LIVIVO - Das Suchportal für Lebenswissenschaften

switch to English language
Zurück zur letzten Suche Suchhistorie
Erweiterte Suche

Ihre letzten Suchen

  1. AU="Lester, Chantel"
  2. AU="Chaintoutis, Christos"

Suchergebnis

Treffer 1 - 5 von insgesamt 5

Suchoptionen

  1. Artikel ; Online: Tetraspanin CD9 and ectonucleotidase CD73 identify an osteochondroprogenitor population with elevated osteogenic properties.

    Singh, Anju / Lester, Chantel / Drapp, Rebecca / Hu, Dorothy Z / Glimcher, Laurie H / Jones, Dallas

    Development (Cambridge, England)

    2015  Band 142, Heft 3, Seite(n) 438–443

    Abstract: Cell-based bone regeneration strategies offer promise for traumatic bone injuries, congenital defects, non-union fractures and other skeletal pathologies. Postnatal bone remodeling and fracture healing provide evidence that an osteochondroprogenitor cell ...

    Abstract Cell-based bone regeneration strategies offer promise for traumatic bone injuries, congenital defects, non-union fractures and other skeletal pathologies. Postnatal bone remodeling and fracture healing provide evidence that an osteochondroprogenitor cell is present in adult life that can differentiate to remodel or repair the fractured bone. However, cell-based skeletal repair in the clinic is still in its infancy, mostly due to poor characterization of progenitor cells and lack of knowledge about their in vivo behavior. Here, we took a combined approach of high-throughput screening, flow-based cell sorting and in vivo transplantation to isolate markers that identify osteochondroprogenitor cells. We show that the presence of tetraspanin CD9 enriches for osteochondroprogenitors within CD105(+) mesenchymal cells and that these cells readily form bone upon transplantation. In addition, we have used Thy1.2 and the ectonucleotidase CD73 to identify subsets within the CD9(+) population that lead to endochondral or intramembranous-like bone formation. Utilization of this unique cell surface phenotype to enrich for osteochondroprogenitor cells will allow for further characterization of the molecular mechanisms that regulate their osteogenic properties.
    Mesh-Begriff(e) 5'-Nucleotidase/metabolism ; Animals ; Biomarkers/metabolism ; Bone Regeneration/physiology ; Chondrocytes/cytology ; Chondrocytes/metabolism ; Chondrocytes/physiology ; Flow Cytometry ; High-Throughput Screening Assays ; Image Processing, Computer-Assisted ; Kidney/diagnostic imaging ; Mice ; Mice, Inbred C57BL ; Microarray Analysis ; Osteoblasts/cytology ; Osteoblasts/metabolism ; Osteoblasts/physiology ; Real-Time Polymerase Chain Reaction ; Stem Cells/physiology ; Tetraspanin-29/metabolism ; X-Ray Microtomography
    Chemische Substanzen Biomarkers ; Cd9 protein, mouse ; Tetraspanin-29 ; 5'-Nucleotidase (EC 3.1.3.5)
    Sprache Englisch
    Erscheinungsdatum 2015-02-01
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 90607-4
    ISSN 1477-9129 ; 0950-1991
    ISSN (online) 1477-9129
    ISSN 0950-1991
    DOI 10.1242/dev.113571
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Ub I Zs.183: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 91: Hefte anzeigen

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  2. Artikel ; Online: iNKT Cells Induce FGF21 for Thermogenesis and Are Required for Maximal Weight Loss in GLP1 Therapy.

    Lynch, Lydia / Hogan, Andrew E / Duquette, Danielle / Lester, Chantel / Banks, Alexander / LeClair, Katherine / Cohen, David E / Ghosh, Abhisek / Lu, Bing / Corrigan, Michelle / Stevanovic, Darko / Maratos-Flier, Eleftheria / Drucker, Daniel J / O'Shea, Donal / Brenner, Michael

    Cell metabolism

    2016  Band 24, Heft 3, Seite(n) 510–519

    Abstract: Adipose-resident invariant natural killer T (iNKT) cells are key players in metabolic regulation. iNKT cells are innate lipid sensors, and their activation, using their prototypic ligand α-galactosylceramide (αGalCer), induces weight loss and restores ... ...

