Proteomics

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Chromatomes of GR and SUMO2/3 identified with RIME

ABSTRACT: We identified GR and SUMO2/3 chromatomes in B-cell acute leukemia cells (NALM6) and studied the impact of SUMOylation inhibition (SUMOi) on them utilizing small molecule inhibitor ML792. Chromatome members were identified with Rapid Immunoprecipitation Mass spectrometry of Endogenous proteins (RIME) in absence and presence of the synthetic glucocorticoid dexamethasone (Dex) and ML792. Mass spectrometry analyses were executed with high resolution mass spectrometry (LC-MS), using the Evosep One liquid chromatography system coupled to a hybrid trapped ion mobility quadrupole TOF mass spectrometer (Bruker timsTOF Pro) via a CaptiveSpray nano-electrospray ion source. Chromatome members were discriminated from background based on spectral count expression filtering and intensity ratio compared to corresponding IgG control sample.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): B Cell, Cell Suspension Culture

DISEASE(S): Acute Leukemia

SUBMITTER: Emma Valima  

LAB HEAD: Jorma Palvimo

PROVIDER: PXD051304 | Pride | 2025-05-06

REPOSITORIES: Pride

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Dataset's files

Source:
Action DRS
GR_CTRL_Dex_rep1-3.d.zip Other
GR_CTRL_EtOH_rep1-3.d.zip Other
GR_SUMOi_Dex_rep1-3.d.zip Other
GR_SUMOi_EtOH_rep1-3.d.zip Other
GR_start.xlsx Xlsx
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Publications

SUMOylation inhibition potentiates the glucocorticoid receptor to program growth arrest of acute lymphoblastic leukemia cells.

Valima Emma E   Varis Vera V   Bureiko Kseniia K   Lempiäinen Joanna K JK   Schroderus Anna-Mari AM   Oksa Laura L   Lohi Olli O   Kinnunen Tuure T   Varjosalo Markku M   Niskanen Einari A EA   Paakinaho Ville V   Palvimo Jorma J JJ  

Oncogene 20250214 18

Glucocorticoids are a mainstay in the treatment of B-cell acute lymphoblastic leukemia (B-ALL). The glucocorticoid receptor (GR), a ligand-activated transcription factor (TF), mediates their actions. Chromatin occupancy, chromatin-protein networks (chromatomes) and gene programmes of GR are regulated by SUMOylation, a post-translational modification with therapeutic implications in other hematomalignancies. To unravel the GR-SUMOylation crosstalk in B-ALL, we induced hypoSUMOylation in NALM6 B-A  ...[more]

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