{"entity": "researcher", "timestamp": "2026-08-20T20:50:37.359Z", "family": "Fernandez-Capetillo", "given": "Oscar", "initials": "O", "orcid": "0000-0002-2690-6885", "affiliations": ["Genomic Instability Group, Spanish National Cancer Research Centre (CNIO), Madrid, Spain.", "Science for Life Laboratory, Division of Genome Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institute, Stockholm, Sweden."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/ab1f07900e6e466d83763e5fe0020ed6.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/ab1f07900e6e466d83763e5fe0020ed6"}}, "publications": [{"entity": "publication", "iuid": "cba67b05ce7f4cd2a8af7b6871e6ccb6", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/cba67b05ce7f4cd2a8af7b6871e6ccb6.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/cba67b05ce7f4cd2a8af7b6871e6ccb6"}}, "title": "Cyclophilin D plays a critical role in the survival of senescent cells.", "authors": [{"family": "Protasoni", "given": "Margherita", "initials": "M"}, {"family": "L\u00f3pez-Polo", "given": "Vanessa", "initials": "V", "orcid": "0000-0001-6165-2510", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6533bccc17664cbe837a56914580d01d.json"}}, {"family": "Stephan-Otto Attolini", "given": "Camille", "initials": "C"}, {"family": "Brandariz", "given": "Julian", "initials": "J", "orcid": "0009-0006-4316-3952", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a03eedc015b64e51bf686044c658b319.json"}}, {"family": "Herranz", "given": "Nicolas", "initials": "N"}, {"family": "Mateo", "given": "Joaquin", "initials": "J"}, {"family": "Ruiz", "given": "Sergio", "initials": "S", "orcid": "0000-0002-0177-6965", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a1df9c89b653456fbcb710b8e749f346.json"}}, {"family": "Fernandez-Capetillo", "given": "Oscar", "initials": "O", "orcid": "0000-0002-2690-6885", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ab1f07900e6e466d83763e5fe0020ed6.json"}}, {"family": "Kovatcheva", "given": "Marta", "initials": "M", "orcid": "0000-0002-2536-1043", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c04ebf2b2e9c4577bf12a901f57b1c06.json"}}, {"family": "Serrano", "given": "Manuel", "initials": "M", "orcid": "0000-0001-7177-9312", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/26e4038046f3446ebcb124419692eed4.json"}}], "type": "journal article", "published": "2024-12-00", "journal": {"title": "EMBO J.", "issn": "1460-2075", "volume": "43", "issue": "23", "pages": "5972-6000", "issn-l": "0261-4189"}, "abstract": "Senescent cells play a causative role in many diseases, and their elimination is a promising therapeutic strategy. Here, through a genome-wide CRISPR/Cas9 screen, we identify the gene PPIF, encoding the mitochondrial protein cyclophilin D (CypD), as a novel senolytic target. Cyclophilin D promotes the transient opening of the mitochondrial permeability transition pore (mPTP), which serves as a failsafe mechanism for calcium efflux. We show that senescent cells exhibit a high frequency of transient CypD/mPTP opening events, known as 'flickering'. Inhibition of CypD using genetic or pharmacologic tools, including cyclosporin A, leads to the toxic accumulation of mitochondrial Ca2+ and the death of senescent cells. Genetic or pharmacological inhibition of NCLX, another mitochondrial calcium efflux channel, also leads to senolysis, while inhibition of the main Ca2+ influx channel, MCU, prevents senolysis induced by CypD inhibition. We conclude that senescent cells are highly vulnerable to elevated mitochondrial Ca2+ ions, and that transient CypD/mPTP opening is a critical adaptation mechanism for the survival of senescent cells.", "doi": "10.1038/s44318-024-00259-2", "pmid": "39448884", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC11612481"}, {"db": "pii", "key": "10.1038/s44318-024-00259-2"}], "notes": [], "created": "2026-08-20T09:26:41.098Z", "modified": "2026-08-20T09:26:41.345Z"}, {"entity": "publication", "iuid": "0f7b8a50618b4b91845b2f05d5c329e5", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/0f7b8a50618b4b91845b2f05d5c329e5.