{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ding Y"],"funding":["NCI NIH HHS"],"pagination":["48545-48562"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5564707"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(30)"],"pubmed_abstract":["Zinc finger domain genes comprise ~3% of the human genome, yet many of their functions remain unknown. Here we investigated roles for the vertebrate-specific BTB domain zinc finger gene ZNF131 in the context of human brain tumors. We report that ZNF131 is broadly required for Glioblastoma stem-like cell (GSC) viability, but dispensable for neural progenitor cell (NPC) viability. Examination of gene expression changes after ZNF131 knockdown (kd) revealed that ZNF131 activity notably promotes expression of Joubert Syndrome ciliopathy genes, including KIF7, NPHP1, and TMEM237, as well as HAUS5, a component of Augmin/HAUS complex that facilitates microtubule nucleation along the mitotic spindle. Of these genes only kd of HAUS5 displayed GSC-specific viability loss. Critically, HAUS5 ectopic ex"],"journal":["Oncotarget"],"pubmed_title":["ZNF131 suppresses centrosome fragmentation in glioblastoma stem-like cells through regulation of HAUS5."],"pmcid":["PMC5564707"],"funding_grant_id":["P30 CA015704","R21 CA170722","R01 CA114567","R01 CA155360","R01 CA190957"],"pubmed_authors":["Delrow JJ","Ding Y","Corrin P","Girard EJ","Paddison PJ","Herman JA","Olson JM","Lang JM","Basom R","Toledo CM"],"additional_accession":[]},"is_claimable":false,"name":"ZNF131 suppresses centrosome fragmentation in glioblastoma stem-like cells through regulation of HAUS5.","description":"Zinc finger domain genes comprise ~3% of the human genome, yet many of their functions remain unknown. Here we investigated roles for the vertebrate-specific BTB domain zinc finger gene ZNF131 in the context of human brain tumors. We report that ZNF131 is broadly required for Glioblastoma stem-like cell (GSC) viability, but dispensable for neural progenitor cell (NPC) viability. Examination of gene expression changes after ZNF131 knockdown (kd) revealed that ZNF131 activity notably promotes expression of Joubert Syndrome ciliopathy genes, including KIF7, NPHP1, and TMEM237, as well as HAUS5, a component of Augmin/HAUS complex that facilitates microtubule nucleation along the mitotic spindle. Of these genes only kd of HAUS5 displayed GSC-specific viability loss. Critically, HAUS5 ectopic ex","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Jul","modification":"2026-07-15T15:23:52.557Z","creation":"2026-07-07T03:07:48.885Z"},"accession":"S-EPMC5564707","cross_references":{"pubmed":["28596487"],"doi":["10.18632/oncotarget.18153"]}}