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Mol. Life Sci."],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Translation of the coding sequence for human C\/EBP homologous protein (CHOP) is highly regulated by its upstream open reading frame (\n                    <jats:italic>uORF<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>chop<\/jats:italic>\n                    <\/jats:sup>\n                    ). ENDOU-1 was shown to play positive roles in mediating\n                    <jats:italic>CHOP<\/jats:italic>\n                    translation through suppressing\n                    <jats:italic>uORF<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>chop<\/jats:italic>\n                    <\/jats:sup>\n                    -mediated translational inhibition (\n                    <jats:italic>uORF<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>chop<\/jats:italic>\n                    <\/jats:sup>\n                    -MTI) during ER stress. However, when we screened for other RNA-binding proteins putatively engaged in the same inhibitory activity, we found that HnRNPA3 associated with zebrafish Endouc and its mammalian orthologue ENDOU-1 and could also be involved in\n                    <jats:italic>uORF<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>chop<\/jats:italic>\n                    <\/jats:sup>\n                    -MTI in a p-eIF2\u03b1-independent manner. A time course experiment showed that the dynamic patterns of ENDOU-1, HnRNPA3 and CHOP were similarly fluctuant and positively correlated during ER stress. Moreover, overexpression of ENDOU-1 induced the increase of HnRNPA3 expression and caused a shift of HnRNPA3 from the nucleus to the cytoplasm. The resultant cytoplasmic HnRNPA3 served as a reader protein to recognize the N6-methyladenosine site on human\n                    <jats:italic>uORF<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>chop<\/jats:italic>\n                    <\/jats:sup>\n                    cassette methylated by Wilms\u2019 tumor 1-associating protein. Collectively, we suggest that HnRNPA3 is a positive effector of ENDOU-1 in an m6A-dependent manner, allowing it to reach maximal\n                    <jats:italic>CHOP<\/jats:italic>\n                    translation during ER stress.\n                  <\/jats:p>","DOI":"10.1007\/s00018-026-06180-7","type":"journal-article","created":{"date-parts":[[2026,3,28]],"date-time":"2026-03-28T13:53:42Z","timestamp":1774706022000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["ENDOU-1-induced cytoplasmic HnRNPA3 recognizes m6A methylation on the upstream reading frame of human CHOP transcripts to achieve maximal CHOP translation"],"prefix":"10.1007","volume":"83","author":[{"given":"Hung-Chieh","family":"Lee","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi-Hsin","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chi-Cheng","family":"Hsieh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi-Nan","family":"Ke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8242-4939","authenticated-orcid":false,"given":"Huai-Jen","family":"Tsai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,3,28]]},"reference":[{"key":"6180_CR1","doi-asserted-by":"publisher","first-page":"4341","DOI":"10.1093\/nar\/29.21.4341","volume":"29","author":"C Jousse","year":"2001","unstructured":"Jousse C, Bruhat A, Carraro V, Urano F, Ferrara M, Ron D, Fafournoux P (2001) Inhibition of CHOP translation by a peptide encoded by an open reading frame localized in the chop 5\u2019UTR. 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