{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Rivera-Correa J"],"funding":["NIDDK NIH HHS","National Institute of Health","NCI NIH HHS","NIAMS NIH HHS","NIH HHS"],"pagination":["e180507"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11949073"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(5)"],"pubmed_abstract":["The mechanisms utilized by differentiating B cells to withstand highly damaging conditions generated during severe infections, like the massive hemolysis that accompanies malaria, are poorly understood. Here, we demonstrate that ROCK1 regulates B cell differentiation in hostile environments replete with pathogen-associated molecular patterns (PAMPs) and high levels of heme by controlling 2 key heme-regulated molecules, BACH2 and heme-regulated eIF2α kinase (HRI). ROCK1 phosphorylates BACH2 and protects it from heme-driven degradation. As B cells differentiate, furthermore, ROCK1 restrains their pro-inflammatory potential and helps them handle the heightened stress imparted by the presence of PAMPs and heme by controlling HRI, a key regulator of the integrated stress response and cytosolic "],"journal":["JCI insight"],"pubmed_title":["ROCK1 promotes B cell differentiation and proteostasis under stress through the heme-regulated proteins, BACH2 and HRI."],"pmcid":["PMC11949073"],"funding_grant_id":["P30 CA008748","R01 DK129946","R01AR078766,R01AI58579,R01DK129946,T32 AR071302,S10OD019986","T32 AR071302","R01 AR078766","S10 OD019986"],"pubmed_authors":["Ricker E","Gupta S","Rivera-Correa J","Jenkins D","Pannellini T","Giannopoulou E","Flores-Castro D","Kim YB","Li Z","Phalke SP","Pernis AB","Zamponi N","Chinenov Y","Cerchietti L","Miele MM","Vulcano S"],"additional_accession":[]},"is_claimable":false,"name":"ROCK1 promotes B cell differentiation and proteostasis under stress through the heme-regulated proteins, BACH2 and HRI.","description":"The mechanisms utilized by differentiating B cells to withstand highly damaging conditions generated during severe infections, like the massive hemolysis that accompanies malaria, are poorly understood. Here, we demonstrate that ROCK1 regulates B cell differentiation in hostile environments replete with pathogen-associated molecular patterns (PAMPs) and high levels of heme by controlling 2 key heme-regulated molecules, BACH2 and heme-regulated eIF2α kinase (HRI). ROCK1 phosphorylates BACH2 and protects it from heme-driven degradation. As B cells differentiate, furthermore, ROCK1 restrains their pro-inflammatory potential and helps them handle the heightened stress imparted by the presence of PAMPs and heme by controlling HRI, a key regulator of the integrated stress response and cytosolic ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Feb","modification":"2026-06-02T07:21:02.043Z","creation":"2025-06-28T03:05:27.13Z"},"accession":"S-EPMC11949073","cross_references":{"pubmed":["39903532"],"doi":["10.1172/jci.insight.180507"]}}