SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Bergö Martin O. 1970) "

Sökning: WFRF:(Bergö Martin O. 1970)

  • Resultat 1-13 av 13
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Akula, Murali K, et al. (författare)
  • Protein prenylation restrains innate immunity by inhibiting Rac1 effector interactions
  • 2019
  • Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 10:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Rho family proteins are prenylated by geranylgeranyltransferase type I (GGTase-I), which normally target proteins to membranes for GTP-loading. However, conditional deletion of GGIase-I in mouse macrophages increases GTP-loading of Rho proteins, leading to enhanced inflammatory responses and severe rheumatoid arthritis. Here we show that heterozygous deletion of the Rho family gene Rac1, but not Rhoa and Cdc42, reverses inflammation and arthritis in GGTase-I-deficient mice. Non-prenylated Rac1 has a high affinity for the adaptor protein Ras GTPase-activating-like protein 1 (Iqgap1), which facilitates both GTP exchange and ubiquitination-mediated degradation of Rac1. Consistently, inactivating lagapl normalizes Rac1 GTP-loading, and reduces inflammation and arthritis in GGTase-I-deficient mice, as well as prevents statins from increasing Rac1 GTP-loading and cytokine production in macrophages. We conclude that blocking prenylation stimulates Rac1 effector interactions and unleashes proinflammatory signaling. Our results thus suggest that prenylation normally restrains innate immune responses by preventing Rac1 effector interactions.
  •  
2.
  • Dalin, Martin, 1982, et al. (författare)
  • Massive parallel sequencing questions the pathogenic role of missense variants in dilated cardiomyopathy
  • 2017
  • Ingår i: International Journal of Cardiology. - : Elsevier BV. - 0167-5273 .- 1874-1754. ; 228, s. 742-748
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Germline genetic variants are an important cause of dilated cardiomyopathy (DCM). However, recent sequencing studies have revealed rare variants in DCM-associated genes also in individuals without known heart disease. In this study, we investigate variant prevalence and genotype-phenotype correlations in Swedish DCM patients, and compare their genetic variants to those detected in reference cohorts. Methods and results: We sequenced the coding regions of 41 DCM-associated genes in 176 unrelated patients with idiopathic DCM and found 102 protein-altering variants with an allele frequency of <0.04% in reference cohorts; the majority were missense variants not previously described in DCM. Fifty-five (31%) patients had one variant, and 24 (14%) patients had two or more variants in the analysed genes. Detection of genetic variants in any gene, and in LMNA, MYII7 or TTN alone, was associated with early onset disease and reduced transplant-free survival. As expected, nonsense and frameshift variants were more common in DCM patients than in healthy individuals of the reference cohort 1000 Genomes Europeans. Surprisingly however, the prevalence, conservation and pathogenicity scores, and localization of missense variants were similar in DCM patients and healthy reference individuals. Conclusion: To our knowledge, this is the first study to identify correlations between genotype and prognosis when sequencing a large number of genes in unselected DCM patients. The similar distribution of missense variants in DCM patients and healthy reference individuals questions the pathogenic role of many variants, and suggests that results from genetic testing of DCM patients should be interpreted with caution.
  •  
3.
  •  
4.
  • Bandaru, Sashidar, et al. (författare)
  • Lack of RAC1 in macrophages protects against atherosclerosis.
  • 2020
  • Ingår i: PLoS One. - : Public Library of Science (PLoS). - 1932-6203. ; 15:9
  • Tidskriftsartikel (refereegranskat)abstract
    • The Rho GTPase RAC1 is an important regulator of cytoskeletal dynamics, but the role of macrophage-specific RAC1 has not been explored during atherogenesis. We analyzed RAC1 expression in human carotid atherosclerotic plaques using immunofluorescence and found higher macrophage RAC1 expression in advanced plaques compared with intermediate human atherosclerotic plaques. We then produced mice with Rac1-deficient macrophages by breeding conditional floxed Rac1 mice (Rac1fl/fl) with mice expressing Cre from the macrophage-specific lysosome M promoter (LC). Atherosclerosis was studied in vivo by infecting Rac1fl/fl and Rac1fl/fl/LC mice with AdPCSK9 (adenoviral vector overexpressing proprotein convertase subtilisin/kexin type 9). Rac1fl/fl/LC macrophages secreted lower levels of IL-6 and TNF-α and exhibited reduced foam cell formation and lipid uptake. The deficiency of Rac1 in macrophages reduced the size of aortic atherosclerotic plaques in AdPCSK9-infected Rac1fl/fl/LC mice. Compare with controls, intima/media ratios, the size of necrotic cores, and numbers of CD68-positive macrophages in atherosclerotic plaques were reduced in Rac1-deficient mice. Moreover, we found that RAC1 interacts with actin-binding filamin A. Macrophages expressed increased RAC1 levels in advanced human atherosclerosis. Genetic inactivation of RAC1 impaired macrophage function and reduced atherosclerosis in mice, suggesting that drugs targeting RAC1 may be useful in the treatment of atherosclerosis.