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/0f7b8a50618b4b91845b2f05d5c329e5"}}, "title": "Emerging concepts in drug discovery for cancer therapy.", "authors": [{"family": "Murga", "given": "Matilde", "initials": "M"}, {"family": "Fernandez-Capetillo", "given": "Oscar", "initials": "O", "orcid": "0000-0002-2690-6885", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ab1f07900e6e466d83763e5fe0020ed6.json"}}], "type": "editorial", "published": "2022-11-00", "journal": {"title": "Mol Oncol", "issn": "1878-0261", "volume": "16", "issue": "21", "pages": "3757-3760", "issn-l": "1574-7891"}, "abstract": null, "doi": "10.1002/1878-0261.13325", "pmid": "36321722", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9627784"}], "notes": [], "created": "2026-08-20T06:26:50.051Z", "modified": "2026-08-20T06:26:50.110Z"}, {"entity": "publication", "iuid": "8358a6013bea4696bba1359b5f692158", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/8358a6013bea4696bba1359b5f692158.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/8358a6013bea4696bba1359b5f692158"}}, "title": "Activation of the integrated stress response is a vulnerability for multidrug-resistant FBXW7-deficient cells.", "authors": [{"family": "Sanchez-Burgos", "given": "Laura", "initials": "L", "orcid": "0000-0002-5196-5828", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/1925f119bd724efabd716a3df6f0c865.json"}}, {"family": "Navarro-Gonz\u00e1lez", "given": "Bel\u00e9n", "initials": "B", "orcid": "0000-0003-4362-3382", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/50bbcc00591344e5b8bc55c0639c68ab.json"}}, {"family": "Garc\u00eda-Mart\u00edn", "given": "Santiago", "initials": "S", "orcid": "0000-0002-4540-9446", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/fa816816d0e048aba3ff21740040773c.json"}}, {"family": "Sirozh", "given": "Oleksandra", "initials": "O"}, {"family": "Mota-Pino", "given": "Jorge", "initials": "J", "orcid": "0000-0003-1421-1450", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6c79064797fd4115ab12a4bb2a3d2dd1.json"}}, {"family": "Fueyo-Marcos", "given": "Elena", "initials": "E", "orcid": "0000-0001-5963-6204", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/6fc6caa5b8e54265b3dff2a3784d21f3.json"}}, {"family": "Tejero", "given": "H\u00e9ctor", "initials": "H"}, {"family": "Ant\u00f3n", "given": "Marta Elena", "initials": "ME"}, {"family": "Murga", "given": "Matilde", "initials": "M"}, {"family": "Al-Shahrour", "given": "F\u00e1tima", "initials": "F"}, {"family": "Fernandez-Capetillo", "given": "Oscar", "initials": "O", "orcid": "0000-0002-2690-6885", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ab1f07900e6e466d83763e5fe0020ed6.json"}}], "type": "journal article", "published": "2022-09-07", "journal": {"title": "EMBO Mol Med", "issn": "1757-4684", "volume": "14", "issue": "9", "pages": "e15855", "issn-l": "1757-4676"}, "abstract": "FBXW7 is one of the most frequently mutated tumor suppressors, deficiency of which has been associated with resistance to some anticancer therapies. Through bioinformatics and genome-wide CRISPR screens, we here reveal that FBXW7 deficiency leads to multidrug resistance (MDR). Proteomic analyses found an upregulation of mitochondrial factors as a hallmark of FBXW7 deficiency, which has been previously linked to chemotherapy resistance. Despite this increased expression of mitochondrial factors, functional analyses revealed that mitochondria are under stress, and genetic or chemical targeting of mitochondria is preferentially toxic for FBXW7-deficient cells. Mechanistically, the toxicity of therapies targeting mitochondrial translation such as the antibiotic tigecycline relates to the activation of