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Deep proteomic and phosphoproteomic profiling of Rhabdoid tumor response to IDA/SEL therapy

ABSTRACT: Different Rhabdoid tumors have different responses to idasanultin/selinexor therapy, which can be identified by quantitative proteomics/phospho-proteomics approach

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Kaiwen Yu

LAB HEAD: Anang Shelat

PROVIDER: PXD049344 | Pride | 2026-03-30

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	TMTchannel.txt	Txt
	checksum.txt	Txt
	shelatgrp_052422_tmt_b1_f10.1.pepXML	Pepxml
	shelatgrp_052422_tmt_b1_f10.raw	Raw
	shelatgrp_052422_tmt_b1_f12.1.pepXML	Pepxml

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Publications

Targeting the p53 pathway to treat atypical teratoid rhabdoid tumors.

Refaat Alaa A Cho Hyekyung P HP Williams Justin S JS Stripay Jennifer J Blankenship Kaley K Mercer Kimberly S KS De Vries Rebekah R Connelly Michele M Ganguly Debolina D Robinson Sarah S Savage Evan E Twarog Nathaniel R NR Attery Ayush A Laha Dipranjan D Yu Kaiwen K Poudel Suresh S Dhanda Sandeep K SK Stewart Clinton F CF Freeman Burgess B BB Roberts Charles W M CWM Tinkle Christopher C Stewart Elizabeth A EA Upadhyaya Santhosh A SA Shelat Anang A AA Roussel Martine F MF

Neuro-oncology pediatrics 20251213 1

<h4>Background</h4>Rhabdoid tumors (RTs) are rare aggressive pediatric cancers that can arise throughout the body, including in the central nervous system (CNS), where they are called atypical teratoid rhabdoid tumors (ATRTs), and in extra-CNS locations such as kidneys and other soft tissues, where they are designated as malignant rhabdoid tumors (MRTs). We previously identified MDM2 as a therapeutic vulnerability in RTs and showed that treatment with the MDM2 inhibitor idasanutlin (IDA) increas ...[more]

PMID: 41890241

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Deep proteomic and phosphoproteomic profiling of DIPG responses to radiation therapy

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

2024-05-21 | PXD028285 | Pride

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

Project description:One of the most striking observations in the S. oneidensis genome regarding nitrate respiration is that napC is missing and nrfBCD is degenerated. To gain insights into candidate genes encoding the protein(s) in place of NapC and NrfBCD function, i.e., delivering electrons to NapA and NrfA, transcriptional profiling was carried out using the S. oneidensis whole-genome cDNA microarray. Cells of MR-1 grown on nitrate or fumarate under anaerobic conditions were sampled at the exponential phase for the analysis. The quality of the array data was statistically assessed using the method reported previously. Keywords: Compararive microarray study Compare transcriptional profiles of MR-1 grown on nitrate and Fumarate aiming at finding the electron transfer proteins to NapA and NrfA.

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

2015-12-28 | E-MTAB-3662 | biostudies-arrayexpress

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

Project description:Attachment of the ubiquitin (UB) peptide to proteins via the E1-E2-E3 enzymatic machinery regulates diverse biological pathways, yet identification of the substrates of E3 UB ligases remains a challenge. We overcame this challenge by constructing an “orthogonal UB transfer (OUT) cascade with yeast E3 Rsp5 to enable the exclusive delivery of an engineered UB (xUB) to Rsp5 and its substrate proteins. The OUT screen uncovered new Rsp5 substrates in yeast, such as Pal1 and Pal2 that are partners of endocytic protein Ede1, and chaperones Hsp70-Ssb, Hsp82, and Hsp104 that counteract protein misfolding and control self-perpetuating amyloid aggregates (prions), resembling those involved in human amyloid diseases. We showed that prion formation and effect of Hsp104 on prion propagation are modulated by Rsp5. Overall, our work demonstrates the capacity of OUT to deconvolute the complex E3-substrate relationships in crucial biological processes such as endocytosis and protein assembly disorders through protein ubiquitination.

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

Project description:Histone acetyltransferases (HATs) and deacetylases (HDACs) function antagonistically to control histone acetylation. As acetylation is a histone mark for active transcription, HATs have been associated with active and HDACs with inactive genes. We describe here genome-wide mapping of HATs and HDACs binding on chromatin and ﬁnd that both are found at active genes with acetylated histones. Our data provide evidence that HATs and HDACs are both targeted to transcribed regions of active genes by phosphorylated RNA Pol II. Furthermore, the majority of HDACs in the human genome function to reset chromatin by removing acetylation at active genes. Inactive genes that are primed by MLL-mediated histone H3K4 methylation are subject to a dynamic cycle of acetylation and deacetylation by transient HAT/HDAC binding, preventing Pol II from binding to these genes but poising them for future activation. Silent genes without any H3K4 methylation signal show no evidence of being bound by HDACs. high throughput sequencing: genome-wide analysis of 5 HATs, 4 HDACs in human CD4+ cells, Tip60 and HDAC6 in activated CD4 cells, genome-wide analysis of 2 histone acetylations and RNA Polymerase II after HDAC inhibitor treatment in CD4, histone modification with WDR5 knock-down and HDAC inhibitor treatment in HeLa cells expression profiling: Global change in gene expression in human CD4+ T cells after HDAC inhibitor treatment for 2hours and 12 hours. (9 samples in total)

2009-08-20 | E-GEOD-15735 | biostudies-arrayexpress

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

Project description:A RNA Seq analysis of 7 tissues from 16 week old male knockout mice. A total of 106 IMPC knockout lines were analysed by David West's group at Children's Hospital Oakland Research Institute.

2017-12-01 | E-MTAB-5131 | biostudies-arrayexpress

Chromatin-to-nucleoprotamine transition is controlled by the histone H2B variant TH2B [ChIP-Seq]

Project description:The conversion of male germ cell chromatin to a nucleoprotamine structure is fundamental to the life cycle yet the underlying molecular details remain obscure. Here we show that an essential step is the genome-wide incorporation of TH2B, a histone H2B variant of hitherto unknown function. Using mouse models in which TH2B is depleted or C-terminally modified we show that TH2B directs the final transformation of dissociating nucleosomes into protamine-packed structures. Depletion of TH2B induces compensatory mechanisms that permit histone removal by up-regulating H2B and programming nucleosome instability through targeted histone modifications, including lysine crotonylation and arginine methylation. Furthermore, after fertilization, TH2B re-assembles onto the male genome during protamine-to-histone exchange. Thus, TH2B is a unique histone variant, which plays a key role in the histone-to-protamine packing of the male genome and guides genome-wide chromatin transitions that both precede and follow transmission of the male genome to the egg. Examination of TH2B binding on chromatin in meiotic (spermatocytes) and post-meiotic (round spermatids) male germ cells from adult Th2b+/tag mice (TH2B C-terminally fused to three consecutive affinity tags: His, Flag and Ha). Examination of TH2B (wild type) binding on chromatin in male germ cells from adult wt mice.

2013-10-18 | E-GEOD-45915 | biostudies-arrayexpress

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