms of human lymphoid chromosomal translocations and their medical relevance.</pubmed_title><pmcid>PMC9632267</pmcid><funding_grant_id>R35 GM118009</funding_grant_id><funding_grant_id>GM118009</funding_grant_id><funding_grant_id>CA196671</funding_grant_id><funding_grant_id>R01 CA196671</funding_grant_id><pubmed_authors>Liu D</pubmed_authors><pubmed_authors>Lieber MR</pubmed_authors></additional><is_claimable>false</is_claimable><name>The mechanisms of human lymphoid chromosomal translocations and their medical relevance.</name><description>The most common human lymphoid chromosomal translocations involve concurrent failures of the recombination activating gene (RAG) complex and Activation-Induced Deaminase (AID). These are two enzymes that are normally expressed for purposes of the two site-specific DNA recombination processes: V(D)J recombination and class switch recombination (CSR). First, though it is rare, a low level of expression of AID can introduce long-lived T:G mismatch lesions at 20-600 bp fragile zones. Second, the V(D)J recombination process can occasionally fail to rejoin coding ends, and this failure may permit an opportunity for Artemis:DNA-dependent kinase catalytic subunit (DNA-PKcs) to convert the T:G mismatch sites at the fragile zones into double-strand breaks. The 20-600 bp fragile zones must be, at lea</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2025-04-26T17:45:32.572Z</modification><creation>2025-04-06T15:35:51.552Z</creation></dates><accession>S-EPMC9632267</accession><cross_references><pubmed>34875186</pubmed><doi>10.1080/10409238.2021.2004576</doi></cross_references></HashMap>