the integrated stress response (ISR) in a GCN2 kinase-dependent manner. Furthermore, the discovery of additional drugs that are toxic for FBXW7-deficient cells showed that all of them unexpectedly activate a GCN2-dependent ISR regardless of their accepted mechanism of action. Our study reveals that while one of the most frequent mutations in cancer reduces the sensitivity to the vast majority of available therapies, it renders cells vulnerable to ISR-activating drugs.", "doi": "10.15252/emmm.202215855", "pmid": "35861150", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9449593"}, {"db": "GEO", "key": "GSE189499"}], "notes": [], "created": "2026-08-20T12:51:46.957Z", "modified": "2026-08-20T12:51:47.194Z"}, {"entity": "publication", "iuid": "71038df5b2f243e797be7fa2a65177b3", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/71038df5b2f243e797be7fa2a65177b3.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/71038df5b2f243e797be7fa2a65177b3"}}, "title": "Distinct roles for PARP-1 and PARP-2 in c-Myc-driven B-cell lymphoma in mice.", "authors": [{"family": "Galindo-Campos", "given": "Miguel A", "initials": "MA", "orcid": "0000-0002-0650-8660", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/10d44079628a440e98da0ce1dd56c9b9.json"}}, {"family": "Lutfi", "given": "Nura", "initials": "N"}, {"family": "Bonnin", "given": "Sarah", "initials": "S", "orcid": "0000-0001-5159-2518", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a3074010e1c34fed9ed35f9d0ca54d92.json"}}, {"family": "Mart\u00ednez", "given": "Carlos", "initials": "C", "orcid": "0000-0003-3307-1326", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e0493b09554543e884ea61ed9d57a692.json"}}, {"family": "Velasco-Hernandez", "given": "Talia", "initials": "T", "orcid": "0000-0003-2183-7443", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/332a43e5a86141afb3b585972de8cfec.json"}}, {"family": "Garc\u00eda-Hern\u00e1ndez", "given": "Violeta", "initials": "V", "orcid": "0000-0003-2328-4360", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e31ccefd7cae4350b56a01f81db1d34c.json"}}, {"family": "Mart\u00edn-Caballero", "given": "Juan", "initials": "J"}, {"family": "Ampurdan\u00e9s", "given": "Coral", "initials": "C"}, {"family": "Gimeno", "given": "Ram\u00f3n", "initials": "R", "orcid": "0000-0002-8758-121X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/317c169baefd42018d5b507b5f320796.json"}}, {"family": "Colomo", "given": "Lluis", "initials": "L"}, {"family": "Rou\u00e9", "given": "Ga\u00ebl", "initials": "G"}, {"family": "Guilbaud", "given": "Guillaume", "initials": "G", "orcid": "0000-0002-4345-6855", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5d0d2b6a3dfd4306b10f875a69297621.json"}}, {"family": "Dantzer", "given": "Fran\u00e7oise", "initials": "F"}, {"family": "Navarro", "given": "Pilar", "initials": "P", "orcid": "0000-0003-4314-4584", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/62b30841008c40de887bc43ec46d13f2.json"}}, {"family": "Murga", "given": "Matilde", "initials": "M", "orcid": "0000-0002-9766-4481", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/bcb1f05248024b948915de2b24ace8a7.json"}}, {"family": "Fern\u00e1ndez-Capetillo", "given": "Oscar", "initials": "O", "orcid": "0000-0002-2690-6885", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ab1f07900e6e466d83763e5fe0020ed6.json"}}, {"family": "Bigas", "given": "Anna", "initials": "A", "orcid": "0000-0003-4801-6899", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/edc911cc937d4184ab4b11594cd34b01.json"}}, {"family": "Men\u00e9ndez", "given": "Pablo", "initials": "P"}, {"family": "Sale", "given": "Julian E", "initials": "JE"}, {"family": "Y\u00e9lamos", "given": "Jos\u00e9", "initials": "J", "orcid": "0000-0003-1195-1496", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3c857e9f548545369bb73b08bf5db754.json"}}], "type": "journal