{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["2"],"submitter":["Hashimoto M"],"pubmed_abstract":["Protooncogene T-cell leukemia 1 (TCL1), which is implicated in human T-cell prolymphocytic leukemia (T-PLL), interacts with Akt and enhances its kinase activity, functioning as an Akt kinase co-activator. Two major isoforms of TCL1 Protooncogenes (TCL1 and TCL1b) are present adjacent to each other on human chromosome 14q.32. In human T-PLL, both TCL1 and TCL1b are activated by chromosomal translocation. Moreover, TCL1b-transgenic mice have never been created. Therefore, it remains unclear whether TCL1b itself, independent of TCL1, exhibits oncogenicity. In co-immunoprecipitation assays, both ectopic and endogenous TCL1b interacted with Akt. In in vitro Akt kinase assays, TCL1b enhanced Akt kinase activity in dose- and time-dependent manners. Bioinformatics approaches utilizing multiregress"],"journal":["Oncogenesis"],"pagination":["e70"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3816220"],"repository":["biostudies-literature"],"pubmed_title":["Protooncogene TCL1b functions as an Akt kinase co-activator that exhibits oncogenic potency in vivo."],"pmcid":["PMC3816220"],"pubmed_authors":["Hirata N","Noguchi H","Tanaka S","Suizu F","Masuzawa M","Edamura T","Tokuyama W","Gotoh N","Hashimoto M","Matsuda-Lennikov M","Noguchi M"],"additional_accession":[]},"is_claimable":false,"name":"Protooncogene TCL1b functions as an Akt kinase co-activator that exhibits oncogenic potency in vivo.","description":"Protooncogene T-cell leukemia 1 (TCL1), which is implicated in human T-cell prolymphocytic leukemia (T-PLL), interacts with Akt and enhances its kinase activity, functioning as an Akt kinase co-activator. Two major isoforms of TCL1 Protooncogenes (TCL1 and TCL1b) are present adjacent to each other on human chromosome 14q.32. In human T-PLL, both TCL1 and TCL1b are activated by chromosomal translocation. Moreover, TCL1b-transgenic mice have never been created. Therefore, it remains unclear whether TCL1b itself, independent of TCL1, exhibits oncogenicity. In co-immunoprecipitation assays, both ectopic and endogenous TCL1b interacted with Akt. In in vitro Akt kinase assays, TCL1b enhanced Akt kinase activity in dose- and time-dependent manners. Bioinformatics approaches utilizing multiregress","dates":{"release":"2013-01-01T00:00:00Z","publication":"2013 Sep","modification":"2025-04-22T16:31:39.939Z","creation":"2019-03-27T01:18:03Z"},"accession":"S-EPMC3816220","cross_references":{"pubmed":["24042734"],"doi":["10.1038/oncsis.2013.30"]}}