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  • 1. Allagnat, F.
    et al.
    Fukaya, M.
    Nogueira, T. C.
    Delaroche, D.
    Welsh, Nils
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk cellbiologi.
    Marselli, L.
    Marchetti, P.
    Haefliger, J. A.
    Eizirik, D. L.
    Cardozo, A. K.
    C/EBP homologous protein contributes to cytokine-induced pro-inflammatory responses and apoptosis in beta-cells2012Inngår i: Cell Death and Differentiation, ISSN 1350-9047, E-ISSN 1476-5403, Vol. 19, nr 11, s. 1836-1846Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Induction of the C/EBP homologous protein (CHOP) is considered a key event for endoplasmic reticulum (ER) stress-mediated apoptosis. Type 1 diabetes (T1D) is characterized by an autoimmune destruction of the pancreatic beta-cells. Pro-inflammatory cytokines are early mediators of beta-cell death in T1D. Cytokines induce ER stress and CHOP overexpression in beta-cells, but the role for CHOP overexpression in cytokine-induced beta-cell apoptosis remains controversial. We presently observed that CHOP knockdown (KD) prevents cytokine-mediated degradation of the anti-apoptotic proteins B-cell lymphoma 2 (Bcl-2) and myeloid cell leukemia sequence 1 (Mcl-1), thereby decreasing the cleavage of executioner caspases 9 and 3, and apoptosis. Nuclear factor-kappa B (NF-kappa B) is a crucial transcription factor regulating beta-cell apoptosis and inflammation. CHOP KD resulted in reduced cytokine-induced NF-kappa B activity and expression of key NF-kappa B target genes involved in apoptosis and inflammation, including iNOS, FAS, IRF-7, IL-15, CCL5 and CXCL10. This was due to decreased I kappa B degradation and p65 translocation to the nucleus. The present data suggest that CHOP has a dual role in promoting beta-cell death: (1) CHOP directly contributes to cytokine-induced beta-cell apoptosis by promoting cytokine-induced mitochondrial pathways of apoptosis; and (2) by supporting the NF-kappa B activation and subsequent cytokine/chemokine expression, CHOP may contribute to apoptosis and the chemo attraction of mononuclear cells to the islets during insulitis. Cell Death and Differentiation (2012) 19, 1836-1846; doi:10.1038/cdd.2012.67; published online 1 June 2012

  • 2. Bellomo, Claudia
    Fabregat, Isabel ()
    Mikulits, Wolfgang ()
    Kardassis, Dimitri
    Heldin, Carl-Henrik
    Moustakas, Aristidis
    Snail mediates crosstalk between TGFβ and LXRα in hepatocellular carcinomaInngår i: Cell Death and Differentiation, ISSN 1350-9047, E-ISSN 1476-5403Artikkel i tidsskrift (Fagfellevurdert)
  • 3.
    Bellomo, Claudia
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwiginstitutet för cancerforskning. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Caja, Laia
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwiginstitutet för cancerforskning. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Fabregat, Isabel
    Bellvitge Biomedical Research Institute (IDIBELL), L’Hospitalet, and Department of Physiological Sciences, School of Medicine, University of Barcelona, ES-08908, Barcelona, Spain.
    Mikulits, Wolfgang
    Department of Medicine I, Division: Institute of Cancer Research, Comprehensive Cancer Center Vienna, Medical University of Vienna, A-1090, Vienna, Austria.
    Kardassis, Dimitris
    Division of Basic Medical Sciences, University of Crete Medical School and Institute of Molecular Biology and Biotechnology, Foundation for Research and Technology of Hellas, GR-71003, Heraklion, Greece.
