Proteomics

Dataset Information

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Pevonedistat inhibits aberrant protein NEDDylation in Polycystic Liver Diseases.


ABSTRACT: Background: Polycystic liver diseases (PLD) are genetic disorders characterized by progressive growth of numerous liver cysts, causing significant morbidity. Previous studies revealed genes affecting protein biogenesis and more recently, protein SUMOylation, a posttranslational modification (PTM), has been implicated in PLD pathobiology. On the other hand, protein NEDDylation is a newly-characterized PTM, modulating a plethora of biological processes and its dysregulation is associated with development and progression of several human diseases. In this regard, the role of NEDDylation in PLD remains elusive and unraveling its role in the pathogenesis of these genetic disorders could open new avenues for the development of novel treatments in the future. Objective: To explore the role of protein NEDDylation in PLD and its potential therapeutic regulatory value. Methods: Expression and function of NEDDylation, including response to Pevonedistat (first-in-class selective inhibitor of the NEDDylation E1 enzyme NAE1), were assessed in vitro. Proteomic analyses of immunoprecipitated NEDDylated proteins were performed by mass spectrometry.

INSTRUMENT(S): timsTOF Pro

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cholangiocyte, Liver

DISEASE(S): Polycystic Liver Disease

SUBMITTER: Mikel Azkargorta  

LAB HEAD: Felix Elortza

PROVIDER: PXD022571 | Pride | 2022-02-16

REPOSITORIES: Pride

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Publications

Inhibition of NAE-dependent protein hyper-NEDDylation in cystic cholangiocytes halts cystogenesis in experimental models of polycystic liver disease.

Lee-Law Pui Y PY   Olaizola Paula P   Caballero-Camino Francisco J FJ   Izquierdo-Sanchez Laura L   Rodrigues Pedro M PM   Perugorria Maria J MJ   Azkargorta Mikel M   Elortza Felix F   Martinez-Chantar Maria L ML   Aspichueta Patricia P   Marzioni Marco M   Bujanda Luis L   Drenth Joost P H JPH   Banales Jesus M JM  

United European gastroenterology journal 20210726 7


<h4>Background</h4>Polycystic liver diseases (PLDs) are genetic inherited disorders characterized by the progressive growth of numerous intrahepatic biliary cysts, which are the main cause of morbidity. Previous studies revealed that cystic cholangiocytes are characterized by endoplasmic reticulum stress and aberrant posttranslational modification (PTM) of proteins, in particular hyper-SUMOylation, that promote PLD pathobiology. Protein NEDDylation is a newly characterized PTM that modulates a p  ...[more]

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