Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chemoproteomic map of compounds candidates to modulate human disease in 293t cells

ABSTRACT: We here present a proteomic platform by implementing in-depth proteome profiling technologies to drug discovery and mechanism of action study.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Ka Yang

LAB HEAD: Ka Yang

PROVIDER: PXD059473 | Pride | 2025-09-18

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	PRIDE_sample_information_Chen_PROTAC.xlsx	Xlsx
	mg_b1_f02.mzXML	Mzxml
	mg_b1_f02.raw	Raw
	mg_b1_f04.mzXML	Mzxml
	mg_b1_f04.raw	Raw

Items per page:

1 - 5 of 195

Similar Datasets

A proteomic study of dual-functional degrader in leukemia cell line

Project description:Here we present the proteomic study of WB156, which is a selective and dual-functional degrader against MDM2 and GSPT1, in leukemia cell line Molt4 and MV4;11.

2025-05-24 | PXD031836 | Pride

Evaluation of a Pooling Chemoproteomics Strategy with an FDA-approved Drug Library

Project description:Chemoproteomics is a key platform for characterizing the mode of action (MoA) for compounds, especially for targeted protein degraders such as proteolysis targeting chimerics (PROTACs) and molecular glues. With deep proteome coverage, multiplexed tandem mass tag-mass spectrometry (TMT-MS) can tackle up to 18 samples in a single experiment. Here, we present a pooling strategy to further enhance the throughput, and apply the strategy to an FDA-approved drug library (95 best-in-class compounds). The TMT-MS-based pooling strategy was evaluated in the following steps. First, we demonstrated the capability of TMT-MS by analyzing over 15,000 unique proteins (>12,000 gene products) in HEK293 cells treated with five PROTACs (two BRD/BET degraders and three degraders for FAK, ALK, and BTK kinases). We then introduced a rationalized pooling strategy to separate structurally similar compounds in different pools, and identified the proteomic response to 14 pools from the drug library. Finally, we validated the proteomic response from one pool by re-profiling the cells under individual drug treatment with sufficient replicates. Interestingly, numerous proteins were found to change upon drug treatment, including AMD1, ODC1, PRKX, PRKY, EXO1, AEN and LRRC58 by 7-Hydroxystaurosporine; C6orf64, HMGCR and RRM2 by Sorafenib; SYS1 and ALAS1 by Venetoclax; and ATF3, CLK1 and CLK4 by Palbocilib. Thus, the pooling chemoproteomics screening provides an efficient method for dissecting the molecular targets of compound libraries.

2023-03-11 | PXD033780 | Pride

A chemoproteomic map of compound candidate to arrest cell growth in pancreatic cancer patient-derived organoids

Project description:We here present a proteomic study of drug inhibiting the cell growth of pancreatic cancer patient-derived organoids

2024-05-27 | PXD031663 | Pride

large scale brain proteome profiling of 3xtg mice

Project description:A large scale profiling of 3xtg mouse brain to invetigate the AD proteomic phenotype.

2024-06-25 | PXD053314 | Pride

Proteome-wide pulse labeling reveals amyloid-impaired protein degradation in Alzheimer’s disease

Project description:We here present a large-scale proteome-wide profiling of protein turnover in Alzheimer's disease mice model. We integrated in vivo pulse-SILAC labeling and TMT multiplexing with novel mass spectrometry to precisely measure protein half-lives.

2024-10-28 | PXD031830 | Pride

A proteomic study of dual-functional degrader in leukemia cell line

Project description:Here we present the proteomic study of WB156, which is a selective and dual-functional degrader against MDM2 and GSPT1, in leukemia cell line Molt4 and MV4;11

2025-05-23 | PXD055642 | Pride

Tetraspanin-enriched Membrane Domains Regulate Vascular Leakage by Membrane Cholesterol Accessibility to Balance Antagonistic GTPases.

Project description:As an endothelium destabilizer, CD82 facilitates vascular leakage by disrupting endothelial barrier and inhibiting its recovery during inflammation. AC at EC surface primes and promotes vascular leakage, mediates the effect of CD82 or TEMD on inflammation, and can be regulated specifically by i) tetraspanins or TEMDs, ii) ORP-mediated transfer of cholesterol, iii) environmental cholesterol, and iv) statin. Thus, tetraspanin-AC interaction and subcellular cholesterol compartmentalization tune the balances between antagonistic signaling axes of Cdc42 versus RhoA, to alter vascular leakage in inflammation. Equally important, we demonstrated anti-vascular leakage and anti-inflammation roles of i) AC reduction and ii) FARP1-Cdc42 elevation/activation in animal models, with promising translational and clinical prospects.

2025-06-19 | PXD065001 | Pride

Ubiquitinome of G401 SMARCB1-deficient rhabdoid tumor cells

Project description:In this study, DCAF5, a substrate receptor that has been shown to modulate the levels of SWI/SNF subunits, which are components of a chromatin remodeling complex. Here we preformed ubiquitinome proteomics to discover the underlying response of DCAF5 loss on ubiquitylation of SWI/SNF subunits. Furthermore, we determine what sites on SWI/SNF components decrease in ubiquitylation upon DCAF5 loss.

2024-03-25 | PXD046463 | Pride

Bipolar and schizophrenia risk gene AKAP11 encodes an autophagy receptor coupling the regulation of PKA kinase network homeostasis to synaptic transmission

Project description:AKAP11 deficiency is associated with autophagy-regulated PKA and neuronal activity in mouse brains. We hypothesized that the differentially expressed proteins (DEPs) and phospho-proteins (pDEPs) in AKAP11 conditional KO mice and human iPSC-induced neurons (iNs) could be identified as potential AKAP11-PKA targets. We have generated AKAP11 F/F; Syn-Cre KO mice, AKAP11-eGFP;Syn-cre KI mice, AKAP11 KO iNs from human iPSCs using CRISPR/Cas9 and constitutive AKAP11 knockout mice

2025-12-08 | PXD067156 | Pride

ATM-knockout on total and phosphorylation proteomes of cortical brain organoids

Project description:ATM (ataxia telangiectasia mutated) kinase is crucial to a wide range of human developmental disorders and adult/pediatric malignancies. Its mutations are causally tied to ataxia telangiectasia, a multi-systemic congenital disorder mainly affecting brain and blood systems. We generated 4 separate ATM-knockout human pluripotent stem cell lines and differentiated them to form 3-dimensional brain cortical brain organoids. Brain cortical organoids are an excellent model of human developing cortex. Using these analyses, we identified ATM-dependent phosphorylation predominantly influences factors in neurogenesis, neuronal differentiation, cell morphogenesis, and microtubule cytoskeleton as well as kinases involved in ATM, BNDF, and WNT signaling, G2/M checkpoint, and p53 regulation. These findings have broad implications about diseases associated with ATM, including ataxia telangiectasia.

2024-07-25 | PXD041699 | Pride