{"entity": "researcher", "timestamp": "2026-06-02T10:41:49.862Z", "family": "Rodrigues-Junior", "given": "Dorival Mendes", "initials": "DM", "orcid": "0000-0002-8861-9240", "affiliations": ["Department of Medical Biochemistry and Microbiology, Science for Life Laboratory, Box 582, Biomedical Center, Uppsala University, SE-751 23 Uppsala, Sweden."], "links": {"self": {"href": "https://publications.scilifelab.se/researcher/3334d6f77c1f42c2b10fd3e9bef23efb.json"}, "display": {"href": "https://publications.scilifelab.se/researcher/3334d6f77c1f42c2b10fd3e9bef23efb"}}, "publications": [{"entity": "publication", "iuid": "8cb122c7905e4043bd3f13414014d2fe", "links": {"self": {"href": "https://publications.scilifelab.se/publication/8cb122c7905e4043bd3f13414014d2fe.json"}, "display": {"href": "https://publications.scilifelab.se/publication/8cb122c7905e4043bd3f13414014d2fe"}}, "title": "The long noncoding RNA VIM-AS1 and nucleoporin Nup358/RanBP2 regulate SMAD nuclear accumulation during TGF-\u03b2 signaling.", "authors": [{"family": "Rodrigues-Junior", "given": "Dorival Mendes", "initials": "DM", "orcid": "0000-0002-8861-9240", "researcher": {"href": "https://publications.scilifelab.se/researcher/3334d6f77c1f42c2b10fd3e9bef23efb.json"}}, {"family": "Ali", "given": "Mohamad Moustafa", "initials": "MM"}, {"family": "Itoh", "given": "Yuka", "initials": "Y"}, {"family": "Ferreira", "given": "Mafalda Sousa", "initials": "MS"}, {"family": "Heldin", "given": "Johan", "initials": "J", "orcid": "0000-0002-0915-5303", "researcher": {"href": "https://publications.scilifelab.se/researcher/d8a546798d014cd3a44537ae5db9f889.json"}}, {"family": "Fu", "given": "Hao", "initials": "H"}, {"family": "Hoelz", "given": "Andr\u00e9", "initials": "A"}, {"family": "Heldin", "given": "Carl-Henrik", "initials": "CH"}, {"family": "Moustakas", "given": "Aristidis", "initials": "A", "orcid": "0000-0001-9131-3827", "researcher": {"href": "https://publications.scilifelab.se/researcher/6c1626d991f3485e81232db174537e6d.json"}}], "type": "journal article", "published": "2026-01-14", "journal": {"title": "Nucleic Acids Res.", "issn": "1362-4962", "volume": "54", "issue": "2", "issn-l": "0305-1048"}, "abstract": "The transforming growth factor \u03b2 (TGF-\u03b2) pathway is a developmental signaling network that regulates tissue homeostasis and malfunctions in human diseases, including cancer. TGF-\u03b2 signals via two receptors, which activate SMAD and alternative signaling pathways. We show that TGF-\u03b2 induces the expression of the mammalian long noncoding RNA (lncRNA) VIM-AS1 (Vimentin antisense RNA1) variant-2 (v.2) via a transcriptional SMAD-GATA6-SPI1 complex. VIM-AS1 v.1 and v.2 localize in different cell compartments, including the nuclear border. Unbiased whole transcriptomic analysis and functional gain and loss of function assays establish that VIM-AS1 v.2 enhances TGF-\u03b2 signaling. Mechanistically, VIM-AS1 v.2 interacts with the nucleoporin Nup358/RanBP2, contributing to the binding of Nup358/RanBP2 to SMAD2/3 and enhancing SMAD nuclear accumulation. In the context of cancer biology, VIM-AS1 did not affect the antiproliferative actions of TGF-\u03b2, yet had an impact on the epithelial-mesenchymal transition gene program, and increased the invasion and motility of tumor cells, whereas its silencing sensitized cancer cells to chemotherapeutic agents. The molecular mechanism highlights how a lncRNA can modulate the nuclear pore's capacity to import SMAD complexes, by facilitating their capture by Nup358/RanBP2 and thereby enhancing nuclear accumulation of SMADs with distinct isoform composition, thus promoting selectively TGF-\u03b2 signaling responses.", "doi": "10.1093/nar/gkaf1526", "pmid": "41556346", "labels": {"NGI Uppsala (SNP&SEQ Technology Platform)": "Service", "NGI Short read": "Service", "National Genomics Infrastructure": "Service"}, "xrefs": [{"db": "pmc", "key": "PMC12817083"}, {"db": "pii", "key": "8431143"}], "notes": [], "created": "2026-06-01T11:10:58.548Z", "modified": "2026-06-01T11:10:58.802Z"}]}