    Heldin, Carl-Henrik
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwiginstitutet för cancerforskning. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Moustakas, Aristidis
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Ludwiginstitutet för cancerforskning. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Snail mediates crosstalk between TGFβ and LXRα in hepatocellular carcinoma2018Inngår i: Cell Death and Differentiation, ISSN 1350-9047, E-ISSN 1476-5403, Vol. 25, nr 5, s. 885-903Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Understanding the complexity of changes in differentiation and cell survival in hepatocellular carcinoma (HCC) is essential for the design of new diagnostic tools and therapeutic modalities. In this context, we have analyzed the crosstalk between transforming growth factor β (TGFβ) and liver X receptor α (LXRα) pathways. TGFβ is known to promote cytostatic and pro-apoptotic responses in HCC, and to facilitate mesenchymal differentiation. We here demonstrate that stimulation of the nuclear LXRα receptor system by physiological and clinically useful agonists controls the HCC response to TGFβ. Specifically, LXRα activation antagonizes the mesenchymal, reactive oxygen species and pro-apoptotic responses to TGFβ and the mesenchymal transcription factor Snail mediates this crosstalk. In contrast, LXRα activation and TGFβ cooperate in enforcing cytostasis in HCC, which preserves their epithelial features. LXRα influences Snail expression transcriptionally, acting on the Snail promoter. These findings propose that clinically used LXR agonists may find further application to the treatment of aggressive, mesenchymal HCCs, whose progression is chronically dependent on autocrine or paracrine TGFβ.

  • 4.
    Cunha, Daniel A.
    et al.
    Univ Libre Bruxelles, ULB Ctr Diabet Res, CP-618,Route Lennik 808, B-1070 Brussels, Belgium..
    Cito, Monia
    Univ Libre Bruxelles, ULB Ctr Diabet Res, CP-618,Route Lennik 808, B-1070 Brussels, Belgium..
    Carlsson, Per-Ola
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk cellbiologi.
    Vanderwinden, Jean-Marie
    Univ Libre Bruxelles, Light Microscopy Facil, B-1070 Brussels, Belgium..
    Molkentin, Jeffery D.
    Cincinnati Childrens Hosp Med Ctr, Dept Pediat, Cincinnati, OH 45229 USA..
    Bugliani, Marco
    Univ Pisa, Dept Endocrinol & Metab, Pisa, Italy..
    Marchetti, Piero
    Univ Pisa, Dept Endocrinol & Metab, Pisa, Italy..
    Eizirik, Decio L.
    Univ Libre Bruxelles, ULB Ctr Diabet Res, CP-618,Route Lennik 808, B-1070 Brussels, Belgium..
    Cnop, Miriam
    Univ Libre Bruxelles, ULB Ctr Diabet Res, CP-618,Route Lennik 808, B-1070 Brussels, Belgium.;Univ Libre Bruxelles, Erasmus Hosp, Div Endocrinol, B-1070 Brussels, Belgium..
    Thrombospondin 1 protects pancreatic beta-cells from lipotoxicity via the PERK-NRF2 pathway2016Inngår i: Cell Death and Differentiation, ISSN 1350-9047, E-ISSN 1476-5403, Vol. 23, nr 12, s. 1995-2006Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The failure of beta-cells has a central role in the pathogenesis of type 2 diabetes, and the identification of novel approaches to improve functional beta-cell mass is essential to prevent/revert the disease. Here we show a critical novel role for thrombospondin 1 (THBS1) in beta-cell survival during lipotoxic stress in rat, mouse and human models. THBS1 acts from within the endoplasmic reticulum to activate PERK and NRF2 and induce a protective antioxidant defense response against palmitate. Prolonged palmitate exposure causes THBS1 degradation, oxidative stress, activation of JNK and upregulation of PUMA, culminating in beta-cell death. These findings shed light on the mechanisms leading to beta-cell failure during metabolic stress and point to THBS1 as an interesting therapeutic target to prevent oxidative stress in type 2 diabetes.

  • 5.
    Fernandez-Alonso, R.
    et al.
    Univ Leon, Dept Biol Mol, Inst Biomed IBIOMED, E-24071 Leon, Spain..
    Martin-Lopez, M.