  •  
5.
  • Bandaru, Sashidar, et al. (författare)
  • Targeting filamin A reduces macrophage activity and atherosclerosis. : Filamin A in atherogenesis
  • 2019
  • Ingår i: Circulation. - 1524-4539. ; 140:1, s. 67-79
  • Tidskriftsartikel (refereegranskat)abstract
    • The actin-binding protein FLNA (filamin A) regulates signal transduction important for cell locomotion, but the role of macrophage-specific FLNA during atherogenesis has not been explored.We analyzed FLNA expression in human carotid atherosclerotic plaques by immunofluorescence. We also produced mice with Flna-deficient macrophages by breeding conditional Flna-knockout mice ( Flna o/fl) with mice expressing Cre from the macrophage-specific lysosome M promoter ( LC). Atherosclerosis in vivo was studied by transplanting bone marrow from male Flna o/fl/ LC mice to atherogenic low-density lipoprotein receptor-deficient ( Ldlr-/-) mice; and by infecting Flna o/fl and Flna o/fl/ LC mice with AdPCSK9 (adenoviral vector overexpressing proprotein convertase subtilisin/kexin type 9). Furthermore, C57BL/6 mice were infected with AdPCSK9 and then treated with the calpain inhibitor calpeptin to inhibit FLNA cleavage.We found that macrophage FLNA expression was higher in advanced than in intermediate human atherosclerotic plaques. Flna o/fl/ LC macrophages proliferated and migrated less than controls; expressed lower levels of phosphorylated AKT and ERK1/2; exhibited reduced foam cell formation and lipid uptake; and excreted more lipids. The deficiency of Flna in macrophages markedly reduced the size of aortic atherosclerotic plaques in both Ldlr-/-BMT: Flnao/fl/LC and AdPCSK9-infected Flna o/fl/ LC mice. Intima/media ratios and numbers of CD68-positive macrophages in atherosclerotic plaques were lower in Flna-deficient mice than in control mice. Moreover, we found that STAT3 interacts with a calpain-cleaved carboxyl-terminal fragment of FLNA. Inhibiting calpain-mediated FLNA cleavage with calpeptin in macrophages reduced nuclear levels of phosphorylated STAT3, interleukin 6 secretion, foam cell formation, and lipid uptake. Finally, calpeptin treatment reduced the size of atherosclerotic plaques in C57BL/6 mice infected with AdPCSK9.Genetic inactivation of Flna and chemical inhibition of calpain-dependent cleavage of FLNA impaired macrophage signaling and function, and reduced atherosclerosis in mice, suggesting that drugs targeting FLNA may be useful in the treatment of atherosclerosis.
  •  
6.
  • Du, X., et al. (författare)
  • Mevalonate metabolism-dependent protein geranylgeranylation regulates thymocyte egress
  • 2020
  • Ingår i: The Journal of experimental medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 217:2
  • Tidskriftsartikel (refereegranskat)abstract
    • Thymocyte egress is a critical determinant of T cell homeostasis and adaptive immunity. Despite the roles of G protein–coupled receptors in thymocyte emigration, the downstream signaling mechanism remains poorly defined. Here, we report the discrete roles for the two branches of mevalonate metabolism–fueled protein prenylation pathway in thymocyte egress and immune homeostasis. The protein geranylgeranyltransferase Pggt1b is up-regulated in single-positive thymocytes, and loss of Pggt1b leads to marked defects in thymocyte egress and T cell lymphopenia in peripheral lymphoid organs in vivo. Mechanistically, Pggt1b bridges sphingosine-1-phosphate and chemokine-induced migratory signals with the activation of Cdc42 and Pak signaling and mevalonate-dependent thymocyte trafficking. In contrast, the farnesyltransferase Fntb, which mediates a biochemically similar process of protein farnesylation, is dispensable for thymocyte egress but contributes to peripheral T cell homeostasis. Collectively, our studies establish context-dependent effects of protein prenylation and unique roles of geranylgeranylation in thymic egress and highlight that the interplay between cellular metabolism and posttranslational modification underlies immune homeostasis.
