LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 5 of total 5

Search options

  1. Book ; Online ; Thesis: Bidirectional Akt and Notch1 signaling triggers CLL toward Richter's Transformation

    Kohlhaas, Vivien [Verfasser] / Wunderlich, Thomas [Gutachter] / Schmitt, Lutz [Gutachter]

    2022  

    Author's details Vivien Kohlhaas ; Gutachter: Thomas Wunderlich, Lutz Schmitt
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Language English
    Publisher Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf
    Publishing place Düsseldorf
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

    Full text online

    More links

    Kategorien

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  2. Article ; Online: CerS6-dependent ceramide synthesis in hypothalamic neurons promotes ER/mitochondrial stress and impairs glucose homeostasis in obese mice.

    Hammerschmidt, Philipp / Steculorum, Sophie M / Bandet, Cécile L / Del Río-Martín, Almudena / Steuernagel, Lukas / Kohlhaas, Vivien / Feldmann, Marvin / Varela, Luis / Majcher, Adam / Quatorze Correia, Marta / Klar, Rhena F U / Bauder, Corinna A / Kaya, Ecem / Porniece, Marta / Biglari, Nasim / Sieben, Anna / Horvath, Tamas L / Hornemann, Thorsten / Brodesser, Susanne /
    Brüning, Jens C

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 7824

    Abstract: Dysregulation of hypothalamic ceramides has been associated with disrupted neuronal pathways in control of energy and glucose homeostasis. However, the specific ceramide species promoting neuronal lipotoxicity in obesity have remained obscure. Here, we ... ...

    Abstract Dysregulation of hypothalamic ceramides has been associated with disrupted neuronal pathways in control of energy and glucose homeostasis. However, the specific ceramide species promoting neuronal lipotoxicity in obesity have remained obscure. Here, we find increased expression of the C
    MeSH term(s) Animals ; Mice ; Ceramides/metabolism ; Diet, High-Fat/adverse effects ; Glucose/metabolism ; Homeostasis ; Hypothalamus/metabolism ; Mice, Obese ; Neurons/metabolism ; Obesity/metabolism ; Pro-Opiomelanocortin/metabolism
    Chemical Substances Ceramides ; Glucose (IY9XDZ35W2) ; Pro-Opiomelanocortin (66796-54-1) ; CERS6 protein, mouse (EC 2.3.1.24)
    Language English
    Publishing date 2023-11-29
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-42595-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Article ; Online: AKT activity orchestrates marginal zone B cell development in mice and humans.

    Cox, Eva-Maria / El-Behi, Mohamed / Ries, Stefanie / Vogt, Johannes F / Kohlhaas, Vivien / Michna, Thomas / Manfroi, Benoît / Al-Maarri, Mona / Wanke, Florian / Tirosh, Boaz / Pondarre, Corinne / Lezeau, Harry / Yogev, Nir / Mittenzwei, Romy / Descatoire, Marc / Weller, Sandra / Weill, Jean-Claude / Reynaud, Claude-Agnès / Boudinot, Pierre /
    Jouneau, Luc / Tenzer, Stefan / Distler, Ute / Rensing-Ehl, Anne / König, Christoph / Staniek, Julian / Rizzi, Marta / Magérus, Aude / Rieux-Laucat, Frederic / Wunderlich, F Thomas / Hövelmeyer, Nadine / Fillatreau, Simon

    Cell reports

    2023  Volume 42, Issue 4, Page(s) 112378

    Abstract: The signals controlling marginal zone (MZ) and follicular (FO) B cell development remain incompletely understood. Here, we show that AKT orchestrates MZ B cell formation in mice and humans. Genetic models that increase AKT signaling in B cells or abolish ...

    Abstract The signals controlling marginal zone (MZ) and follicular (FO) B cell development remain incompletely understood. Here, we show that AKT orchestrates MZ B cell formation in mice and humans. Genetic models that increase AKT signaling in B cells or abolish its impact on FoxO transcription factors highlight the AKT-FoxO axis as an on-off switch for MZ B cell formation in mice. In humans, splenic immunoglobulin (Ig) D
    MeSH term(s) Humans ; Mice ; Animals ; Proto-Oncogene Proteins c-akt ; B-Lymphocytes ; Lymphoid Tissue ; Signal Transduction ; Spleen
    Chemical Substances Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2023-04-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2023.112378
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article ; Online: Insulin Resistance and Vulnerability to Cardiac Ischemia.

    Jelenik, Tomas / Flögel, Ulrich / Álvarez-Hernández, Elisa / Scheiber, Daniel / Zweck, Elric / Ding, Zhaoping / Rothe, Maik / Mastrototaro, Lucia / Kohlhaas, Vivien / Kotzka, Jörg / Knebel, Birgit / Müller-Wieland, Dirk / Moellendorf, Sarah / Gödecke, Axel / Kelm, Malte / Westenfeld, Ralf / Roden, Michael / Szendroedi, Julia

    Diabetes

    2018  Volume 67, Issue 12, Page(s) 2695–2702

    Abstract: Hepatic and myocardial ectopic lipid deposition has been associated with insulin resistance (IR) and cardiovascular risk. Lipid overload promotes increased hepatic oxidative capacity, oxidative stress, and impaired mitochondrial efficiency, driving the ... ...