    Univ Leon, Dept Biol Mol, Inst Biomed IBIOMED, E-24071 Leon, Spain..
    Gonzalez-Cano, L.
    Univ Leon, Dept Biol Mol, Inst Biomed IBIOMED, E-24071 Leon, Spain..
    Garcia, S.
    Univ Leon, Dept Biol Mol, Inst Biomed IBIOMED, E-24071 Leon, Spain..
    Castrillo, F.
    Univ Leon, Dept Biol Mol, Inst Biomed IBIOMED, E-24071 Leon, Spain..
    Diez-Prieto, I.
    Univ Leon, Dept Biol Mol, Inst Biomed IBIOMED, E-24071 Leon, Spain.;Univ Leon, Dept Med Cirugia & Anat Vet, E-24071 Leon, Spain..
    Fernandez-Corona, A.
    Univ Leon, Dept Biol Mol, Inst Biomed IBIOMED, E-24071 Leon, Spain.;Complejo Hosp Leon, Leon 24071, Spain..
    Lorenzo-Marcos, M. E.
    Univ Leon, Dept Biol Mol, Inst Biomed IBIOMED, E-24071 Leon, Spain.;Complejo Hosp Leon, Leon 24071, Spain..
    Li, Xiujuan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Vaskulärbiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Claesson-Welsh, Lena
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Vaskulärbiologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala Univ, Dept Immunol Genet & Pathol, Rudbeck Lab, S-75185 Uppsala, Sweden.;Uppsala Univ, Dept Immunol Genet & Pathol, Sci Life Lab, S-75185 Uppsala, Sweden..
    Marques, M.
    Univ Leon, Inst Desarrollo Ganadero, E-24071 Leon, Spain..
    Marin, M. C.
    Univ Leon, Dept Biol Mol, Inst Biomed IBIOMED, E-24071 Leon, Spain..
    p73 is required for endothelial cell differentiation, migration and the formation of vascular networks regulating VEGF and TGF beta signaling2015Inngår i: Cell Death and Differentiation, ISSN 1350-9047, E-ISSN 1476-5403, Vol. 22, nr 8, s. 1287-+Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Vasculogenesis, the establishment of the vascular plexus and angiogenesis, branching of new vessels from the preexisting vasculature, involves coordinated endothelial differentiation, proliferation and migration. Disturbances in these coordinated processes may accompany diseases such as cancer. We hypothesized that the p53 family member p73, which regulates cell differentiation in several contexts, may be important in vascular development. We demonstrate that p73 deficiency perturbed vascular development in the mouse retina, decreasing vascular branching, density and stability. Furthermore, p73 deficiency could affect non endothelial cells (ECs) resulting in reduced in vivo proangiogenic milieu. Moreover, p73 functional inhibition, as well as p73 deficiency, hindered vessel sprouting, tubulogenesis and the assembly of vascular structures in mouse embryonic stem cell and induced pluripotent stem cell cultures. Therefore, p73 is necessary for EC biology and vasculogenesis and, in particular, that DNp73 regulates EC migration and tube formation capacity by regulation of expression of pro-angiogenic factors such as transforming growth factor-beta and vascular endothelial growth factors. DNp73 expression is upregulated in the tumor environment, resulting in enhanced angiogenic potential of B16-F10 melanoma cells. Our results demonstrate, by the first time, that differential p73-isoform regulation is necessary for physiological vasculogenesis and angiogenesis and DNp73 overexpression becomes a positive advantage for tumor progression due to its pro-angiogenic capacity.

  • 6. Sleeper, E
    et al.
    Tamm, C
    Frisén, J
    Zhivotovsky, B
    Orrenius, S
    Ceccatelli, S
    Cell death in adult neural stem cells.2002Inngår i: Cell Death and Differentiation, ISSN 1350-9047, E-ISSN 1476-5403, Vol. 9, nr 12, s. 1377-8Artikkel i tidsskrift (Fagfellevurdert)
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