article", "published": "2022-01-13", "journal": {"title": "Blood", "issn": "1528-0020", "volume": "139", "issue": "2", "pages": "228-239", "issn-l": "0006-4971"}, "abstract": "Dysregulation of the c-Myc oncogene occurs in a wide variety of hematologic malignancies, and its overexpression has been linked with aggressive tumor progression. Here, we show that poly (ADP-ribose) polymerase 1 (PARP-1) and PARP-2 exert opposing influences on progression of c-Myc-driven B-cell lymphoma. PARP-1 and PARP-2 catalyze the synthesis and transfer of ADP-ribose units onto amino acid residues of acceptor proteins in response to DNA strand breaks, playing a central role in the response to DNA damage. Accordingly, PARP inhibitors have emerged as promising new cancer therapeutics. However, the inhibitors currently available for clinical use are not able to discriminate between individual PARP proteins. We found that genetic deletion of PARP-2 prevents c-Myc-driven B-cell lymphoma, whereas PARP-1 deficiency accelerates lymphomagenesis in the E\u03bc-Myc mouse model of aggressive B-cell lymphoma. Loss of PARP-2 aggravates replication stress in preleukemic E\u03bc-Myc B cells, resulting in accumulation of DNA damage and concomitant cell death that restricts the c-Myc-driven expansion of B cells, thereby providing protection against B-cell lymphoma. In contrast, PARP-1 deficiency induces a proinflammatory response and an increase in regulatory T cells, likely contributing to immune escape of B-cell lymphoma, resulting in an acceleration of lymphomagenesis. These findings pinpoint specific functions for PARP-1 and PARP-2 in c-Myc-driven lymphomagenesis with antagonistic consequences that may help inform the design of new PARP-centered therapeutic strategies, with selective PARP-2 inhibition potentially representing a new therapeutic approach for the treatment of c-Myc-driven tumors.", "doi": "10.1182/blood.2021012805", "pmid": "34359075", "labels": [], "xrefs": [{"db": "pii", "key": "S0006-4971(21)01451-8"}], "notes": [], "created": "2026-08-20T12:17:51.508Z", "modified": "2026-08-20T12:17:51.921Z"}, {"entity": "publication", "iuid": "a9924f0b5427486390e3b236da64b749", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/a9924f0b5427486390e3b236da64b749.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/a9924f0b5427486390e3b236da64b749"}}, "title": "Widespread displacement of DNA- and RNA-binding factors underlies toxicity of arginine-rich cell-penetrating peptides.", "authors": [{"family": "Lafarga", "given": "Vanesa", "initials": "V"}, {"family": "Sirozh", "given": "Oleksandra", "initials": "O"}, {"family": "D\u00edaz-L\u00f3pez", "given": "Irene", "initials": "I"}, {"family": "Galarreta", "given": "Antonio", "initials": "A", "orcid": "0000-0003-2358-7927", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/afa6e99550224076bf06615778479685.json"}}, {"family": "Hisaoka", "given": "Misaru", "initials": "M"}, {"family": "Zarzuela", "given": "Eduardo", "initials": "E"}, {"family": "Boskovic", "given": "Jasminka", "initials": "J"}, {"family": "Jovanovic", "given": "Bogdan", "initials": "B"}, {"family": "Fernandez-Leiro", "given": "Rafael", "initials": "R", "orcid": "0000-0002-7941-0357", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/082cd4d551754cbd91af9bcf249a3912.json"}}, {"family": "Mu\u00f1oz", "given": "Jaime", "initials": "J"}, {"family": "Stoecklin", "given": "Georg", "initials": "G", "orcid": "0000-0001-9284-9834", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/65fee664b61c42b1ad51358fe34e2608.json"}}, {"family": "Ventoso", "given": "Iv\u00e1n", "initials": "I"}, {"family": "Fernandez-Capetillo", "given": "Oscar", "initials": "O", "orcid": "0000-0002-2690-6885", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ab1f07900e6e466d83763e5fe0020ed6.json"}}], "type": "journal article", "published": "2021-07-01", "journal": {"title": "EMBO