  •  
7.
  • Lopez-Posadas, R., et al. (författare)
  • Inhibiting PGGT1B Disrupts Function of RHOA, Resulting in T-cell Expression of Integrin alpha 4 beta 7 and Development of Colitis in Mice
  • 2019
  • Ingår i: Gastroenterology. - : Elsevier BV. - 0016-5085. ; 157:5, s. 1293-1309
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND & AIMS: It is not clear how regulation of T-cell function is altered during development of inflammatory bowel diseases (IBD). We studied the mechanisms by which geranylgeranyltransferase-mediated prenylation controls T-cell localization to the intestine and chronic inflammation. METHODS: We generated mice with T-cell-specific disruption of the geranylgeranyltransferase type I, beta subunit gene (Pggt1b), called Pggt1b(Delta CD4) mice, or the ras homolog family member A gene (Rhoa), called Rhoa(Delta CD4) mice. We also studied mice with knockout of CDC42 or RAC1 and wild-type mice (controls). Intestinal tissues were analyzed by histology, multiphoton and confocal microscopy, and real-time polymerase chain reaction. Activation of CDC42, RAC1, and RHOA were measured with G-LISA, cell fractionation, and immunoblots. T cells and lamina propria mononuclear cells from mice were analyzed by flow cytometry or transferred to Rag1(-/-) mice. Mice were given injections of antibodies against integrin alpha4beta7 or gavaged with the RORC antagonist GSK805. We obtained peripheral blood and intestinal tissue samples from patients with and without IBD and analyzed them by flow cytometry. RESULTS: Pggt1b(Delta CD4) mice developed spontaneous colitis, characterized by thickening of the intestinal wall, edema, fibrosis, accumulation of T cells in the colon, and increased expression of inflammatory cytokines. Compared with control CD4+ T cells, PGGT1B-deficient CD4+ T cells expressed significantly higher levels of integrin alpha4beta7, which regulates their localization to the intestine. Inflammation induced by transfer of PGGT1B-deficient CD4+ T cells to Rag1(-/-) mice was blocked by injection of an antibody against integrin alpha4beta7. Lamina propria of Pggt1b(Delta CD4) mice had increased numbers of CD4+ T cells that expressed RORC and higher levels of cytokines produced by T-helper 17 cells (granulocyte-macrophage colony-stimulating factor, interleukin [IL]17A, IL17F, IL22, and tumor necrosis factor [TNF]). The RORC inverse agonist GSK805, but not antibodies against IL17A or IL17F, prevented colitis in Pggt1b(Delta CD4) mice. PGGT1B-deficient CD4+ T cells had decreased activation of RHOA. RhoA(Delta CD4) mice had a similar phenotype to Pggt1b(Delta CD4) mice, including development of colitis, increased numbers of CD4+ T cells in colon, increased expression of integrin alpha4beta7 by CD4+ T cells, and increased levels of IL17A and other inflammatory cytokines in lamina propria. T cells isolated from intestinal tissues from patients with IBD had significantly lower levels of PGGT1B than tissues from individuals without IBD. CONCLUSION: Loss of PGGT1B from T cells in mice impairs RHOA function, increasing CD4+ T-cell expression of integrin alpha4beta7 and localization to colon, resulting in increased expression of inflammatory cytokines and colitis. T cells isolated from gut tissues from patients with IBD have lower levels of PGGT1B than tissues from patients without IBD.
  •  
8.