    Abstract Hepatic and myocardial ectopic lipid deposition has been associated with insulin resistance (IR) and cardiovascular risk. Lipid overload promotes increased hepatic oxidative capacity, oxidative stress, and impaired mitochondrial efficiency, driving the progression of nonalcoholic fatty liver disease (NAFLD). We hypothesized that higher lipid availability promotes ischemia-induced cardiac dysfunction and decreases myocardial mitochondrial efficiency. Mice with adipose tissue-specific overexpression of sterol element-binding protein 1c as model of lipid overload with combined NAFLD-IR and controls underwent reperfused acute myocardial infarcts (AMIs). Whereas indexes of left ventricle (LV) contraction were similar in both groups at baseline, NAFLD-IR showed severe myocardial dysfunction post-AMI, with prominent LV reshaping and increased end-diastolic and end-systolic volumes. Hearts of NAFLD-IR displayed hypertrophy, steatosis, and IR due to 18:1/18:1-diacylglycerol-mediated protein kinase Cε (PKCε) activation. Myocardial fatty acid-linked respiration and oxidative stress were increased, whereas mitochondrial efficiency was decreased. In humans, decreased myocardial mitochondrial efficiency of ventricle biopsies related to IR and troponin levels, a marker of impaired myocardial integrity. Taken together, increased lipid availability and IR favor susceptibility to ischemia-induced cardiac dysfunction. The diacylglycerol-PKCε pathway and reduced mitochondrial efficiency both caused by myocardial lipotoxicity may contribute to the impaired LV compensation of the noninfarcted region of the myocardium.
    MeSH term(s) Animals ; Disease Models, Animal ; Humans ; Insulin Resistance/physiology ; Mice ; Mitochondria, Heart/metabolism ; Myocardial Infarction/complications ; Myocardial Infarction/metabolism ; Myocardium/metabolism ; Non-alcoholic Fatty Liver Disease/complications ; Non-alcoholic Fatty Liver Disease/metabolism ; Oxidative Stress/physiology
    Language English
    Publishing date 2018-09-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/db18-0449
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.175: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article ; Online: Active Akt signaling triggers CLL toward Richter transformation via overactivation of Notch1.

    Kohlhaas, Vivien / Blakemore, Stuart James / Al-Maarri, Mona / Nickel, Nadine / Pal, Martin / Roth, Andreas / Hövelmeyer, Nadine / Schäfer, Stephan C / Knittel, Gero / Lohneis, Philipp / Nikolic, Milos / Wiederstein, Janica L / Franitza, Marek / Georgomonolis, Theodoros / Reinart, Nina / Herling, Marco / Herling, Carmen / Hartmann, Elena M / Rosenwald, Andreas /
    Klapper, Wolfram / Büttner, Reinhard / Moia, Riccardo / Rossi, Davide / Boldorini, Renzo / Gaidano, Gianluca / Frenzel, Lukas P / Reinhardt, Hans Christian / Brüning, Jens C / Hallek, Michael / Krüger, Marcus / Peifer, Martin / Pallasch, Christian P / Wunderlich, F Thomas

    Blood

    2021  Volume 137, Issue 5, Page(s) 646–660

    Abstract: Richter's transformation (RT) is an aggressive lymphoma that occurs upon progression from chronic lymphocytic leukemia (CLL). Transformation has been associated with genetic aberrations in the CLL phase involving TP53, CDKN2A, MYC, and NOTCH1; however, a ...

    Abstract Richter's transformation (RT) is an aggressive lymphoma that occurs upon progression from chronic lymphocytic leukemia (CLL). Transformation has been associated with genetic aberrations in the CLL phase involving TP53, CDKN2A, MYC, and NOTCH1; however, a significant proportion of RT cases lack CLL phase-associated events. Here, we report that high levels of AKT phosphorylation occur both in high-risk CLL patients harboring TP53 and NOTCH1 mutations as well as in patients with RT. Genetic overactivation of Akt in the murine Eµ-TCL1 CLL mouse model resulted in CLL transformation to RT with significantly reduced survival and an aggressive lymphoma phenotype. In the absence of recurrent mutations, we identified a profile of genomic aberrations intermediate between CLL and diffuse large B-cell lymphoma. Multiomics assessment by phosphoproteomic/proteomic and single-cell transcriptomic profiles of this Akt-induced murine RT revealed an S100 protein-defined subcluster of highly aggressive lymphoma cells that developed from CLL cells, through activation of Notch via Notch ligand expressed by T cells. Constitutively active Notch1 similarly induced RT of murine CLL. We identify Akt activation as an initiator of CLL transformation toward aggressive lymphoma by inducing Notch signaling between RT cells and microenvironmental T cells.
    MeSH term(s) Animals ; Clonal Evolution ; Disease Progression ; Enzyme Activation ; Gene Expression Regulation, Neoplastic ; Genes, p53 ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Leukemia, Lymphocytic, Chronic, B-Cell/physiopathology ; Lymphocytes, Tumor-Infiltrating/immunology ; Lymphoma, Large B-Cell, Diffuse/genetics ; Lymphoma, Large B-Cell, Diffuse/pathology ; Lymphoma, Large B-Cell, Diffuse/physiopathology ; Mice ; Mice, Inbred C57BL ; Neoplasm Proteins/physiology ; Phenotype ; Phosphoproteins/physiology ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/physiology ; Receptor, Notch1/physiology ; Receptors, Antigen, B-Cell/immunology ; Signal Transduction/physiology ; Transcriptome ; Tumor Microenvironment ; Tumor Suppressor Protein p53/physiology ; Up-Regulation
    Chemical Substances NOTCH1 protein, human ; Neoplasm Proteins ; Phosphoproteins ; Receptor, Notch1 ; Receptors, Antigen, B-Cell ; TP53 protein, human ; Tumor Suppressor Protein p53 ; AKT1 protein, human (EC 2.7.11.1) ; Akt1 protein, mouse (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2021-02-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2020005734
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.140: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 364: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top