{"entity": "journal", "iuid": "1ef8053a50854c54930c1b90d6e0109e", "timestamp": "2026-08-25T23:23:19.997Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/journal/J%20Mol%20Cell%20Biol.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/journal/J%20Mol%20Cell%20Biol"}}, "title": "J Mol Cell Biol", "issn": "1759-4685", "issn-l": null, "publications_count": 3, "publications": [{"entity": "publication", "iuid": "7d64204d683a4e45876e5e9a47090cfc", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/7d64204d683a4e45876e5e9a47090cfc.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/7d64204d683a4e45876e5e9a47090cfc"}}, "title": "Transcriptional output, cell-type densities, and normalization in spatial transcriptomics.", "authors": [{"family": "Saiselet", "given": "Manuel", "initials": "M"}, {"family": "Rodrigues-Vit\u00f3ria", "given": "Jo\u00ebl", "initials": "J"}, {"family": "Tourneur", "given": "Adrien", "initials": "A"}, {"family": "Craciun", "given": "Ligia", "initials": "L"}, {"family": "Spinette", "given": "Alex", "initials": "A"}, {"family": "Larsimont", "given": "Denis", "initials": "D"}, {"family": "Andry", "given": "Guy", "initials": "G"}, {"family": "Lundeberg", "given": "Joakim", "initials": "J"}, {"family": "Maenhaut", "given": "Carine", "initials": "C"}, {"family": "Detours", "given": "Vincent", "initials": "V"}], "type": "letter", "published": "2020-06-23", "journal": {"title": "J Mol Cell Biol", "issn": "1759-4685", "volume": "12", "issue": "11", "pages": "906-908", "issn-l": null}, "abstract": null, "doi": "10.1093/jmcb/mjaa028", "pmid": "32573704", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC7883818"}, {"db": "pii", "key": "5861536"}], "notes": [], "created": "2026-08-20T09:42:14.788Z", "modified": "2026-08-20T09:42:14.854Z"}, {"entity": "publication", "iuid": "b6b24b49300c4341b6b5c79e50f06ece", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/b6b24b49300c4341b6b5c79e50f06ece.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/b6b24b49300c4341b6b5c79e50f06ece"}}, "title": "Small molecule activators of the p53 response.", "authors": [{"family": "Ladds", "given": "Marcus J G W", "initials": "MJGW"}, {"family": "La\u00edn", "given": "Sonia", "initials": "S"}], "type": "journal article", "published": "2019-03-01", "journal": {"title": "J Mol Cell Biol", "issn": "1759-4685", "volume": "11", "issue": "3", "pages": "245-254", "issn-l": null}, "abstract": "Drugging the p53 pathway has been a goal for both academics and pharmaceutical companies since the designation of p53 as the 'guardian of the genome'. Through growing understanding of p53 biology, we can see multiple routes for activation of both wild-type p53 function and restoration of mutant p53. In this review, we focus on small molecules that activate wild-type p53 and that do so in a non-genotoxic manner. In particular, we will describe potential approaches to targeting proteins that alter p53 stability and function through posttranslational modification, affect p53's subcellular localization, or target RNA synthesis or the synthesis of ribonucleotides. The plethora of pathways for exploitation of p53, as well as the wide-ranging response to p53 activation, makes it an attractive target for anti-cancer therapy.", "doi": "10.1093/jmcb/mjz006", "pmid": "30689917", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC6478124"}, {"db": "pii", "key": "5301296"}], "notes": [], "created": "2026-08-21T12:10:11.510Z", "modified": "2026-08-21T12:10:11.522Z"}, {"entity": "publication", "iuid": "33a7a80bfb4b4633b42ca6e1a3036ede", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/33a7a80bfb4b4633b42ca6e1a3036ede.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/33a7a80bfb4b4633b42ca6e1a3036ede"}}, "title": "A calreticulin/gC1qR complex prevents cells from dying: a conserved mechanism from arthropods to humans.", "authors": [{"family": "Watthanasurorot", "given": "Apiruck", "initials": "A"}, {"family": "Jiravanichpaisal", "given": "Pikul", "initials": "P"}, {"family": "S\u00f6derh\u00e4ll", "given": "Kenneth", "initials": "K"}, {"family": "S\u00f6derh\u00e4ll", "given": "Irene", "initials": "I"}], "type": "journal article", "published": "2013-04-00", "journal": {"title": "J Mol Cell Biol", "issn": "1759-4685", "volume": "5", "issue": "2", "pages": "120-131", "issn-l": null}, "abstract": "The crossroad between cell death and proliferation is a general target for viral infections because viruses need to obstruct apoptosis to use cells for their own replication. Inducing immunogenic cell death in proliferating cells is also an important aim of anticancer chemotherapy. The C1q-binding proteins calreticulin (CRT) and gC1qR are highly conserved ubiquitous proteins, which are putative targets for viral manipulation and are associated with cancer. Here we show that these proteins form a complex in the cytoplasm as a response to viral infection resulting in apoptosis prevention. The formation of a cytosolic CRT/gC1qR complex prevents cell death by reducing gC1qR translocation into the mitochondria, and we provide evidence that this mechanism is conserved from arthropods to human cancer cells. Furthermore, we show that it is possible to prevent this complex from being formed in cancer cells. When the peptides of the complex proteins are overexpressed in these cells, the cells undergo apoptosis. This finding shows a causal link between virus and cancer and may be used to develop new tools in anticancer or antiviral therapy.", "doi": "10.1093/jmcb/mjt005", "pmid": "23378602", "labels": [], "xrefs": [{"db": "pii", "key": "mjt005"}], "notes": [], "created": "2026-08-21T12:10:07.803Z", "modified": "2026-08-21T12:10:07.816Z"}], "created": "2026-08-20T09:42:14.811Z", "modified": "2026-08-20T09:42:14.811Z"}