Proteomics

Dataset Information

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EZH1/2 function mostly within canonical PRC2 and exhibit proliferation-dependent redundancy that shapes mutational signatures in cancer

ABSTRACT: The project aimed at determining whether the Polycomb complex PRC2 has a unique composition in androgen independent prostate cancer cells and the project aimed at determining whether EZH2, the enzymatic subunit of PRC2, retains any functional role in the context of Malignant peripheral nerve sheath tumor (MPNST) where either EED or SUZ12, two essential subunits of PRC2 are inactivated.

OTHER RELATED OMICS DATASETS IN: GSE118183GSE118185GSE118186

INSTRUMENT(S): Orbitrap Fusion ETD, Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Nerve, Cell Culture, Prostate Epithelium

DISEASE(S): Malignant Peripheral Nerve Sheath Tumor,Prostate Cancer

SUBMITTER: Pascal Jansen  

LAB HEAD: Raphaël Margueron

PROVIDER: PXD012547 | Pride | 2019-03-01

REPOSITORIES: Pride

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20150605_Q1_SA_IrBa_IP_88-14-EZH2-Flag_1.raw Raw
20150605_Q1_SA_IrBa_IP_88-14-EZH2-Flag_2.raw Raw
20150605_Q1_SA_IrBa_IP_88-14-EZH2-Flag_3.raw Raw
20150605_Q1_SA_IrBa_IP_88-14-EZH2-Flag_txt.zip Other
20150605_Q1_SA_IrBa_IP_88-14-Flag_1.raw Raw
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EZH1/2 function mostly within canonical PRC2 and exhibit proliferation-dependent redundancy that shapes mutational signatures in cancer.

Wassef Michel M   Luscan Armelle A   Aflaki Setareh S   Zielinski Dina D   Jansen Pascal W T C PWTC   Baymaz H Irem HI   Battistella Aude A   Kersouani Carole C   Servant Nicolas N   Wallace Margaret R MR   Romero Pierre P   Kosmider Olivier O   Just Pierre-Alexandre PA   Hivelin Mikaël M   Jacques Sébastien S   Vincent-Salomon Anne A   Vermeulen Michiel M   Vidaud Michel M   Pasmant Eric E   Margueron Raphaël R  

Proceedings of the National Academy of Sciences of the United States of America 20190313 13

Genetic mutations affecting chromatin modifiers are widespread in cancers. In malignant peripheral nerve sheath tumors (MPNSTs), Polycomb repressive complex 2 (PRC2), which plays a crucial role in gene silencing, is inactivated through recurrent mutations in core subunits embryonic ectoderm development (EED) and suppressor of zeste 12 homolog (SUZ12), but mutations in PRC2's main catalytic subunit enhancer of zeste homolog 2 (EZH2) have never been found. This is in contrast to myeloid and lympho  ...[more]

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