    Abstract Adipose-resident invariant natural killer T (iNKT) cells are key players in metabolic regulation. iNKT cells are innate lipid sensors, and their activation, using their prototypic ligand α-galactosylceramide (αGalCer), induces weight loss and restores glycemic control in obesity. Here, iNKT activation induced fibroblast growth factor 21 (FGF21) production and thermogenic browning of white fat. Complete metabolic analysis revealed that iNKT cell activation induced increased body temperature, V02, VC02, and fatty acid oxidation, without affecting food intake or activity. FGF21 induction played a major role in iNKT cell-induced weight loss, as FGF21 null mice lost significantly less weight after αGalCer treatment. The glucagon-like peptide 1 (GLP-1) receptor agonist, liraglutide, also activated iNKT cells in humans and mice. In iNKT-deficient mice, liraglutide promoted satiety but failed to induce FGF21, resulting in less weight loss. These findings reveal an iNKT cell-FGF21 axis that defines a new immune-mediated pathway that could be targeted for glycemic control and weight regulation.
    Mesh-Begriff(e) Adipose Tissue, Brown/drug effects ; Adipose Tissue, Brown/metabolism ; Adipose Tissue, White/drug effects ; Adipose Tissue, White/metabolism ; Animals ; Fibroblast Growth Factors/metabolism ; Glucagon-Like Peptide 1/analogs & derivatives ; Glucagon-Like Peptide 1/therapeutic use ; Humans ; Liraglutide/pharmacology ; Liraglutide/therapeutic use ; Mice, Inbred C57BL ; Natural Killer T-Cells/drug effects ; Natural Killer T-Cells/metabolism ; Thermogenesis/drug effects ; Weight Loss/drug effects
    Chemische Substanzen fibroblast growth factor 21 ; Fibroblast Growth Factors (62031-54-3) ; Liraglutide (839I73S42A) ; Glucagon-Like Peptide 1 (89750-14-1)
    Sprache Englisch
    Erscheinungsdatum 2016-09-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2016.08.003
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 6169: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  3. Artikel ; Online: Regulatory iNKT cells lack expression of the transcription factor PLZF and control the homeostasis of T(reg) cells and macrophages in adipose tissue.

    Lynch, Lydia / Michelet, Xavier / Zhang, Sai / Brennan, Patrick J / Moseman, Ashley / Lester, Chantel / Besra, Gurdyal / Vomhof-Dekrey, Emilie E / Tighe, Mike / Koay, Hui-Fern / Godfrey, Dale I / Leadbetter, Elizabeth A / Sant'Angelo, Derek B / von Andrian, Ulrich / Brenner, Michael B

    Nature immunology

    2014  Band 16, Heft 1, Seite(n) 85–95

    Abstract: Invariant natural killer T cells (iNKT cells) are lipid-sensing innate T cells that are restricted by the antigen-presenting molecule CD1d and express the transcription factor PLZF. iNKT cells accumulate in adipose tissue, where they are anti- ... ...

    Abstract Invariant natural killer T cells (iNKT cells) are lipid-sensing innate T cells that are restricted by the antigen-presenting molecule CD1d and express the transcription factor PLZF. iNKT cells accumulate in adipose tissue, where they are anti-inflammatory, but the factors that contribute to their anti-inflammatory nature, as well as their targets in adipose tissue, are unknown. Here we found that iNKT cells in adipose tissue had a unique transcriptional program and produced interleukin 2 (IL-2) and IL-10. Unlike other iNKT cells, they lacked PLZF but expressed the transcription factor E4BP4, which controlled their IL-10 production. The adipose iNKT cells were a tissue-resident population that induced an anti-inflammatory phenotype in macrophages and, through the production of IL-2, controlled the number, proliferation and suppressor function of regulatory T cells (Treg cells) in adipose tissue. Thus, iNKT cells in adipose tissue are unique regulators of immunological homeostasis in this tissue.
    Mesh-Begriff(e) Adipose Tissue/cytology ; Adipose Tissue/immunology ; Animals ; Basic-Leucine Zipper Transcription Factors/genetics ; Basic-Leucine Zipper Transcription Factors/immunology ; Cell Growth Processes/immunology ; Female ; Flow Cytometry ; Gene Expression Regulation ; Homeostasis/immunology ; Interleukin-10/genetics ; Interleukin-10/immunology ; Interleukin-2/genetics ; Interleukin-2/immunology ; Kruppel-Like Transcription Factors/biosynthesis ; Kruppel-Like Transcription Factors/deficiency ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/immunology ; Macrophages/cytology ; Macrophages/immunology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Natural Killer T-Cells/cytology ; Natural Killer T-Cells/immunology ; Natural Killer T-Cells/metabolism ; Promyelocytic Leukemia Zinc Finger Protein ; Specific Pathogen-Free Organisms ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
    Chemische Substanzen Basic-Leucine Zipper Transcription Factors ; Interleukin-2 ; Kruppel-Like Transcription Factors ; Nfil3 protein, mouse ; Promyelocytic Leukemia Zinc Finger Protein ; Zbtb16 protein, mouse ; Interleukin-10 (130068-27-8)
    Sprache Englisch
    Erscheinungsdatum 2014-12-01
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/ni.3047
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 5294: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 42: Hefte anzeigen

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  4. Artikel ; Online: Cdh1 regulates osteoblast function through an APC/C-independent modulation of Smurf1.