  • Malmhäll-Bah, Eric, et al. (författare)
  • Rho-GTPase dependent leukocyte interaction generates pro-inflammatory thymic Tregs and causes arthritis
  • 2022
  • Ingår i: Journal of Autoimmunity. - : Elsevier BV. - 0896-8411 .- 1095-9157. ; 130
  • Tidskriftsartikel (refereegranskat)abstract
    • Conditional mutation of protein geranylgeranyltransferase type I (GGTase-I) in macrophages (GLC) activates Rho-GTPases and causes arthritis in mice. Knocking out Rag1 in GLC mice alleviates arthritis which indicates that lymphocytes are required for arthritis development in those mice. To study GLC dependent changes in the adaptive immunity, we isolated CD4(+) T cells from GLC mice (CD4(+)GLCs). Spleen and joint draining lymph nodes (dLN) CD4(+)GLCs exhibited high expression of Cdc42 and Rac1, which repressed the caudal HOXA proteins and activated the mechanosensory complex to facilitate migration. These CDC42/RAC1 rich CD4(+)GLCs presented a complete signature of GARP(+)NRP1(+)IKZF2(+)FOXP3(+) regulatory T cells (Tregs) of thymic origin. Activation of the beta-catenin/Lef1 axis promoted a pro-inflammatory Th1 phenotype of Tregs, which was strongly associated with arthritis severity. Knockout of Cdc42 in macrophages of GLC mice affected CD4(+) cell biology and triggered development of non-thymic Tregs. Knockout of Rac1 and RhoA had no such effects on CD4(+) cells although it alleviated arthritis in GLC mice. Disrupting macrophage and T cell interaction with CTLA4 fusion protein reduced the Th1-driven inflammation and enrichment of thymic Tregs into dLNs. Antigen challenge reinforced the CD4(+)GLC phenotype in non-arthritic heterozygote GLC mice and increased accumulation of Rho-GTPase expressing thymic Tregs in dLNs. Our study demonstrates an unexpected role of macrophages in stimulating the development of pro-inflammatory thymic Tregs and reveal activation of Rho-GTPases behind their arthri-togenic phenotype.
  •  
9.
  • Nilton, Anna, et al. (författare)
  • Targeting Zfp148 activates p53 and reduces tumor initiation in the gut
  • 2016
  • Ingår i: OncoTarget. - : Impact Journals, LLC. - 1949-2553. ; 7:35, s. 56183-56192
  • Tidskriftsartikel (refereegranskat)abstract
    • The transcription factor Zinc finger protein 148 (Zfp148, ZBP-89, BFCOL, BERF1, htβ) interacts physically with the tumor suppressor p53, but the significance of this interaction is not known. We recently showed that knockout of Zfp148 in mice leads to ectopic activation of p53 in some tissues and cultured fibroblasts, suggesting that Zfp148 represses p53 activity. Here we hypothesize that targeting Zfp148 would unleash p53 activity and protect against cancer development, and test this idea in the APCMin/+ mouse model of intestinal adenomas. Loss of one copy of Zfp148 markedly reduced tumor numbers and tumor-associated intestinal bleedings, and improved survival. Furthermore, after activation of β-catenin-the initiating event in colorectal cancer-Zfp148 deficiency activated p53 and induced apoptosis in intestinal explants of APCMin/+ mice. The anti-tumor effect of targeting Zfp148 depended on p53, as Zfp148 deficiency did not affect tumor numbers in APCMin/+ mice lacking one or both copies of Trp53. The results suggest that Zfp148 controls the fate of newly transformed intestinal tumor cells by repressing p53 and that targeting Zfp148 might be useful in the treatment of colorectal cancer.
  •  
10.
  • Taube, Magdalena, et al. (författare)
  • Association of Bariatric Surgery With Skin Cancer Incidence in Adults With Obesity: A Nonrandomized Controlled Trial.
