Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TBC1D3 Associates with the Histone Lysine N-methyltransferase G9a to Affect the Promotion of Neural Progenitors and Cortical Expansion in an Epigenetic Way [RNA-Seq]

ABSTRACT: TBC1D3 Associates with the Histone Lysine N-methyltransferase G9a to Affect the Promotion of Neural Progenitors and Cortical Expansion in an Epigenetic Way [RNA-Seq]

PROVIDER: PRJNA543055 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9058898_1.fastq.gz	Fastqsanger.gz
	SRR9058898_2.fastq.gz	Fastqsanger.gz
	SRR9058899_1.fastq.gz	Fastqsanger.gz
	SRR9058899_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

TBC1D3 Associates with the Histone Lysine N-methyltransferase G9a to Affect the Promotion of Neural Progenitors and Cortical Expansion in an Epigenetic Way

Project description:TBC1D3 Associates with the Histone Lysine N-methyltransferase G9a to Affect the Promotion of Neural Progenitors and Cortical Expansion in an Epigenetic Way

| PRJNA543058 | ENA

TBC1D3 Associates with the Histone Lysine N-methyltransferase G9a to Affect the Promotion of Neural Progenitors and Cortical Expansion in an Epigenetic Way [ChIP-Seq]

Project description:TBC1D3 Associates with the Histone Lysine N-methyltransferase G9a to Affect the Promotion of Neural Progenitors and Cortical Expansion in an Epigenetic Way [ChIP-Seq]

| PRJNA542629 | ENA

TBC1D3 Associates with the Histone Lysine N-methyltransferase G9a to Affect the Promotion of Neural Progenitors and Cortical Expansion in an Epigenetic Way [ChIP-Seq]

Project description:we conducted chromotin Immunoprecipitation sequencing (ChIP-seq) using mouse cortical tissues from TBC1D3-transgenic mice and wild-typed mice

2021-12-01 | GSE131080 | GEO

TBC1D3 Associates with the Histone Lysine N-methyltransferase G9a to Affect the Promotion of Neural Progenitors and Cortical Expansion in an Epigenetic Way

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-12-01 | GSE131254 | GEO

TBC1D3 Associates with the Histone Lysine N-methyltransferase G9a to Affect the Promotion of Neural Progenitors and Cortical Expansion in an Epigenetic Way [RNA-Seq]

Project description:we conducted RNA sequencing using human cerebral organoids treated with TAT peptides

2021-12-01 | GSE131250 | GEO

TBC1D3 suppression of the Histone Lysine N-methyltransferase G9a promotes the generation of neural progenitors and cortical expansion [ChIP-seq]

Project description:we conducted chromotin Immunoprecipitation sequencing (ChIP-seq) using human cerebral organoids treated with TAT-Scrambled (Short for TAT-Scr) with the sequence of YGRKKRRQRRR-FRVRYWFQGCHSEDPWR and TAT-465-481, a special peoptide designed for inhibition of TBC1D3, with the sequence of YGRKKRRQRRR-EGPWFRHYDFRQSCWVR.

2021-02-08 | GSE136281 | GEO

TBC1D3 suppression of the Histone Lysine N-methyltransferase G9a promotes the generation of neural progenitors and cortical expansion

Project description:TBC1D3 suppression of the Histone Lysine N-methyltransferase G9a promotes the generation of neural progenitors and cortical expansion

| PRJNA561829 | ENA

A role for Widely Interspaced Zinc finger (WIZ) in retention of the G9a methyltransferase on chromatin

Project description:G9a and GLP lysine methyltransferases form a heterodimeric complex that is responsible for the bulk of cellular mono- and di-methylation on histone H3 lysine 9 (H3K9me1/me2). Widely Interspaced Zinc finger (WIZ) associates with the G9a/GLP protein complex, but its role in lysine methylation is poorly defined. Here, we show that WIZ regulates global H3K9me2 levels through a mechanism that involves retention of G9a on chromatin. We also show that WIZ-mediated chromatin loss of G9a/GLP results in altered gene expression and protein-protein interactions that are distinguishable from that of using a molecule-induced enzymatic inhibitor towards G9a/GLP – thus providing evidence that the G9a/GLP/WIZ complex has unique functions when bound to chromatin that are independent of the H3K9me2 mark DMSO, UNC0638, NS, and siWIZ treatments to HEK293T cells, assessing G9a and H3K9me2 localization, each performed in duplicate, plus one input control for each cell condition. 30 samples total.

2015-09-03 | E-GEOD-67317 | biostudies-arrayexpress

TBC1D3 promotes neural progenitor proliferation by suppressing the histone methyltransferase G9a.

Project description:Genomic changes during human linage evolution contribute to the expansion of the cerebral cortex to allow more advanced thought processes. The hominoid-specific gene TBC1D3 displays robust capacity of promoting the generation and proliferation of neural progenitors (NPs), which are thought to contribute to cortical expansion. However, the underlying mechanisms remain unclear. Here, we found that TBC1D3 interacts with G9a, a euchromatic histone lysine N-methyltransferase, which mediates dimethylation of histone 3 in lysine 9 (H3K9me2), a suppressive mark for gene expression. TBC1D3 displayed an inhibitory role in G9a's histone methyltransferase activity. Treatment with G9a inhibitor markedly increased NP proliferation and promoted human cerebral organoid expansion, mimicking the effects caused by TBC1D3 up-regulation. By contrast, blockade of TBC1D3/G9a interaction to disinhibit G9a caused up-regulation of H3K9me2, suppressed NP proliferation, and impaired organoid development. Together, this study has demonstrated a mechanism underlying the role of a hominoid-specific gene in promoting cortical expansion.

| S-EPMC7810367 | biostudies-literature

MYC interacts with the G9a histone methyltransferase to drive transcriptional repression and tumorigenesis

Project description:MYC is an oncogenic driver that regulates transcriptional activation and repression, yet molecular mechanisms of MYC transformation remain unclear. We demonstrate that MYC interacts with the G9a H3K9-methyltransferase complex to control transcriptional repression. Inhibiting G9a hinders MYC chromatin binding at MYC-repressed genes and de-represses gene expression to antagonize cellular transformation. By identifying the MYC Box II region as essential for MYC-G9a interaction, a long-standing missing link between MYC transformation and gene repression is unveiled. In breast cancer, anti-proliferative sensitivity to G9a pharmacological inhibition associates with MYC sensitivity and the basal subtype. Inhibiting G9a in vivo suppresses MYC-dependent basal breast tumor growth. Our findings reveal G9a as an epigenetic regulator of MYC-mediated transcriptional repression and a therapeutic vulnerability in MYC-driven cancers.

2018-10-08 | GSE115024 | GEO

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