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Affinity switching of the LEDGF/p75 IBD interactome is governed by kinase-dependent phosphorylation

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F18%3A10403787" target="_blank" >RIV/00216208:11310/18:10403787 - isvavai.cz</a>

  • Alternative codes found

    RIV/61388971:_____/18:00492184 RIV/68378050:_____/18:00495066 RIV/61388963:_____/18:00492184

  • Result on the web

    <a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=e-iI2r9BE7" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=e-iI2r9BE7</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1073/pnas.1803909115" target="_blank" >10.1073/pnas.1803909115</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Affinity switching of the LEDGF/p75 IBD interactome is governed by kinase-dependent phosphorylation

  • Original language description

    Lens epithelium-derived growth factor/p75 (LE DGF/p75, or PSIP1) is a transcriptional coactivator that tethers other proteins to gene bodies. The chromatin tethering function of LEDGF/p75 is hijacked by HIV integrase to ensure viral integration at sites of active transcription. LEDGF/p75 is also important for the development of mixed-lineage leukemia (MLL), where it tethers the MLL1 fusion complex at aberrant MLL targets, inducing malignant transformation. However, little is known about how the LEDGF/p75 protein interaction network is regulated. Here, we obtained solution structures of the complete interfaces between the LEDGF/p75 integrase binding domain (IBD) and its cellular binding partners and validated another binding partner, Mediator subunit 1 (MED1). We reveal that structurally conserved IBD-binding motifs (IBMs) on known LEDGF/ p75 binding partners can be regulated by phosphorylation, permitting switching between low- and high-affinity states. Finally, we show that elimination of IBM phosphorylation sites on MLL1 disrupts the oncogenic potential of primary MLL1-rearranged leukemic cells. Our results demonstrate that kinase-dependent phosphorylation of MLL1 represents a previously unknown oncogenic dependency that may be harnessed in the treatment of MLL-rearranged leukemia.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10601 - Cell biology

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2018

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Proceedings of the National Academy of Sciences of the United States of America

  • ISSN

    0027-8424

  • e-ISSN

  • Volume of the periodical

    115

  • Issue of the periodical within the volume

    30

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    10

  • Pages from-to

    "E7053"-"E7062"

  • UT code for WoS article

    000439574700012

  • EID of the result in the Scopus database

    2-s2.0-85052021815