Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome profiling based on the presence of PHF23 and amino acid starvation

ABSTRACT: Autophagy is a conserved self-digestion pathway essential for maintaining cellular homeostasis and catabolism. Under normal conditions, autophagic activity remains minimal but is rapidly upregulated in response to stresses such as nutrient deprivation. While the transcriptional and epigenetic activation of autophagy under nutrient deprived condition has been widely studied, less is known about the repression mechanisms of autophagy under normal conditions. Here, we identify PHF23 as an epigenetic repressor of autophagy through a CRISPR interference (CRISPRi) screening. PHF23 inhibits the expression of autophagy genes by recruiting the NuRD complex and reducing chromatin accessibility, particularly at enhancer regions. This repressive function of PHF23 requires an intact PHD domain and is attenuated under amino acid starvation or mTOR inhibition conditions. Notably, inhibiting PHF23 enhances the autophagic clearance of pathological protein aggregates including Tau and a1 antitrypsin Z variant (ATZ), underscoring its potential as a therapeutic target in diseases characterized by proteotoxic stress.

ORGANISM(S): Homo sapiens

PROVIDER: GSE300095 | GEO | 2025/12/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	GSE300095_PHF23_featurecounts.txt.gz	Txt

Items per page:

1 - 2 of 2

Similar Datasets

Genome binding/occupancy profiling of PHF23 and changes in H3K27ac based on the presence of PHF23

Project description:Autophagy is a conserved self-digestion pathway essential for maintaining cellular homeostasis and catabolism. Under normal conditions, autophagic activity remains minimal but is rapidly upregulated in response to stresses such as nutrient deprivation. While the transcriptional and epigenetic activation of autophagy under nutrient deprived condition has been widely studied, less is known about the repression mechanisms of autophagy under normal conditions. Here, we identify PHF23 as an epigenetic repressor of autophagy through a CRISPR interference (CRISPRi) screening. PHF23 inhibits the expression of autophagy genes by recruiting the NuRD complex and reducing chromatin accessibility, particularly at enhancer regions. This repressive function of PHF23 requires an intact PHD domain and is attenuated under amino acid starvation or mTOR inhibition conditions. Notably, inhibiting PHF23 enhances the autophagic clearance of pathological protein aggregates including Tau and a1 antitrypsin Z variant (ATZ), underscoring its potential as a therapeutic target in diseases characterized by proteotoxic stress.

2025-12-17 | GSE300094 | GEO

chromatin accessibility profiling by ATAC-seq based on the presence of PHF23

2025-12-17 | GSE300092 | GEO

CRISPRi screen identifying epigenetic regulators of autophagic flux

2025-12-17 | GSE300093 | GEO

PHF20 Activates Autophagy Genes through Enhancer Activation via H3K36me2 Binding Activity [ChIP-seq]

Project description:Autophagy is a catabolic pathway that maintains cellular homeostasis under various stress conditions, including nutrient-deprived conditions. To elevate autophagic flux to a sufficient level under stress conditions, transcriptional activation of autophagy genes occurs to replenish autophagy components. Here, using combination of RNA-seq, ATAC-seq and ChIP-seq, we demonstrated found that plant homeodomain finger protein 20 (Phf20PHF20), which is an epigenetic reader possessing methyl binding activity, plays a key role in controlling the expression of autophagy genes. PHF20 activates autophagy genes through enhancer activation via H3K36me2 binding activity as an epigenetic reader and that our findings emphasize the importance of nuclear regulation of autophagy.

2022-06-23 | GSE193217 | GEO

PHF20 Activates Autophagy Genes through Enhancer Activation via H3K36me2 Binding Activity [ATAC-seq]

2022-06-23 | GSE193215 | GEO

PHF20 Activates Autophagy Genes through Enhancer Activation via H3K36me2 Binding Activity [RNA-seq]

2022-06-23 | GSE193392 | GEO

Bulk RNA sequencing of mouse embryonic fibroblasts in autophagy processes

Project description:Autophagy, a catabolic process to remove unnecessary or dysfunctional cells, is triggered by various signals including nutrient starvation. Depending on the type of the nutrient deficiency, diverse sensing mechanisms and pathways are used for autophagy, suggesting subsequent nutrient dependent transcriptional regulation. Still, however, our knowledge about nutrient specific transcriptional regulation during autophagy is limited. To understand nutrient type dependent transcriptional mechanisms during autophagy, we performed single cell RNA sequencing (scRNAseq) for the mouse embryonic fibroblasts (MEFs) before and after applying glucose- (GS) as well as amino acid starvation (AAS). Trajectory analysis using scRNAseq identified sequential induction of potential transcriptional regulators for each deficiency condition. Gene regulatory rules inferred using TENET newly identified CCAAT/enhancer binding protein γ (C/EBPγ) regulates autophagy processes specifically to AAS condition. Strikingly, knockdown of C/EBPγ attenuated the autophagic process only in the AAS condition. Cell biological and biochemical studies validated that C/EBPγ plays a switching role for ATF4 to activate autophagy genes under AAS, but not under GS. Together, our data identified C/EBPγ as a previously unidentified key regulator under amino acid starvation-induced autophagy.

2022-04-04 | GSE199923 | GEO

Single cell RNA sequencing of mouse embryonic fibroblasts in autophagy processes

2021-12-01 | GSE189710 | GEO

Epigenetic and transcriptional regulation of starvation-induced atrophy and autophagy programs by Foxk1 and Sin3A

Project description:Autophagy is the primary catabolic process triggered in response to starvation. Although autophagic regulation within the cytosolic compartment is well established, it is becoming clear that nuclear events also regulate the induction or repression of autophagy. Nevertheless, a thorough understanding of the mechanisms by which sequence-specific transcription factors modulate expression of genes required for autophagy is lacking. Here, we identify Foxk proteins (Foxk1 and Foxk2) as transcriptional repressors of autophagy in muscle cells and fibroblasts. Interestingly, Foxk1/2 serve to counter-balance another forkhead transcription factor, Foxo3, which induces an overlapping set of autophagic and atrophic targets in muscle. Foxk1/2 specifically recruits Sin3A-HDAC complexes to restrict acetylation of histone H4 and expression of critical autophagy genes. Remarkably, mTOR promotes the transcriptional activity of Foxk1 by facilitating nuclear entry to specifically limit basal levels of autophagy in nutrient-rich conditions. Our study highlights an ancient, conserved mechanism whereby nutritional status is interpreted by mTOR to restrict autophagy by repressing essential autophagy genes via Foxk-Sin3-mediated transcriptional control. Examination of (1) chromatin binding of Foxk1 and Sin3A in non-starved myoblasts and (2) gene expression profiling upon either starvation or siRNA-mediated depletion of Foxk1 relative to a non-starved control.

2014-11-17 | E-GEOD-56932 | biostudies-arrayexpress

Genome wide localization of chromatin bound NUP98-PHF23 (NP23)

Project description:We analyzed the genome wide localization of H3K4me3, H3K27me3 and the NUP98-PHF23 (with V5 tag) fusion protein which binds H3K4me3 via its PHD finger, using ChIP-seq. Results correlated with gene expression profiles. NUP98-PHF23 bound only 1.6% of H3K4me3 marks including Hoxa/b + Meis1. Assess H3K4me3 and H3K27me3 histone marks, and correlate these marks with chromatin binding of the NP23 fusion protein using lymphoblast and myeloblast cell lines derived from NP23 leukemias.

2014-03-06 | E-GEOD-54786 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data