    Wan, Lixin / Zou, Weiguo / Gao, Daming / Inuzuka, Hiroyuki / Fukushima, Hidefumi / Berg, Anders H / Drapp, Rebecca / Shaik, Shavali / Hu, Dorothy / Lester, Chantel / Eguren, Manuel / Malumbres, Marcos / Glimcher, Laurie H / Wei, Wenyi

    Molecular cell

    2011  Band 44, Heft 5, Seite(n) 721–733

    Abstract: The APC/Cdh1 E3 ubiquitin ligase plays an essential role in both mitotic exit and G1/S transition by targeting key cell-cycle regulators for destruction. There is mounting evidence indicating that Cdh1 has other functions in addition to cell-cycle ... ...

    Abstract The APC/Cdh1 E3 ubiquitin ligase plays an essential role in both mitotic exit and G1/S transition by targeting key cell-cycle regulators for destruction. There is mounting evidence indicating that Cdh1 has other functions in addition to cell-cycle regulation. However, it remains unclear whether these additional functions depend on its E3 ligase activity. Here, we report that Cdh1, but not Cdc20, promotes the E3 ligase activity of Smurf1. This is mediated by disruption of an autoinhibitory Smurf1 homodimer and is independent of APC/Cdh1 E3 ligase activity. As a result, depletion of Cdh1 leads to reduced Smurf1 activity and subsequent activation of multiple downstream targets, including the MEKK2 signaling pathway, inducing osteoblast differentiation. Our studies uncover a cell-cycle-independent function of Cdh1, establishing Cdh1 as an upstream component that governs Smurf1 activity. They further suggest that modulation of Cdh1 is a potential therapeutic option for treatment of osteoporosis.
    Mesh-Begriff(e) Anaphase-Promoting Complex-Cyclosome ; Animals ; Antigens, CD ; Cadherins/metabolism ; Cdh1 Proteins ; Cell Cycle Proteins/metabolism ; Cell Differentiation ; Humans ; MAP Kinase Kinase Kinase 2/metabolism ; MAP Kinase Signaling System ; Mice ; Osteoblasts/cytology ; Osteoblasts/metabolism ; Protein Binding ; Protein Multimerization ; Ubiquitin-Protein Ligase Complexes/metabolism ; Ubiquitin-Protein Ligases/antagonists & inhibitors ; Ubiquitin-Protein Ligases/chemistry ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination
    Chemische Substanzen Antigens, CD ; CDH1 protein, human ; Cadherins ; Cdh1 Proteins ; Cell Cycle Proteins ; Fzr1 protein, mouse ; Ubiquitin-Protein Ligase Complexes (EC 2.3.2.23) ; SMURF1 protein, human (EC 2.3.2.26) ; Smurf1 protein, mouse (EC 2.3.2.26) ; Anaphase-Promoting Complex-Cyclosome (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; MAP Kinase Kinase Kinase 2 (EC 2.7.11.25)
    Sprache Englisch
    Erscheinungsdatum 2011-12-07
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2011.09.024
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 5055: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  5. Artikel: Cdh1 Regulates Osteoblast Function through an APC/C-Independent Modulation of Smurf1

    Wan, Lixin / Zou, Weiguo / Gao, Daming / Inuzuka, Hiroyuki / Fukushima, Hidefumi / Berg, Anders H. / Drapp, Rebecca / Shaik, Shavali / Hu, Dorothy / Lester, Chantel / Eguren, Manuel / Malumbres, Marcos / Glimcher, Laurie H. / Wei, Wenyi

    Molecular cell

    Band v. 44,, Heft no. 5

    Abstract: The APC/Cdh1 E3 ubiquitin ligase plays an essential role in both mitotic exit and G1/S transition by targeting key cell-cycle regulators for destruction. There is mounting evidence indicating that Cdh1 has other functions in addition to cell-cycle ... ...

    Abstract The APC/Cdh1 E3 ubiquitin ligase plays an essential role in both mitotic exit and G1/S transition by targeting key cell-cycle regulators for destruction. There is mounting evidence indicating that Cdh1 has other functions in addition to cell-cycle regulation. However, it remains unclear whether these additional functions depend on its E3 ligase activity. Here, we report that Cdh1, but not Cdc20, promotes the E3 ligase activity of Smurf1. This is mediated by disruption of an autoinhibitory Smurf1 homodimer and is independent of APC/Cdh1 E3 ligase activity. As a result, depletion of Cdh1 leads to reduced Smurf1 activity and subsequent activation of multiple downstream targets, including the MEKK2 signaling pathway, inducing osteoblast differentiation. Our studies uncover a cell-cycle-independent function of Cdh1, establishing Cdh1 as an upstream component that governs Smurf1 activity. They further suggest that modulation of Cdh1 is a potential therapeutic option for treatment of osteoporosis.
    Schlagwörter ubiquitin-protein ligase ; osteoporosis ; osteoblasts ; cell cycle ; signal transduction
    Sprache Englisch
    Dokumenttyp Artikel
    ISSN 1097-2765
    Datenquelle AGRIS - International Information System for the Agricultural Sciences and Technology

    Zusatzmaterialien

    Kategorien

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

Zum Seitenanfang