{"entity": "researcher", "timestamp": "2026-09-23T18:26:26.267Z", "family": "Lindskog", "given": "Magnus", "initials": "M", "orcid": "0000-0001-9484-1983", "affiliations": ["Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden; Department of Pelvic Cancer, Genitourinary Oncology, Karolinska University Hospital, Stockholm, Sweden; Department of Oncology-Pathology, Karolinska Institute, Stockholm, Sweden."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/de1f718eadcd41b7b3d5834bf34886b1.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/de1f718eadcd41b7b3d5834bf34886b1"}}, "publications": [{"entity": "publication", "iuid": "449343954cd54135937eb684c181d4ab", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/449343954cd54135937eb684c181d4ab.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/449343954cd54135937eb684c181d4ab"}}, "title": "Baseline laboratory values and metastatic burden predict survival in addition to IMDC risk in real-world renal cell carcinoma patients treated with ipilimumab-nivolumab.", "authors": [{"family": "Kheir", "given": "Alaa", "initials": "A", "orcid": "0009-0000-0558-8622", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/869e67d188b94e87b31171a086ab253c.json"}}, {"family": "Johannsdottir", "given": "Berglind", "initials": "B"}, {"family": "Gr\u00f6nn-Weiss", "given": "Alexandra", "initials": "A"}, {"family": "Liu", "given": "Lisa L", "initials": "LL"}, {"family": "Ull\u00e9n", "given": "Anders", "initials": "A"}, {"family": "Laurell", "given": "Anna", "initials": "A"}, {"family": "H\u00e5kansson", "given": "Annika", "initials": "A"}, {"family": "Verbien\u00e9", "given": "Ingrida", "initials": "I"}, {"family": "Ullenhag", "given": "Gustav", "initials": "G", "orcid": "0000-0003-4949-3267", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c8495fa495c94c8f87f09658aedf19d5.json"}}, {"family": "Carlhed", "given": "Rickard", "initials": "R"}, {"family": "Costa Svedman", "given": "Fernanda", "initials": "F"}, {"family": "Lindskog", "given": "Magnus", "initials": "M", "orcid": "0000-0001-9484-1983", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/de1f718eadcd41b7b3d5834bf34886b1.json"}}, {"family": "Harmenberg", "given": "Ulrika", "initials": "U"}], "type": "journal article", "published": "2025-10-03", "journal": {"title": "Acta Oncol", "issn": "1651-226X", "volume": "64", "pages": "1355-1364", "issn-l": "0284-186X"}, "abstract": "Clinical tools to optimally select real-world metastatic renal cell carcinoma (mRCC) patients for treatment with ipilimumab-nivolumab remain to be identified.\n\nMedical records of the first 100 mRCC patients treated with ipilimumab-nivolumab at three Swedish centers were retrospectively analyzed. Data on International Metastatic Renal Cell Carcinoma Database Consortium (IMDC) risk, baseline levels of routine blood markers, and tumor burden were collected. Outcome variables were progression-free survival (PFS), overall survival (OS), and radiological response (RR) according to clinical routine imaging.\n\nAt a median follow-up of 22 months, 65% had progressed or died with a median PFS of 7 months and an estimated median OS of 28 months. The RR rate was 45%, including 11% complete responses (CR). 29% had progressive disease as best response. IMDC poor-risk patients had shorter mPFS (4 vs 14 months; HR [hazard ratio] 1.90; P = 0.009), shorter mOS (12.5 months vs not reached; HR 4.27; P < 0.0001), and lower CR rate (3% vs 16%, P = 0.06) than IMDC intermediate/favorable patients. C-reactive protein (aHR 2.67; P = 0.040), albumin (aHR, 2.13; P = 0.039), neutrophil-lymphocyte-ratio (aHR, 2.8; P = 0.009), and > 2 metastatic sites (aHR, 2.13; P = 0.024) were associated with OS after adjusting for IMDC risk. Prior nephrectomy was not (aHR, 0.84; P = 0.62). A normal C-reactive protein was associated with an increased likelihood of CR (OR 7.2; P = 0.017).