<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhang J</submitter><funding>Youth project of Wuxi commission of Health</funding><funding>National Natural Science Foundation of China</funding><funding>Wuxi Taihu Lake Talent Plan</funding><funding>Scientific Research Project of Wuxi Health Commission</funding><pagination>2518679</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12184166</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(1)</volume><pubmed_abstract>Glioblastoma (GBM) exhibits elevated TRIM22 expression correlated with tumor progression, as validated in TCGA/GEO databases. The effects of TRIM22 knockdown and overexpression on GBM proliferation were evaluated with cellular assays. TRIM22 was identified as a potential Bcl-2 activator via a ubiquitination microarray. Flow cytometry (FCM) was utilized to investigate cell apoptosis. Additionally, the expression levels of Bcl-2 and proteins associated with Bcl-2 were evaluated using Western blot analysis. The interaction and ubiquitination of TRIM22 and Bcl-2 were analyzed via immunoprecipitation (IP). TRIM22 overexpression is correlated with glioma progression, and TRIM22 deficiency inhibits GBM cell proliferation. FCM revealed that TRIM22 knockdown promotes GBM cell apoptosis. A TRIM22-ov</pubmed_abstract><journal>Molecular &amp; cellular oncology</journal><pubmed_title>TRIM22 promotes glioblastoma development by ubiquitinating Bcl-2.</pubmed_title><pmcid>PMC12184166</pmcid><funding_grant_id>82172955</funding_grant_id><funding_grant_id>Q202133</funding_grant_id><funding_grant_id>2020ZHYB16</funding_grant_id><funding_grant_id>DJYX-2020</funding_grant_id><pubmed_authors>Cheng C</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Shao J</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Huang J</pubmed_authors><pubmed_authors>Huang H</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Wang G</pubmed_authors><pubmed_authors>Jiao J</pubmed_authors></additional><is_claimable>false</is_claimable><name>TRIM22 promotes glioblastoma development by ubiquitinating Bcl-2.</name><description>Glioblastoma (GBM) exhibits elevated TRIM22 expression correlated with tumor progression, as validated in TCGA/GEO databases. The effects of TRIM22 knockdown and overexpression on GBM proliferation were evaluated with cellular assays. TRIM22 was identified as a potential Bcl-2 activator via a ubiquitination microarray. Flow cytometry (FCM) was utilized to investigate cell apoptosis. Additionally, the expression levels of Bcl-2 and proteins associated with Bcl-2 were evaluated using Western blot analysis. The interaction and ubiquitination of TRIM22 and Bcl-2 were analyzed via immunoprecipitation (IP). TRIM22 overexpression is correlated with glioma progression, and TRIM22 deficiency inhibits GBM cell proliferation. FCM revealed that TRIM22 knockdown promotes GBM cell apoptosis. A TRIM22-ov</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025</publication><modification>2026-06-03T07:03:38.175Z</modification><creation>2026-04-25T03:21:58.598Z</creation></dates><accession>S-EPMC12184166</accession><cross_references><pubmed>40552115</pubmed><doi>10.1080/23723556.2025.2518679</doi></cross_references></HashMap>