Proteomics

Dataset Information

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Immediate adaption – Quantitative Proteomics of BCL6 silencing and EGFR TK inhibition


ABSTRACT: We aimed to identify the response mechanism to EGFR tyrosine kinase inhibition. A431 cells were transfected with mock siRNA or BCL6 siRNA. Cells were then treated with gefitinib. Harvesting was done at 0h, at 24h and at 48h. Two TMT10plex sets were organized as follows: TMT set1: mock 0h (3x, channels 126, 127N and 127C), mock 24h (3x, 128N, 128C and 129N), mock 48h (3x, 129C, 130N, 130C) and internal pooled standard (131) composed from equal aliquots of all samples (mock siRNA and BCL6 siRNA). TMT set2: siBCL6 0h (3x, channels 126, 127N and 127C), siBCL6 24h (3x, 128N, 128C and 129N), siBCL6 48h (3x, 129C, 130N, 130C) and the same internal pooled standard (131) as for set 1.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell

DISEASE(S): Lung Cancer

SUBMITTER: Rui Branca  

LAB HEAD: Janne Lehtiö

PROVIDER: PXD016605 | Pride | 2020-12-09

REPOSITORIES: pride

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Publications

Immediate Adaptation Analysis Implicates BCL6 as an EGFR-TKI Combination Therapy Target in NSCLC.

Zhou Tran Yan Y   Minozada Rezan R   Cao Xiaofang X   Johansson Henrik J HJ   Branca Rui M RM   Seashore-Ludlow Brinton B   Orre Lukas M LM  

Molecular & cellular proteomics : MCP 20200331 6


Drug resistance is a major obstacle to curative cancer therapies, and increased understanding of the molecular events contributing to resistance would enable better prediction of therapy response, as well as contribute to new targets for combination therapy. Here we have analyzed the early molecular response to epidermal growth factor receptor (EGFR) inhibition using RNA sequencing data covering 13,486 genes and mass spectrometry data covering 10,138 proteins. This analysis revealed a massive re  ...[more]

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