J.", "issn": "1460-2075", "volume": "40", "issue": "13", "pages": "e103311", "issn-l": "0261-4189"}, "abstract": "Due to their capability to transport chemicals or proteins into target cells, cell-penetrating peptides (CPPs) are being developed as therapy delivery tools. However, and despite their interesting properties, arginine-rich CPPs often show toxicity for reasons that remain poorly understood. Using a (PR)n dipeptide repeat that has been linked to amyotrophic lateral sclerosis (ALS) as a model of an arginine-rich CPP, we here show that the presence of (PR)n leads to a generalized displacement of RNA- and DNA-binding proteins from chromatin and mRNA. Accordingly, any reaction involving nucleic acids, such as RNA transcription, translation, splicing and degradation, or DNA replication and repair, is impaired by the presence of the CPPs. Interestingly, the effects of (PR)n are fully mimicked by protamine, a small arginine-rich protein that displaces histones from chromatin during spermatogenesis. We propose that widespread coating of nucleic acids and consequent displacement of RNA- and DNA-binding factors from chromatin and mRNA accounts for the toxicity of arginine-rich CPPs, including those that have been recently associated with the onset of ALS.", "doi": "10.15252/embj.2019103311", "pmid": "33978236", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8246256"}], "notes": [], "created": "2026-08-20T12:51:31.926Z", "modified": "2026-08-20T12:51:32.043Z"}, {"entity": "publication", "iuid": "7760d431e3664f2d8e55416b641390f8", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/7760d431e3664f2d8e55416b641390f8.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/7760d431e3664f2d8e55416b641390f8"}}, "title": "USP7 limits CDK1 activity throughout the cell cycle.", "authors": [{"family": "Galarreta", "given": "Antonio", "initials": "A", "orcid": "0000-0003-2358-7927", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/afa6e99550224076bf06615778479685.json"}}, {"family": "Valledor", "given": "Pablo", "initials": "P", "orcid": "0000-0001-8215-7914", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/311d8e1c65bf437f94e35fdb90453ebd.json"}}, {"family": "Ubieto-Capella", "given": "Patricia", "initials": "P"}, {"family": "Lafarga", "given": "Vanesa", "initials": "V"}, {"family": "Zarzuela", "given": "Eduardo", "initials": "E"}, {"family": "Mu\u00f1oz", "given": "Javier", "initials": "J", "orcid": "0000-0003-3288-3496", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0f5947eb1a88407097be793853f3b08c.json"}}, {"family": "Malumbres", "given": "Marcos", "initials": "M", "orcid": "0000-0002-0829-6315", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3da3462ae875499a98fda83ecb8406ac.json"}}, {"family": "Lecona", "given": "Emilio", "initials": "E", "orcid": "0000-0002-1687-2562", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/16cf65e3590d430bbd2f3fbf1fddfa39.json"}}, {"family": "Fernandez-Capetillo", "given": "Oscar", "initials": "O", "orcid": "0000-0002-2690-6885", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ab1f07900e6e466d83763e5fe0020ed6.json"}}], "type": "journal article", "published": "2021-06-01", "journal": {"title": "EMBO J.", "issn": "1460-2075", "volume": "40", "issue": "11", "pages": "e99692", "issn-l": "0261-4189"}, "abstract": "Chemical inhibitors of the deubiquitinase USP7 are currently being developed as anticancer agents based on their capacity to stabilize P53. Regardless of this activity, USP7 inhibitors also generate DNA damage in a p53-independent manner. However, the mechanism of this genotoxicity and its contribution to the anticancer effects of USP7 inhibitors are still under debate. Here we show that, surprisingly, even if USP7 inhibitors stop DNA replication, they also induce a widespread activation of CDK1 throughout the cell cycle, which leads to DNA damage and is toxic for mammalian cells. In addition, USP7 