<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Drosopoulos WC</submitter><funding>NIGMS NIH HHS</funding><pagination>191-208</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4508891</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>210(2)</volume><pubmed_abstract>Based on its in vitro unwinding activity on G-quadruplex (G4) DNA, the Bloom syndrome-associated helicase BLM is proposed to participate in telomere replication by aiding fork progression through G-rich telomeric DNA. Single molecule analysis of replicated DNA (SMARD) was used to determine the contribution of BLM helicase to telomere replication. In BLM-deficient cells, replication forks initiating from origins within the telomere, which copy the G-rich strand by leading strand synthesis, moved slower through the telomere compared with the adjacent subtelomere. Fork progression through the telomere was further slowed in the presence of a G4 stabilizer. Using a G4-specific antibody, we found that deficiency of BLM, or another G4-unwinding helicase, the Werner syndrome-associated helicase WR</pubmed_abstract><journal>The Journal of cell biology</journal><pubmed_title>BLM helicase facilitates telomere replication during leading strand synthesis of telomeres.</pubmed_title><pmcid>PMC4508891</pmcid><funding_grant_id>R01 GM045751</funding_grant_id><funding_grant_id>5R01-GM045751</funding_grant_id><pubmed_authors>Drosopoulos WC</pubmed_authors><pubmed_authors>Kosiyatrakul ST</pubmed_authors><pubmed_authors>Schildkraut CL</pubmed_authors></additional><is_claimable>false</is_claimable><name>BLM helicase facilitates telomere replication during leading strand synthesis of telomeres.</name><description>Based on its in vitro unwinding activity on G-quadruplex (G4) DNA, the Bloom syndrome-associated helicase BLM is proposed to participate in telomere replication by aiding fork progression through G-rich telomeric DNA. Single molecule analysis of replicated DNA (SMARD) was used to determine the contribution of BLM helicase to telomere replication. In BLM-deficient cells, replication forks initiating from origins within the telomere, which copy the G-rich strand by leading strand synthesis, moved slower through the telomere compared with the adjacent subtelomere. Fork progression through the telomere was further slowed in the presence of a G4 stabilizer. Using a G4-specific antibody, we found that deficiency of BLM, or another G4-unwinding helicase, the Werner syndrome-associated helicase WR</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Jul</publication><modification>2025-04-26T08:15:06.109Z</modification><creation>2019-03-27T01:55:30Z</creation></dates><accession>S-EPMC4508891</accession><cross_references><pubmed>26195664</pubmed><doi>10.1083/jcb.201410061</doi></cross_references></HashMap>