{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Humbert M"],"funding":["Swiss National Science Foundation","NHLBI NIH HHS","Bernese Foundation of Cancer Research","Ursula-Hecht-Foundation for Leukemia Research","Marlies-Schwegler Foundation","U.S. National Institutes of Health","Joyce Klein Stock Gift","Werner and Hedy Berger-Janser Foundation of Cancer Research","Bern University Research Foundation"],"pagination":["83-93"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3868189"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["95(1)"],"pubmed_abstract":["DAPK2 is a proapoptotic protein that is mostly expressed in the hematopoietic tissue. A detailed DAPK2 expression analysis in two large AML patient cohorts revealed particularly low DAPK2 mRNA levels in APL. DAPK2 levels were restored in APL patients undergoing ATRA therapy. PML-RARA is the predominant lesion in APL causing transcriptional repression of genes important for neutrophil differentiation. We found binding of PML-RARA and PU.1, a myeloid master regulator, to RARA and PU.1 binding sites in the DAPK2 promoter. Ectopic expression of PML-RARA in non-APL, as well as knocking down PU.1 in APL cells, resulted in a significant reduction of DAPK2 expression. Restoring DAPK2 expression in PU.1 knockdown APL cells partially rescued neutrophil differentiation, thereby identifying DAPK2 as a"],"journal":["Journal of leukocyte biology"],"pubmed_title":["The tumor suppressor gene DAPK2 is induced by the myeloid transcription factors PU.1 and C/EBPα during granulocytic differentiation but repressed by PML-RARα in APL."],"pmcid":["PMC3868189"],"funding_grant_id":["R01 HL091219","129702","129955","R01HL091219","31003A_129955","31003A_129702"],"pubmed_authors":["Haferlach T","Valk PJ","Schlafli AM","Fey MF","Torbett BE","Tschan MP","Simon HU","Britschgi A","Behre G","Humbert M","Kaufmann T","Federzoni EA"],"additional_accession":[]},"is_claimable":false,"name":"The tumor suppressor gene DAPK2 is induced by the myeloid transcription factors PU.1 and C/EBPα during granulocytic differentiation but repressed by PML-RARα in APL.","description":"DAPK2 is a proapoptotic protein that is mostly expressed in the hematopoietic tissue. A detailed DAPK2 expression analysis in two large AML patient cohorts revealed particularly low DAPK2 mRNA levels in APL. DAPK2 levels were restored in APL patients undergoing ATRA therapy. PML-RARA is the predominant lesion in APL causing transcriptional repression of genes important for neutrophil differentiation. We found binding of PML-RARA and PU.1, a myeloid master regulator, to RARA and PU.1 binding sites in the DAPK2 promoter. Ectopic expression of PML-RARA in non-APL, as well as knocking down PU.1 in APL cells, resulted in a significant reduction of DAPK2 expression. Restoring DAPK2 expression in PU.1 knockdown APL cells partially rescued neutrophil differentiation, thereby identifying DAPK2 as a","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Jan","modification":"2026-04-14T17:12:58.273Z","creation":"2025-07-28T03:04:00.684Z"},"accession":"S-EPMC3868189","cross_references":{"pubmed":["24038216"],"doi":["10.1189/jlb.1112608"]}}