\n\nBaseline blood markers and number of metastatic sites add prognostic value independently of IMDC risk in real-word mRCC patients treated with ipililmumab-nivolumab.", "doi": "10.2340/1651-226X.2025.44533", "pmid": "41039982", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC12509422"}], "notes": [], "created": "2026-09-23T11:37:16.836Z", "modified": "2026-09-23T11:37:16.988Z"}, {"entity": "publication", "iuid": "ae10dde75f17468cb23f7cc1868588e2", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/ae10dde75f17468cb23f7cc1868588e2.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/ae10dde75f17468cb23f7cc1868588e2"}}, "title": "ATP1A3 dysfunction causes motor hyperexcitability and afterhyperpolarization loss in a dystonia model.", "authors": [{"family": "Akkuratov", "given": "Evgeny E", "initials": "EE", "orcid": "0000-0002-2552-9512", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/abd9e4662bb543eebb0451af868bc319.json"}}, {"family": "Sorrell", "given": "Francesca", "initials": "F"}, {"family": "Picton", "given": "Laurence D", "initials": "LD"}, {"family": "Sousa", "given": "Vasco C", "initials": "VC", "orcid": "0000-0003-3575-0875", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/f8257f3d6561484d8f1a2e88ede975b9.json"}}, {"family": "Paucar", "given": "Martin", "initials": "M", "orcid": "0000-0003-3735-1480", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d09ae68f3253456bae5112ee04a3b542.json"}}, {"family": "Jans", "given": "Daniel", "initials": "D", "orcid": "0000-0002-6356-9742", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9ff40f8719c944e6b0ff27ded3b05a27.json"}}, {"family": "Svensson", "given": "Lill-Britt", "initials": "LB"}, {"family": "Lindskog", "given": "Maria", "initials": "M", "orcid": "0000-0001-9484-1983", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/de1f718eadcd41b7b3d5834bf34886b1.json"}}, {"family": "Fritz", "given": "Nicolas", "initials": "N", "orcid": "0000-0002-9722-7425", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c191a09238064a52b559e43ee867de61.json"}}, {"family": "Liebmann", "given": "Thomas", "initials": "T"}, {"family": "Sillar", "given": "Keith T", "initials": "KT"}, {"family": "Rosewich", "given": "Hendrik", "initials": "H", "orcid": "0000-0003-4692-5511", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d75db0ebcee1483496fb5067e27fe10c.json"}}, {"family": "Svenningsson", "given": "Per", "initials": "P", "orcid": "0000-0001-6727-3802", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b01bbacfa24e4b9794734bf1121d1c38.json"}}, {"family": "Brismar", "given": "Hjalmar", "initials": "H", "orcid": "0000-0003-0578-4003", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/04321d9fb805493db538489927a42c8f.json"}}, {"family": "Miles", "given": "Gareth B", "initials": "GB"}, {"family": "Aperia", "given": "Anita", "initials": "A"}], "type": "journal article", "published": "2025-04-03", "journal": {"title": "Brain", "issn": "1460-2156", "volume": "148", "issue": "4", "pages": "1099-1105", "issn-l": "0006-8950"}, "abstract": "Mutations in the gene encoding the alpha3 Na+/K+-ATPase isoform (ATP1A3) lead to movement disorders that manifest with dystonia, a common neurological symptom with many different origins, but for which the underlying molecular mechanisms remain poorly understood. We have generated an ATP1A3 mutant mouse that displays motor impairments and a hyperexcitable motor phenotype compatible with dystonia. We show that neurons harbouring this mutation are compromised in their ability to extrude raised levels of intracellular sodium, highlighting a profound deficit in neuronal sodium homeostasis. We show that the spinal motor network in ATP1A3 mutant mice has a reduced responsiveness to activity-dependent rises in intracellular sodium and that this is accompanied by loss of the Na+/K+-ATPase-mediated afterhyperpolarization in motor neurons. Taken together, our data support that the