{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lama B"],"funding":["Intramural NIH HHS","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["e202403140"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11806350"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(4)"],"pubmed_abstract":["Either inhibiting or stabilizing SUMOylation in mitosis causes defects in chromosome segregation, suggesting that dynamic mitotic SUMOylation of proteins is critical to maintain integrity of the genome. Polo-like kinase 1-interacting checkpoint helicase (PICH), a mitotic chromatin remodeling enzyme, interacts with SUMOylated chromosomal proteins via three SUMO-interacting motifs (SIMs) to control their association with chromosomes. Using cell lines with conditional PICH depletion/PICH replacement, we revealed mitotic defects associated with compromised PICH functions toward SUMOylated chromosomal proteins. Defects in either remodeling activity or SIMs of PICH delayed mitotic progression caused by activation of the spindle assembly checkpoint (SAC) indicated by extended"],"journal":["Life science alliance"],"pubmed_title":["PICH impacts the spindle assembly checkpoint via its DNA translocase and SUMO-interaction activities."],"pmcid":["PMC11806350"],"funding_grant_id":["P20 GM103418","ZIA HD001902","R01 GM130858","R01 GM112793","R21 CA259718"],"pubmed_authors":["Saito-Fujita T","Lama B","Saitoh N","Azuma Y","Park H","Keifenheim D","Arnaoutov A","Saraf A","Dasso M","Hassebroek V","Aksenova V","Clarke DJ"],"additional_accession":[]},"is_claimable":false,"name":"PICH impacts the spindle assembly checkpoint via its DNA translocase and SUMO-interaction activities.","description":"Either inhibiting or stabilizing SUMOylation in mitosis causes defects in chromosome segregation, suggesting that dynamic mitotic SUMOylation of proteins is critical to maintain integrity of the genome. Polo-like kinase 1-interacting checkpoint helicase (PICH), a mitotic chromatin remodeling enzyme, interacts with SUMOylated chromosomal proteins via three SUMO-interacting motifs (SIMs) to control their association with chromosomes. Using cell lines with conditional PICH depletion/PICH replacement, we revealed mitotic defects associated with compromised PICH functions toward SUMOylated chromosomal proteins. Defects in either remodeling activity or SIMs of PICH delayed mitotic progression caused by activation of the spindle assembly checkpoint (SAC) indicated by extended","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2026-05-29T12:47:56.874Z","creation":"2025-04-03T23:58:17.946Z"},"accession":"S-EPMC11806350","cross_references":{"pubmed":["39919802"],"doi":["10.26508/lsa.202403140"]}}