interacts with the phosphatase PP2A and supports its active localization in the cytoplasm. Accordingly, inhibition of USP7 or PP2A triggers very similar changes of the phosphoproteome, including a widespread increase in the phosphorylation of CDK1 targets. Importantly, the toxicity of USP7 inhibitors is alleviated by lowering CDK1 activity or by chemical activation of PP2A. Our work reveals that USP7 limits CDK1 activity at all cell cycle stages, providing a novel mechanism that explains the toxicity of USP7 inhibitors through untimely activation of CDK1.", "doi": "10.15252/embj.201899692", "pmid": "33856059", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8167359"}], "notes": [], "created": "2026-08-20T12:51:30.021Z", "modified": "2026-08-20T12:51:30.253Z"}, {"entity": "publication", "iuid": "79d8a8a0a7e04cfa8c7f5011ad71a8f8", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/79d8a8a0a7e04cfa8c7f5011ad71a8f8.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/79d8a8a0a7e04cfa8c7f5011ad71a8f8"}}, "title": "ATR expands embryonic stem cell fate potential in response to replication stress", "authors": [{"family": "Atashpaz", "given": "Sina", "initials": "S", "orcid": "0000-0003-0566-5629", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c8836292554646f8b1db4da6fb341107.json"}}, {"family": "Shams", "given": "Sara Samadi", "initials": "SS", "orcid": "0000-0002-1697-9343", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c0769a0706764b6f85f3949e31f73d36.json"}}, {"family": "Gonzalez", "given": "Javier Martin", "initials": "JM"}, {"family": "Sebesty\u00e9n", "given": "Endre", "initials": "E", "orcid": "0000-0001-5470-2161", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a6cad94788f84d2d8ce3e18f7dd21d68.json"}}, {"family": "Arghavanifard", "given": "Negar", "initials": "N", "orcid": "0000-0003-3039-7603", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/98744fc5a644426b80f96f5fafd8daca.json"}}, {"family": "Gnocchi", "given": "Andrea", "initials": "A", "orcid": "0000-0003-3290-9449", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/e402b4ef8af042308ca805bb2d739c6a.json"}}, {"family": "Albers", "given": "Eliene", "initials": "E", "orcid": "0000-0003-3207-0348", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9b2b5a33864b452f96b54001a426d83e.json"}}, {"family": "Minardi", "given": "Simone", "initials": "S", "orcid": "0000-0001-7303-3821", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9a6733b6b3734030a4a0bbfa059a6ba3.json"}}, {"family": "Faga", "given": "Giovanni", "initials": "G"}, {"family": "Soffientini", "given": "Paolo", "initials": "P"}, {"family": "Allievi", "given": "Elisa", "initials": "E"}, {"family": "Cancila", "given": "Valeria", "initials": "V"}, {"family": "Bachi", "given": "Angela", "initials": "A"}, {"family": "Fernandez-Capetillo", "given": "Oscar", "initials": "O", "orcid": "0000-0002-2690-6885", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ab1f07900e6e466d83763e5fe0020ed6.json"}}, {"family": "Tripodo", "given": "Claudio", "initials": "C"}, {"family": "Ferrari", "given": "Francesco", "initials": "F", "orcid": "0000-0002-9811-3753", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/04dd46220caf47cbb4db412cd976b373.json"}}, {"family": "L\u00f3pez-Contreras", "given": "Andr\u00e9s Joaquin", "initials": "AJ", "orcid": "0000-0002-5517-7327", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/4c57e2d4e1734bc3bf9dfafd705eb0d6.json"}}, {"family": "Costanzo", "given": "Vincenzo", "initials": "V", "orcid": "0000-0002-2920-9508", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/fa58e20a668c49b2ba09a935b2f3c74f.json"}}], "type": "posted-content", "published": "2020-01-01", "journal": {"issn-l": null}, "abstract": null, "doi": "10.1101/2020.01.01.888354", "pmid": null, "labels": [], "xrefs": [], "notes": [], "created": "2026-08-20T09:55:19.358Z", "modified": "2026-08-20T09:55:19.813Z"}]}