alpha3 Na+/K+-ATPase is important for cellular and spinal motor network homeostasis. These insights suggest that it may be useful to consider ways to compensate for this loss of a critical afterhyperpolarization-dependent control of neuronal excitability when developing future therapies for dystonia.", "doi": "10.1093/brain/awae373", "pmid": "39533828", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC11967811"}, {"db": "pii", "key": "7896743"}], "notes": [], "created": "2026-09-23T12:29:54.670Z", "modified": "2026-09-23T14:47:46.364Z"}, {"entity": "publication", "iuid": "5c451956fb8140fe954f54dc9e90a7fe", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/5c451956fb8140fe954f54dc9e90a7fe.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/5c451956fb8140fe954f54dc9e90a7fe"}}, "title": "Amyloid-\u03b2 accumulation in human astrocytes induces mitochondrial disruption and changed energy metabolism.", "authors": [{"family": "Zy\u015bk", "given": "Marlena", "initials": "M"}, {"family": "Beretta", "given": "Chiara", "initials": "C"}, {"family": "Naia", "given": "Luana", "initials": "L", "orcid": "0000-0002-0886-4634", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/594bb6850d604a64bc5ebe6752562231.json"}}, {"family": "Dakhel", "given": "Abdulkhalek", "initials": "A"}, {"family": "P\u00e5v\u00e9nius", "given": "Linnea", "initials": "L", "orcid": "0000-0001-6730-2458", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/832383b2182344d995d2722d2bea9800.json"}}, {"family": "Brismar", "given": "Hjalmar", "initials": "H", "orcid": "0000-0003-0578-4003", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/04321d9fb805493db538489927a42c8f.json"}}, {"family": "Lindskog", "given": "Maria", "initials": "M", "orcid": "0000-0001-9484-1983", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/de1f718eadcd41b7b3d5834bf34886b1.json"}}, {"family": "Ankarcrona", "given": "Maria", "initials": "M", "orcid": "0000-0002-7022-3694", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ba3f69568d294081aa201e131eba2620.json"}}, {"family": "Erlandsson", "given": "Anna", "initials": "A"}], "type": "journal article", "published": "2023-02-20", "journal": {"title": "J Neuroinflammation", "issn": "1742-2094", "volume": "20", "issue": "1", "pages": "43", "issn-l": "1742-2094"}, "abstract": "Astrocytes play a central role in maintaining brain energy metabolism, but are also tightly connected to the pathogenesis of Alzheimer's disease (AD). Our previous studies demonstrate that inflammatory astrocytes accumulate large amounts of aggregated amyloid-beta (A\u03b2). However, in which way these A\u03b2 deposits influence their energy production remain unclear.\n\nThe aim of the present study was to investigate how A\u03b2 pathology in astrocytes affects their mitochondria functionality and overall energy metabolism. For this purpose, human induced pluripotent cell (hiPSC)-derived astrocytes were exposed to sonicated A\u03b242 fibrils for 7 days and analyzed over time using different experimental approaches.\n\nOur results show that to maintain stable energy production, the astrocytes initially increased their mitochondrial fusion, but eventually the A\u03b2-mediated stress led to abnormal mitochondrial swelling and excessive fission. Moreover, we detected increased levels of phosphorylated DRP-1 in the A\u03b2-exposed astrocytes, which co-localized with lipid droplets. Analysis of ATP levels, when blocking certain stages of the energy pathways, indicated a metabolic shift to peroxisomal-based fatty acid \u03b2-oxidation and glycolysis.\n\nTaken together, our data conclude that A\u03b2 pathology profoundly affects human astrocytes and changes their entire energy metabolism, which could result in disturbed brain homeostasis and aggravated disease progression.", "doi": "10.1186/s12974-023-02722-z", "pmid": "36803838", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9940442"}, {"db": "pii", "key": "10.1186/s12974-023-02722-z"}], "notes": [], "created": "2026-08-20T12:20:59.588Z", "modified": "2026-09-23T14:50:16.430Z"}, {"entity": "publication", "iuid": "295acc6b2ccb49fd9b02c72d1d92764e", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/295acc6b2ccb49fd9b02c72d1d92764e.