<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10(23)</volume><submitter>Guo XJ</submitter><pubmed_abstract>Background Atrial fibrillation (AF) is the most common form of clinical cardiac dysrhythmia responsible for thromboembolic cerebral stroke, congestive heart failure, and death. Aggregating evidence highlights the strong genetic basis of AF. Nevertheless, AF is of pronounced genetic heterogeneity, and in an overwhelming majority of patients, the genetic determinants underpinning AF remain elusive. Methods and Results By genome-wide screening with polymorphic microsatellite markers and linkage analysis in a 4-generation Chinese family affected with autosomal-dominant AF, a novel locus for AF was mapped to chromosome 1q24.2-q25.1, a 3.20-cM (≈4.19 Mbp) interval between markers D1S2851 and D1S218, with the greatest 2-point logarithm of odds score of 4.8165 for the marker D1S452 at recombinatio</pubmed_abstract><journal>Journal of the American Heart Association</journal><pagination>e023517</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9075371</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>PRRX1 Loss-of-Function Mutations Underlying Familial Atrial Fibrillation.</pubmed_title><pmcid>PMC9075371</pmcid><pubmed_authors>Ke ZP</pubmed_authors><pubmed_authors>Guo YH</pubmed_authors><pubmed_authors>Qiu XB</pubmed_authors><pubmed_authors>Di RM</pubmed_authors><pubmed_authors>Xu YJ</pubmed_authors><pubmed_authors>Yang YQ</pubmed_authors><pubmed_authors>Guo XJ</pubmed_authors><pubmed_authors>Yang CX</pubmed_authors><pubmed_authors>Wang J</pubmed_authors><pubmed_authors>Li L</pubmed_authors><pubmed_authors>Sun YM</pubmed_authors><pubmed_authors>Gao RF</pubmed_authors></additional><is_claimable>false</is_claimable><name>PRRX1 Loss-of-Function Mutations Underlying Familial Atrial Fibrillation.</name><description>Background Atrial fibrillation (AF) is the most common form of clinical cardiac dysrhythmia responsible for thromboembolic cerebral stroke, congestive heart failure, and death. Aggregating evidence highlights the strong genetic basis of AF. Nevertheless, AF is of pronounced genetic heterogeneity, and in an overwhelming majority of patients, the genetic determinants underpinning AF remain elusive. Methods and Results By genome-wide screening with polymorphic microsatellite markers and linkage analysis in a 4-generation Chinese family affected with autosomal-dominant AF, a novel locus for AF was mapped to chromosome 1q24.2-q25.1, a 3.20-cM (≈4.19 Mbp) interval between markers D1S2851 and D1S218, with the greatest 2-point logarithm of odds score of 4.8165 for the marker D1S452 at recombinatio</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2025-04-04T10:01:43.397Z</modification><creation>2025-04-04T10:01:43.397Z</creation></dates><accession>S-EPMC9075371</accession><cross_references><pubmed>34845933</pubmed><doi>10.1161/JAHA.121.023517</doi></cross_references></HashMap>