{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,15]],"date-time":"2026-08-15T17:27:11Z","timestamp":1786814831487,"version":"build-2736575974"},"reference-count":39,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T00:00:00Z","timestamp":1783900800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T00:00:00Z","timestamp":1783900800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[2026,7,31]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    The activation of endoplasmic reticulum stress (ERS), specifically the PERK\/eIF2\u03b1\/CHOP signaling, is a recognized consequence of ischemic stroke. However, the roles and mechanisms of CRM\u20101 regulating ERS in stroke are poorly elucidated. A murine model of stroke was generated via transient middle cerebral artery occlusion (MCAO). The endpoints included TTC\u2010derived infarct volume, H&amp;E\/TUNEL histopathology, p\u2010PERK immunohistochemistry, and Western blot. Oxygen\u2013glucose deprivation\/reoxygenation (OGD\/R) was employed in HT22 neurons. The CRM1\u2013ALKBH5 interaction and subcellular distribution were assessed by co\u2010immunoprecipitation (co\u2010IP), cytoplasm\u2013nucleus fractionation, and confocal microscopy. m\n                    <jats:sup>6<\/jats:sup>\n                    A regulation of BANF1 was examined using MeRIP\u2010qPCR, RIP\u2010qPCR, and a dual\u2010luciferase reporter assay. Knockdown of CRM\u20101 reduced the infarct size, decreased ER stress activation, decreased apoptosis in\u00a0vivo, and improved cell viability after OGD\/R. CRM\u20101 was attached to ALKBH5 and promoted its export from the nucleus, which increased m\n                    <jats:sup>6<\/jats:sup>\n                    A modification and expression on BANF1. IGF2BP2 and YTHDF1, respectively, enhanced the stability and translation of BANF1 mRNA, thereby upregulating its expression. BANF1 overexpression restored PERK\/eIF2\u03b1\/CHOP activation and apoptosis in the CRM\u20101 knockdown context. CRM\u20101 exacerbated ischemic stroke injury by exporting ALKBH5 to upregulate BANF1 in an m\n                    <jats:sup>6<\/jats:sup>\n                    A\u2010IGF2BP2\/YTHDF1\u2010dependent manner. This cascade subsequently activated the PERK\/eIF2\u03b1\/CHOP ERS pathway.\n                  <\/jats:p>","DOI":"10.1096\/fj.202601304r","type":"journal-article","created":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T14:57:25Z","timestamp":1783954645000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<scp>CRM<\/scp>\n                    \u20101 Aggravates Stroke Injury by Promoting\n                    <scp>BANF1<\/scp>\n                    \u2010Mediated Unfolded Protein Response Through Inducing Nuclear Export of\n                    <scp>ALKBH5<\/scp>"],"prefix":"10.1096","volume":"40","author":[{"ORCID":"https:\/\/orcid.org\/0009-0009-3079-2380","authenticated-orcid":false,"given":"Chujuan","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Neurological Rehabilitation Hunan Provincial People's Hospital (The First Affiliated Hospital of Hunan Normal University)  Changsha P.R. 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