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/295acc6b2ccb49fd9b02c72d1d92764e"}}, "title": "Matched Analyses of Brain Metastases versus Primary Non-Small Cell Lung Cancer Reveal a Unique microRNA Signature.", "authors": [{"family": "Tsakonas", "given": "Georgios", "initials": "G", "orcid": "0000-0003-4397-7391", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a1c9fc21bce24b4d88318890c9d24435.json"}}, {"family": "Koulouris", "given": "Andreas", "initials": "A"}, {"family": "Kazmierczak", "given": "Dominika", "initials": "D"}, {"family": "Botling", "given": "Johan", "initials": "J"}, {"family": "Ortiz-Villalon", "given": "Cristian", "initials": "C"}, {"family": "Nord", "given": "Helena", "initials": "H"}, {"family": "Lindskog", "given": "Magnus", "initials": "M", "orcid": "0000-0001-9484-1983", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/de1f718eadcd41b7b3d5834bf34886b1.json"}}, {"family": "Sandelin", "given": "Martin", "initials": "M"}, {"family": "Micke", "given": "Patrick", "initials": "P", "orcid": "0000-0003-1210-5961", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8b4b9d0f748440e19db93d4543bbe25f.json"}}, {"family": "Hydbring", "given": "Per", "initials": "P"}, {"family": "Ekman", "given": "Simon", "initials": "S", "orcid": "0000-0002-8343-6226", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/bf1c75b77c534ce486a6213c7b110b03.json"}}], "type": "journal article", "published": "2022-12-22", "journal": {"title": "Int J Mol Sci", "issn": "1422-0067", "volume": "24", "issue": "1", "issn-l": null}, "abstract": "Distant spreading of tumor cells to the central nervous system in non-small cell lung cancer (NSCLC) occurs frequently and poses major clinical issues due to limited treatment options. RNAs displaying differential expression in brain metastasis versus primary NSCLC may explain distant tumor growth and may potentially be used as therapeutic targets. In this study, we conducted systematic microRNA expression profiling from tissue biopsies of primary NSCLC and brain metastases from 25 patients. RNA analysis was performed using the nCounter Human v3 miRNA Expression Assay, NanoString technologies, followed by differential expression analysis and in silico target gene pathway analysis. We uncovered a panel of 11 microRNAs with differential expression and excellent diagnostic performance in brain metastasis versus primary NSCLC. Five microRNAs were upregulated in brain metastasis (miR-129-2-3p, miR-124-3p, miR-219a-2-3p, miR-219a-5p, and miR-9-5p) and six microRNAs were downregulated in brain metastasis (miR-142-3p, miR-150-5p, miR-199b-5p, miR-199a-3p, miR-199b-5p, and miR-199a-5p). The differentially expressed microRNAs were predicted to converge on distinct target gene networks originating from five to twelve core target genes. In conclusion, we uncovered a unique microRNA profile linked to two target gene networks. Our results highlight the potential of specific microRNAs as biomarkers for brain metastasis in NSCLC and indicate plausible mechanistic connections.", "doi": "10.3390/ijms24010193", "pmid": "36613642", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9820685"}, {"db": "pii", "key": "ijms24010193"}], "notes": [], "created": "2026-09-23T12:11:42.910Z", "modified": "2026-09-23T12:11:43.038Z"}, {"entity": "publication", "iuid": "026e176cc2744047a1ae797684e42264", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/026e176cc2744047a1ae797684e42264.