<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Hoelbl A</submitter><funding>Austrian Science Fund FWF</funding><pagination>4898-906</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2875852</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>107(12)</volume><pubmed_abstract>The Stat5 transcription factors Stat5a and Stat5b have been implicated in lymphoid development and transformation. Most studies have employed Stat5a/b-deficient mice where gene targeting disrupted the first protein-coding exon, resulting in the expression of N-terminally truncated forms of Stat5a/b (Stat5a/b(DeltaN/DeltaN) mice). We have now reanalyzed lymphoid development in Stat5a/b(null/null) mice having a complete deletion of the Stat5a/b gene locus. The few surviving Stat5a/b(null/null) mice lacked CD8(+) T lymphocytes. A massive reduction of CD8(+) T cells was also found in Stat5a/b(fl/fl) lck-cre transgenic animals. While gammadelta T-cell receptor-positive (gammadeltaTCR(+)) cells were expressed at normal levels in Stat5a/b(DeltaN/DeltaN) mice, they were completely absent in Stat5a</pubmed_abstract><journal>Blood</journal><pubmed_title>Clarifying the role of Stat5 in lymphoid development and Abelson-induced transformation.</pubmed_title><pmcid>PMC2875852</pmcid><funding_grant_id>F 2810</funding_grant_id><funding_grant_id>F 2810-B20</funding_grant_id><funding_grant_id>F 2807-B20</funding_grant_id><funding_grant_id>F 2807</funding_grant_id><funding_grant_id>F 2802-B20</funding_grant_id><funding_grant_id>F 2801</funding_grant_id><funding_grant_id>F 2802</funding_grant_id><funding_grant_id>F 2801-B20</funding_grant_id><pubmed_authors>Hennighausen L</pubmed_authors><pubmed_authors>Moriggl R</pubmed_authors><pubmed_authors>Sexl V</pubmed_authors><pubmed_authors>Cui Y</pubmed_authors><pubmed_authors>Hoelbl A</pubmed_authors><pubmed_authors>Kovacic B</pubmed_authors><pubmed_authors>Beug H</pubmed_authors><pubmed_authors>Warsch W</pubmed_authors><pubmed_authors>Kerenyi MA</pubmed_authors><pubmed_authors>Simma O</pubmed_authors></additional><is_claimable>false</is_claimable><name>Clarifying the role of Stat5 in lymphoid development and Abelson-induced transformation.</name><description>The Stat5 transcription factors Stat5a and Stat5b have been implicated in lymphoid development and transformation. Most studies have employed Stat5a/b-deficient mice where gene targeting disrupted the first protein-coding exon, resulting in the expression of N-terminally truncated forms of Stat5a/b (Stat5a/b(DeltaN/DeltaN) mice). We have now reanalyzed lymphoid development in Stat5a/b(null/null) mice having a complete deletion of the Stat5a/b gene locus. The few surviving Stat5a/b(null/null) mice lacked CD8(+) T lymphocytes. A massive reduction of CD8(+) T cells was also found in Stat5a/b(fl/fl) lck-cre transgenic animals. While gammadelta T-cell receptor-positive (gammadeltaTCR(+)) cells were expressed at normal levels in Stat5a/b(DeltaN/DeltaN) mice, they were completely absent in Stat5a</description><dates><release>2006-01-01T00:00:00Z</release><publication>2006 Jun</publication><modification>2025-06-01T12:33:21.332Z</modification><creation>2025-06-01T12:33:21.332Z</creation></dates><accession>S-EPMC2875852</accession><cross_references><pubmed>16493008</pubmed><doi>10.1182/blood-2005-09-3596</doi></cross_references></HashMap>