  • 2020
  • Ingår i: JAMA dermatology. - : American Medical Association (AMA). - 2168-6084 .- 2168-6068. ; 156:1, s. 38-43
  • Tidskriftsartikel (refereegranskat)abstract
    • Obesity is a cancer risk factor, and bariatric surgery in patients with obesity is associated with reduced cancer risk. However, evidence of an association among obesity, bariatric surgery, and skin cancer, including melanoma, is limited.To investigate the association of bariatric surgery with skin cancer (squamous cell carcinoma and melanoma) and melanoma incidence.This nonrandomized controlled trial, the Swedish Obese Subjects (SOS) study, is ongoing at 25 surgical departments and 480 primary health care centers in Sweden and was designed to examine outcomes after bariatric surgery. The study included 2007 patients with obesity who underwent bariatric surgery and 2040 contemporaneously matched controls who received conventional obesity treatment. Patients were enrolled between September 1, 1987, and January 31, 2001. Data analysis was performed from June 29, 2018, to November 22, 2018.Patients in the surgery group underwent gastric bypass (n=266), banding (n=376), or vertical banded gastroplasty (n=1365). The control group (n=2040) received the customary treatment for obesity at their primary health care centers.The SOS study was cross-linked to the Swedish National Cancer Registry, the Cause of Death Registry, and the Registry of the Total Population for data on cancer incidence, death, and emigration.The study included 4047 participants (mean [SD] age, 47.9 [6.1] years; 2867 [70.8%] female). Information on cancer events was available for 4042 patients. The study found that bariatric surgery was associated with a markedly reduced risk of melanoma (adjusted subhazard ratio, 0.43; 95% CI, 0.21-0.87; P=.02; median follow-up, 18.1 years) and risk of skin cancer in general (adjusted subhazard ratio, 0.59; 95% CI, 0.35-0.99; P=.047). The skin cancer risk reduction was not associated with baseline body mass index or weight; insulin, glucose, lipid, and creatinine levels; diabetes; blood pressure; alcohol intake; or smoking.The results of this study suggest that bariatric surgery in individuals with obesity is associated with a reduced risk of skin cancer, including melanoma.ClinicalTrials.gov identifier: NCT01479452.
  •  
11.
  • Wiel, Clotilde, 1987, et al. (författare)
  • BACH1 Stabilization by Antioxidants Stimulates Lung Cancer Metastasis
  • 2019
  • Ingår i: Cell. - : Elsevier BV. - 0092-8674 .- 1097-4172. ; 178:2, s. 330-345
  • Tidskriftsartikel (refereegranskat)abstract
    • For tumors to progress efficiently, cancer cells must overcome barriers of oxidative stress. Although dietary antioxidant supplementation or activation of endogenous antioxidants by NRF2 reduces oxidative stress and promotes early lung tumor progression, little is known about its effect on lung cancer metastasis. Here, we show that long-term supplementation with the antioxidants N-acetylcysteine and vitamin E promotes KRAS-driven lung cancer metastasis. The antioxidants stimulate metastasis by reducing levels of free heme and stabilizing the transcription factor BACH1. BACH1 activates transcription of Hexokinase 2 and Gapdh and increases glucose uptake, glycolysis rates, and lactate secretion, thereby stimulating glycolysis-dependent metastasis of mouse and human lung cancer cells. Targeting BACH1 normalized glycolysis and prevented antioxidant-induced metastasis, while increasing endogenous BACH1 expression stimulated glycolysis and promoted metastasis, also in the absence of antioxidants. We conclude that BACH1 stimulates glycolysis-dependent lung cancer metastasis and that BACH1 is activated under conditions of reduced oxidative stress.
  •  
12.
  • Zhong, H., et al. (författare)
  • SOX9 drives KRAS-induced lung adenocarcinoma progression and suppresses anti-tumor immunity
  • 2023
  • Ingår i: Oncogene. - 0950-9232. ; 42, s. 2183-2194
  • Tidskriftsartikel (refereegranskat)abstract
    • The SOX9 transcription factor ensures proper tissue development and homeostasis and has been implicated in promoting tumor progression. However, the role of SOX9 as a driver of lung adenocarcinoma (LUAD), or any cancer, remains unclear. Using CRISPR/Cas9 and Cre-LoxP gene knockout approaches in the Kras(G12D)-driven mouse LUAD model, we found that loss of Sox9 significantly reduces lung tumor development, burden and progression, contributing to significantly longer overall survival. SOX9 consistently drove organoid growth in vitro, but SOX9-promoted tumor growth was significantly attenuated in immunocompromised mice compared to syngeneic mice. We demonstrate that SOX9 suppresses immune cell infiltration and functionally suppresses tumor associated CD8(+) T, natural killer and dendritic cells. These data were validated by flow cytometry, gene expression, RT-qPCR, and immunohistochemistry analyses in Kras(G12D)-driven murine LUAD, then confirmed by interrogating bulk and single-cell gene expression repertoires and immunohistochemistry in human LUAD. Notably, SOX9 significantly elevates collagen-related gene expression and substantially increases collagen fibers. We propose that SOX9 increases tumor stiffness and inhibits tumor-infiltrating dendritic cells, thereby suppressing CD8(+) T cell and NK cell infiltration and activity. Thus, SOX9 drives Kras(G12D)-driven lung tumor progression and inhibits anti-tumor immunity at least partly by modulating the tumor microenvironment.