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/026e176cc2744047a1ae797684e42264"}}, "title": "A missense mutation converts the Na+,K+-ATPase into an ion channel and causes therapy-resistant epilepsy.", "authors": [{"family": "Ygberg", "given": "Sofia", "initials": "S", "orcid": "0000-0002-3854-2716", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/0b032359f6bf48be84cbb595142d9382.json"}}, {"family": "Akkuratov", "given": "Evgeny E", "initials": "EE", "orcid": "0000-0002-2552-9512", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/abd9e4662bb543eebb0451af868bc319.json"}}, {"family": "Howard", "given": "Rebecca J", "initials": "RJ", "orcid": "0000-0003-2049-3378", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5ce04593b5b24aaa8978fda1447dd0bf.json"}}, {"family": "Taylan", "given": "Fulya", "initials": "F", "orcid": "0000-0002-2907-0235", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/fc9bc4b87d0f43b9a0528e936921e5ae.json"}}, {"family": "Jans", "given": "Daniel C", "initials": "DC", "orcid": "0000-0002-6356-9742", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/9ff40f8719c944e6b0ff27ded3b05a27.json"}}, {"family": "Mahato", "given": "Dhani R", "initials": "DR"}, {"family": "Katz", "given": "Adriana", "initials": "A"}, {"family": "Kinoshita", "given": "Paula F", "initials": "PF"}, {"family": "Portal", "given": "Benjamin", "initials": "B"}, {"family": "Nennesmo", "given": "Inger", "initials": "I"}, {"family": "Lindskog", "given": "Maria", "initials": "M", "orcid": "0000-0001-9484-1983", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/de1f718eadcd41b7b3d5834bf34886b1.json"}}, {"family": "Karlish", "given": "Steven J D", "initials": "SJD"}, {"family": "Andersson", "given": "Magnus", "initials": "M"}, {"family": "Lindstrand", "given": "Anna", "initials": "A", "orcid": "0000-0003-0806-5602", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3d28fb4cc61f4033b2ac525fed3d6b94.json"}}, {"family": "Brismar", "given": "Hjalmar", "initials": "H", "orcid": "0000-0003-0578-4003", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/04321d9fb805493db538489927a42c8f.json"}}, {"family": "Aperia", "given": "Anita", "initials": "A"}], "type": "case reports", "published": "2021-12-00", "journal": {"title": "J Biol Chem", "issn": "1083-351X", "volume": "297", "issue": "6", "pages": "101355", "issn-l": "0021-9258"}, "abstract": "The ion pump Na+,K+-ATPase is a critical determinant of neuronal excitability; however, its role in the etiology of diseases of the central nervous system (CNS) is largely unknown. We describe here the molecular phenotype of a Trp931Arg mutation of the Na+,K+-ATPase catalytic \u03b11 subunit in an infant diagnosed with therapy-resistant lethal epilepsy. In addition to the pathological CNS phenotype, we also detected renal wasting of Mg2+. We found that membrane expression of the mutant \u03b11 protein was low, and ion pumping activity was lost. Arginine insertion into membrane proteins can generate water-filled pores in the plasma membrane, and our molecular dynamic (MD) simulations of the principle states of Na+,K+-ATPase transport demonstrated massive water inflow into mutant \u03b11 and destabilization of the ion-binding sites. MD simulations also indicated that a water pathway was created between the mutant arginine residue and the cytoplasm, and analysis of oocytes expressing mutant \u03b11 detected a nonspecific cation current. Finally, neurons expressing mutant \u03b11 were observed to be depolarized compared with neurons expressing wild-type protein, compatible with a lowered threshold for epileptic seizures. The results imply that Na+,K+-ATPase should be considered a neuronal locus minoris resistentia in diseases associated with epilepsy and with loss of plasma membrane integrity.", "doi": "10.1016/j.jbc.2021.101355", "pmid": "34717959", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC8637647"}, {"db": "pii", "key": "S0021-9258(21)01161-3"}], "notes": [], "created": "2026-09-23T10:14:51.669Z", "modified": "2026-09-23T14:51:35.637Z"}]}