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Deep proteomic and phosphoproteomic profiling of DIPG responses to radiation therapy

ABSTRACT: Different DIPG tumor models have different responses to radiation therapy, which can be identified by quantitative proteomics/phospho-proteomics approach

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Brain, Neutrophil

DISEASE(S): Brain Glioblastoma Multiforme

SUBMITTER: Hong Wang

LAB HEAD: Hong Wang

PROVIDER: PXD028285 | Pride | 2024-05-21

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	Shelatgrp_TMTpro_WHL_Xie_20210405.xlsx	Xlsx
	Shelatgrp_TMTpro_deepPhos_Xie_20210107.xlsx	Xlsx
	Shelatgrp_whl01.1.pepXML	Pepxml
	Shelatgrp_whl01.raw	Raw
	Shelatgrp_whl02.1.pepXML	Pepxml

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Publications

ATM inhibition enhances the efficacy of radiation across distinct molecular subgroups of pediatric high-grade glioma.

Xie Jia J Kuriakose Teneema T Bianski Brandon B Twarog Nathaniel N Savage Evan E Xu Ke K Zhu Xiaoyan X He Chen C Hansen Baranda B Wang Hong H High Anthony A Li Yuxin Y Rehg Jerold E JE Tillman Heather S HS Freeman Burgess B BB Rankovic Zoran Z Onar-Thomas Arzu A Fan Yiping Y Wu Gang G Peng Junmin J Miller Shondra S Baker Suzanne J SJ Shelat Anang A AA Tinkle Christopher L CL

Neuro-oncology 20231001 10

<h4>Background</h4>Pediatric high-grade glioma (pHGG) is largely incurable and accounts for most brain tumor-related deaths in children. Radiation is a standard therapy, yet the benefit from this treatment modality is transient, and most children succumb to disease within 2 years. Recent large-scale genomic studies suggest that pHGG has alterations in DNA damage response (DDR) pathways that induce resistance to DNA damaging agents. The aim of this study was to evaluate the therapeutic potential ...[more]

PMID: 36971093

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Deep proteomic and phosphoproteomic profiling of neuroblastoma treated with XPO1 inhibitor Selinexor

Project description:Neuroblastoma accounts for 15% of cancer-related deaths in children, highlighting an unmet need for novel therapies. Selinexor is a small molecule inhibitor of XPO1 that shuffles cargo proteins with a nuclear export sequence, many of which are essential for cancer growth and cell maintenance, from the nucleus to the cytosol. We systematically tested the effect of selinexor against neuroblastoma cells in vitro and in vivo and used a proteomics screening approach to interrogate unknown mechanisms of action. We found that selinexor induces its cytotoxic effects in neuroblastoma through the nuclear accumulation of p53. By combining selinexor with an aurora kinase inhibitor, alisertib that is already in clinical use for neuroblastoma, we show that p53-mediated lethality can be further augmented supporting clinical testing of this drug combination against neuroblastoma

2023-03-11 | PXD026454 | Pride

Acute depletion of CTCF rewires genome-wide chromatin accessibility

Project description:The transcription factor CTCF appears indispensable in defining topologically associated domain boundaries and maintaining chromatin loop structures within these domains, supported by numerous functional studies. However, acute depletion of CTCF globally reduces chromatin interactions but does not significantly alter transcription. Here we systematically integrated multi-omics data including ATAC-seq, RNA-seq, WGBS, Hi-C, Cut&Run, CRISPR-Cas9 survival dropout screening, time-solved deep proteomic and phosphoproteomic analyses in cells carrying auxin-induced degron at endogenous CTCF locus. Acute CTCF protein degradation markedly rewired genome-wide chromatin accessibility. Increased accessible chromatin regions were largely located adjacent to CTCF-binding sites at promoter regions and insulator sites and were associated with enhanced transcription of nearby genes. In addition, we used CTCF-associated multi-omics data to establish a combinatorial data analysis pipeline to discover CTCF co-regulatory partners in regulating downstream gene expression. We successfully identified 40 candidates, including multiple established partners (i.e., MYC) supported by all layers of evidence. Interestingly, many CTCF co-regulators (e.g., YY1, ZBTB7A) that have evident alterations of respective downstream gene expression do not show changes at their expression levels across the multi-omics measurements upon acute CTCF loss, highlighting the strength of our system to discover hidden co-regulatory partners associated with CTCF-mediated transcription. This study highlights CTCF loss rewires genome-wide chromatin accessibility, which plays a critical role in transcriptional regulation

2021-07-04 | PXD026484 | Pride

MR-1 nitrate sample to fumarate sample

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2010-05-19 | E-GEOD-11198 | biostudies-arrayexpress

Pilot KOMP knockout mouse strains

Project description:This is a test case of D. West's RNA-seq from KOMP2 mutant strains

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Regulation of the Endocytosis and Prion Chaperoning Machineries by Yeast E3 Ubiquitin Ligase Rsp5 as Revealed by Orthogonal Ubiquitin Transfer

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2022-10-13 | PXD023688 | Pride

RNAseq of coding RNA in the liver, spleen, kidney, abdominal muscle and gonadal adipose tissue of knock out mice and wild type controls as part of the KOMP2 project.

Project description:This is a pilot study from the Knockout Mouse Phenotyping Program (KOMP2). The program provides broad, standardized phenotyping of a genome-wide collection of mouse knockouts generated by the International Knockout Mouse Consortium (IKMC), funded by the NIH, European Union, Wellcome Trust, Canada, and the Texas Enterprise Fund. In this experiment RNAseq was performed to profile expression of coding RNA in the liver, spleen, kidney, abdominal muscle and gonadal adipose tissue of knock out mice (1810027O10Rik knockout, Sik1 knockout, 3110043O21Rik knockout, 3110043O21Rik knockout) compared with wild type controls.

2017-12-31 | E-MTAB-4035 | biostudies-arrayexpress

Genome-wide mapping of HATs and HDACs in human CD4+ T cells

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IMPC (international mouse phenotyping consortium) high throughput RNA seq of 1143 samples from 106 IMPC knockout lines

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