Summary of project PR001402

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001402. The data can be accessed directly via it's Project DOI: 10.21228/M8H42P This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

Project ID: PR001402
Project DOI:doi: 10.21228/M8H42P
Project Title:FOXA2 controls the anti-oxidant response in FH-deficient cells independent of NRF2
Project Summary:Hereditary Leiomyomatosis and renal cell cancer is caused by fumarate hydratase loss of heterozygosity and subsequence accumulation of fumarate. Fumarate is known to activate the anti-oxidant response and is key for cellular survival. Fumarate succinates KEAP1 which releases NRF2 to activate the antioxidant response. The role of fumarate on the global regulatory chromatin landscape is less understood. Here, by integrating chromatin accessibility and histone ChIP-seq profiles, we identify complex transcription factor networks involved in the highly remodelled chromatin landscape of FH-deficient cells. We implicate FOXA2 in the maintenance of FH-deficient cells by regulating anti-oxidant response genes and subsequent metabolic output, independent of NRF2. These results identify new redox and amino acid metabolism regulators and provide new avenues for therapeutic intervention.
Institute:CECAD Research Center
Last Name:Yang
First Name:Ming
Address:Joseph-Stelzmann-Straße 26, Köln, Koeln, 50931, Germany
Email:ming.yang@uni-koeln.de
Phone:4922147884306

Summary of all studies in project PR001402

Study IDStudy TitleSpeciesInstituteAnalysis
(* : Contains Untargted data)		 Release
Date		VersionSamplesDownload
(* : Contains raw data)
ST002199 FOXA2 controls the anti-oxidant response in FH-deficient cells independent of NRF2 Mus musculus CECAD Research Center MS 2022-07-14 1 30 Uploaded data (5.3G)*
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