LIVIVO - Das Suchportal für Lebenswissenschaften

switch to English language
Erweiterte Suche

Ihre letzten Suchen

  1. AU="Räsch, Felix"
  2. TI=The vesicular transfer of CLIC1 from glioblastoma to microvascular endothelial cells requires TRPM7
  3. AU=Dinda Biswanath AU=Dinda Biswanath

Suchergebnis

Treffer 1 - 4 von insgesamt 4

Suchoptionen

  1. Buch ; Online ; Dissertation / Habilitation: Das musikalische Aufführungsrecht in Deutschland im 19. Jahrhundert

    Rasch, Felix [Verfasser]

    2019  

    Verfasserangabe Felix Rasch
    Schlagwörter Recht ; Law
    Thema/Rubrik (Code) sg340
    Sprache Deutsch
    Verlag Peter Lang GmbH, Internationaler Verlag der Wissenschaften
    Erscheinungsort Frankfurt a.M.
    Dokumenttyp Buch ; Online ; Dissertation / Habilitation
    ISBN 978-3-631-80452-0 ; 3-631-80452-0
    Datenquelle Digitale Dissertationen im Internet

    Zusatzmaterialien

    Kategorien

  2. Buch ; Online ; Dissertation / Habilitation: The role of 4E-T in translational regulation and mRNA decay

    Räsch, Felix Alexander Paul [Verfasser]

    2020  

    Verfasserangabe Felix Alexander Paul Räsch
    Schlagwörter Biowissenschaften, Biologie ; Life Science, Biology
    Thema/Rubrik (Code) sg570
    Sprache Englisch
    Verlag Universitätsbibliothek Tübingen
    Erscheinungsort Tübingen
    Dokumenttyp Buch ; Online ; Dissertation / Habilitation
    Datenquelle Digitale Dissertationen im Internet

    Zusatzmaterialien

    Kategorien

  3. Artikel ; Online: 4E-T-bound mRNAs are stored in a silenced and deadenylated form.

    Räsch, Felix / Weber, Ramona / Izaurralde, Elisa / Igreja, Cátia

    Genes & development

    2020  Band 34, Heft 11-12, Seite(n) 847–860

    Abstract: Human 4E-T is an eIF4E-binding protein (4E-BP) present in processing (P)-bodies that represses translation and regulates decay of mRNAs destabilized by AU-rich elements and microRNAs (miRNAs). However, the underlying regulatory mechanisms are still ... ...

    Abstract Human 4E-T is an eIF4E-binding protein (4E-BP) present in processing (P)-bodies that represses translation and regulates decay of mRNAs destabilized by AU-rich elements and microRNAs (miRNAs). However, the underlying regulatory mechanisms are still unclear. Here, we show that upon mRNA binding 4E-T represses translation and promotes deadenylation via the recruitment of the CCR4-NOT deadenylase complex. The interaction with CCR4-NOT is mediated by previously uncharacterized sites in the middle region of 4E-T. Importantly, mRNA decapping and decay are inhibited by 4E-T and the deadenylated target is stored in a repressed form. Inhibition of mRNA decapping requires the interaction of 4E-T with the cap-binding proteins eIF4E/4EHP. We further show that regulation of decapping by 4E-T participates in mRNA repression by the miRNA effector protein TNRC6B and that 4E-T overexpression interferes with tristetraprolin (TTP)- and NOT1-mediated mRNA decay. Thus, we postulate that 4E-T modulates 5'-to-3' decay by swapping the fate of a deadenylated mRNA from complete degradation to storage. Our results provide insight into the mechanism of mRNA storage that controls localized translation and mRNA stability in P-bodies.
    Mesh-Begriff(e) Gene Expression Regulation/genetics ; Gene Silencing/physiology ; Nucleocytoplasmic Transport Proteins/genetics ; Nucleocytoplasmic Transport Proteins/metabolism ; Protein Binding/genetics ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; RNA-Binding Proteins/metabolism ; Transcription Factors/metabolism
    Chemische Substanzen EIF4ENIF1 protein, human ; Nucleocytoplasmic Transport Proteins ; RNA, Messenger ; RNA-Binding Proteins ; TNRC6B protein, human ; Transcription Factors
    Sprache Englisch
    Erscheinungsdatum 2020-04-30
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.336073.119
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

  4. Artikel ; Online: HELZ directly interacts with CCR4-NOT and causes decay of bound mRNAs.

    Hanet, Aoife / Räsch, Felix / Weber, Ramona / Ruscica, Vincenzo / Fauser, Maria / Raisch, Tobias / Kuzuoğlu-Öztürk, Duygu / Chang, Chung-Te / Bhandari, Dipankar / Igreja, Cátia / Wohlbold, Lara

    Life science alliance

    2019  Band 2, Heft 5

    Abstract: Eukaryotic superfamily (SF) 1 helicases have been implicated in various aspects of RNA metabolism, including transcription, processing, translation, and degradation. Nevertheless, until now, most human SF1 helicases remain poorly understood. Here, we ... ...

    Abstract Eukaryotic superfamily (SF) 1 helicases have been implicated in various aspects of RNA metabolism, including transcription, processing, translation, and degradation. Nevertheless, until now, most human SF1 helicases remain poorly understood. Here, we have functionally and biochemically characterized the role of a putative SF1 helicase termed "helicase with zinc-finger," or HELZ. We discovered that HELZ associates with various mRNA decay factors, including components of the carbon catabolite repressor 4-negative on TATA box (CCR4-NOT) deadenylase complex in human and
    Mesh-Begriff(e) Animals ; Cell Line ; Drosophila melanogaster ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; HEK293 Cells ; Humans ; Nervous System/growth & development ; Nervous System/metabolism ; Protein Binding ; Protein Biosynthesis ; RNA Helicases/genetics ; RNA Helicases/metabolism ; RNA Stability ; Receptors, CCR4/chemistry ; Receptors, CCR4/metabolism ; TATA Box
    Chemische Substanzen Receptors, CCR4 ; RNA Helicases (EC 3.6.4.13)
    Sprache Englisch
    Erscheinungsdatum 2019-09-30
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2575-1077
    ISSN (online) 2575-1077
    DOI 10.26508/lsa.201900405
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

Zum Seitenanfang