LIVIVO - Das Suchportal für Lebenswissenschaften

switch to English language
Zurück zur letzten Suche Suchhistorie
Erweiterte Suche

Ihre letzten Suchen

  1. AU="Blaize, Justin L"
  2. AU="R, Ram Babu"
  3. AU="Khalili Arash"
  4. AU="Bhatia, Sandeep"
  5. AU="Ticha, Johnson M"
  6. AU="Aranzabal Barrio, N"

Suchergebnis

Treffer 1 - 3 von insgesamt 3

Suchoptionen

  1. Artikel: Differential Regulation of Retinoic Acid Metabolism in Fanconi Anemia.

    Blaize, Justin L / Noori, Bahaa M / Hunter, Kelsey P / Henrikson, Kathryn A / Atoyan, Janet A / Ardito, Alan A / Donovan, Frank X / Chandrasekharappa, Settara C / Schindler, Detlev / Howlett, Niall G

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Fanconi anemia (FA) is a rare genetic disease characterized by heterogeneous congenital abnormalities and increased risk for bone marrow failure and cancer. FA is caused by mutation of any one of 23 genes, the protein products of which function primarily ...

    Abstract Fanconi anemia (FA) is a rare genetic disease characterized by heterogeneous congenital abnormalities and increased risk for bone marrow failure and cancer. FA is caused by mutation of any one of 23 genes, the protein products of which function primarily in the maintenance of genome stability. An important role for the FA proteins in the repair of DNA interstrand crosslinks (ICLs) has been established
    Sprache Englisch
    Erscheinungsdatum 2023-04-27
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2023.04.06.535759
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    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.

  2. Artikel ; Online: Cyclin-Dependent Kinase-Mediated Phosphorylation of FANCD2 Promotes Mitotic Fidelity

    Cantres-Velez, Juan A. / Blaize, Justin L. / Vierra, David A. / Boisvert, Rebecca A. / Garzon, Jada L. / Piraino, Benjamin / Tan, Winnie / Deans, Andrew J. / Howlett, Niall G.

    Molecular and Cellular Biology. 2021 Aug. 1, v. 41, no. 8 p.e00234-21-

    2021  

    Abstract: Fanconi anemia (FA) is a rare genetic disease characterized by increased risk for bone marrow failure and cancer. The FA proteins function together to repair damaged DNA. A central step in the activation of the FA pathway is the monoubiquitination of the ...

    Abstract Fanconi anemia (FA) is a rare genetic disease characterized by increased risk for bone marrow failure and cancer. The FA proteins function together to repair damaged DNA. A central step in the activation of the FA pathway is the monoubiquitination of the FANCD2 and FANCI proteins, which occurs upon exposure to DNA-damaging agents and during the S phase of the cell cycle. The regulatory mechanisms governing S-phase monoubiquitination, in particular, are poorly understood. In this study, we have identified a cyclin-dependent kinase (CDK) regulatory phosphosite (S592) proximal to the site of FANCD2 monoubiquitination. FANCD2 S592 phosphorylation was detected by liquid chromatography-tandem mass spectrometry (LC-MS/MS) and by immunoblotting with an S592 phospho-specific antibody. Mutation of S592 leads to abrogated monoubiquitination of FANCD2 during the S phase. Furthermore, FA-D2 (FANCD2⁻/⁻) patient cells expressing S592 mutants display reduced proliferation under conditions of replication stress and increased mitotic aberrations, including micronuclei and multinucleated cells. Our findings describe a novel cell cycle-specific regulatory mechanism for the FANCD2 protein that promotes mitotic fidelity.
    Schlagwörter DNA ; Fanconi anemia ; antibodies ; bone marrow ; cyclin-dependent kinase ; immunoblotting ; interphase ; liquid chromatography ; mitosis ; mutation ; patients ; phosphorylation ; risk ; tandem mass spectrometry ; FANCD2 ; CDK phosphorylation ; cell cycle ; chromosome stability ; ubiquitination ; ubiquitin
    Sprache Englisch
    Erscheinungsverlauf 2021-0801
    Erscheinungsort Taylor & Francis
    Dokumenttyp Artikel ; Online
    ZDB-ID 779397-2
    ISSN 1098-5549 ; 0270-7306
    ISSN (online) 1098-5549
    ISSN 0270-7306
    DOI 10.1128/MCB.00234-21
    Datenquelle NAL Katalog (AGRICOLA)

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 1666: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.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.

  3. Artikel ; Online: Cyclin-Dependent Kinase-Mediated Phosphorylation of FANCD2 Promotes Mitotic Fidelity.

    Cantres-Velez, Juan A / Blaize, Justin L / Vierra, David A / Boisvert, Rebecca A / Garzon, Jada L / Piraino, Benjamin / Tan, Winnie / Deans, Andrew J / Howlett, Niall G

    Molecular and cellular biology

    2021  Band 41, Heft 8, Seite(n) e0023421

    Abstract: Fanconi anemia (FA) is a rare genetic disease characterized by increased risk for bone marrow failure and cancer. The FA proteins function together to repair damaged DNA. A central step in the activation of the FA pathway is the monoubiquitination of the ...

    Abstract Fanconi anemia (FA) is a rare genetic disease characterized by increased risk for bone marrow failure and cancer. The FA proteins function together to repair damaged DNA. A central step in the activation of the FA pathway is the monoubiquitination of the FANCD2 and FANCI proteins, which occurs upon exposure to DNA-damaging agents and during the S phase of the cell cycle. The regulatory mechanisms governing S-phase monoubiquitination, in particular, are poorly understood. In this study, we have identified a cyclin-dependent kinase (CDK) regulatory phosphosite (S592) proximal to the site of FANCD2 monoubiquitination. FANCD2 S592 phosphorylation was detected by liquid chromatography-tandem mass spectrometry (LC-MS/MS) and by immunoblotting with an S592 phospho-specific antibody. Mutation of S592 leads to abrogated monoubiquitination of FANCD2 during the S phase. Furthermore, FA-D2 (
    Mesh-Begriff(e) Cell Cycle/physiology ; Cyclin-Dependent Kinases/genetics ; Cyclin-Dependent Kinases/metabolism ; Fanconi Anemia/genetics ; Fanconi Anemia/metabolism ; Fanconi Anemia Complementation Group D2 Protein/genetics ; Fanconi Anemia Complementation Group D2 Protein/metabolism ; Fanconi Anemia Complementation Group Proteins/chemistry ; Fanconi Anemia Complementation Group Proteins/genetics ; Fanconi Anemia Complementation Group Proteins/metabolism ; Humans ; Phosphorylation/physiology ; Tandem Mass Spectrometry/methods ; Ubiquitination/physiology
    Chemische Substanzen Fanconi Anemia Complementation Group D2 Protein ; Fanconi Anemia Complementation Group Proteins ; Cyclin-Dependent Kinases (EC 2.7.11.22)
    Sprache Englisch
    Erscheinungsdatum 2021-07-23
    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 779397-2
    ISSN 1098-5549 ; 0270-7306
    ISSN (online) 1098-5549
    ISSN 0270-7306
    DOI 10.1128/MCB.00234-21
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 1666: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.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.

Zum Seitenanfang