  •  
13.
  • Zou, Zhiyuan V., et al. (författare)
  • Genomic profiling of the transcription factor Zfp148 and its impact on the p53 pathway
  • 2020
  • Ingår i: Scientific Reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 10:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Recent data suggest that the transcription factor Zfp148 represses activation of the tumor suppressor p53 in mice and that therapeutic targeting of the human orthologue ZNF148 could activate the p53 pathway without causing detrimental side effects. We have previously shown that Zfp148 deficiency promotes p53-dependent proliferation arrest of mouse embryonic fibroblasts (MEFs), but the underlying mechanism is not clear. Here, we showed that Zfp148 deficiency downregulated cell cycle genes in MEFs in a p53-dependent manner. Proliferation arrest of Zfp148-deficient cells required increased expression of ARF, a potent activator of the p53 pathway. Chromatin immunoprecipitation showed that Zfp148 bound to the ARF promoter, suggesting that Zfp148 represses ARF transcription. However, Zfp148 preferentially bound to promoters of other transcription factors, indicating that deletion of Zfp148 may have pleiotropic effects that activate ARF and p53 indirectly. In line with this, we found no evidence of genetic interaction between TP53 and ZNF148 in CRISPR and siRNA screen data from hundreds of human cancer cell lines. We conclude that Zfp148 deficiency, by increasing ARF transcription, downregulates cell cycle genes and cell proliferation in a p53-dependent manner. However, the lack of genetic interaction between ZNF148 and TP53 in human cancer cells suggests that therapeutic targeting of ZNF148 may not increase p53 activity in humans.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-13 av 13
Typ av publikation
tidskriftsartikel (13)
Typ av innehåll
refereegranskat (13)
Författare/redaktör
Bergö, Martin O., 19 ... (12)
Sayin, Volkan I., 19 ... (5)
Akula, Murali K (4)
Akyürek, Levent, 196 ... (3)
Bandaru, Sashidar (3)
Bergström, Göran, 19 ... (2)
visa fler...
Borén, Jan, 1963 (2)
Bokarewa, Maria, 196 ... (2)
Ivarsson, Emil G., 1 ... (2)
Erlandsson, Malin, 1 ... (2)
Xu, X. F. (2)
Brisslert, Mikael, 1 ... (2)
Ekstrand, Matias (2)
Liu, S. (1)
Wei, Y. (1)
Wang, D. (1)
Cao, J. (1)
El Zowalaty, Ahmed E (1)
Nilsson, Ola, 1957 (1)
Unneberg, Per (1)
Kashif, M (1)
Lu, W (1)
Svensson, Per-Arne, ... (1)
Sjöholm, Kajsa, 1971 (1)
Anveden, Åsa (1)
Jacobson, Peter, 196 ... (1)
Andersson-Assarsson, ... (1)
Taube, Magdalena (1)
Forssell-Aronsson, E ... (1)
Kanduri, Chandrasekh ... (1)
Larsson, Erik, 1975 (1)
Bergö, Martin, 1970 (1)
Ibrahim, Mohamed X (1)
Khan, O. M. (1)
Kumar, Israiel T. (1)
Karlsson, Christin, ... (1)
Brakebusch, C. (1)
Karlsson, Joakim (1)
Gilljam, Thomas (1)
Levin, Max, 1969 (1)
Mondal, Tanmoy, 1981 (1)
Devarakonda, Sravani (1)
Lena, Carlsson (1)
Andersson, Bert, 195 ... (1)
Dalin, Martin, 1982 (1)
Andersson, Karin, 19 ... (1)
Fogelstrand, Per, 19 ... (1)
Tivesten, Åsa, 1969 (1)
Peltonen, Markku, 19 ... (1)
Staffas, Anna, 1982 (1)
visa färre...
Lärosäte
Göteborgs universitet (13)
Karolinska Institutet (10)
Stockholms universitet (1)
Språk
Engelska (13)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (12)
Naturvetenskap (1)

År

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy