Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell transcriptome analysis of Myt1l mutant mouse cortices at birth.

ABSTRACT: Single-cell transcriptome analysis of Myt1l mutant mouse cortices at birth.

PROVIDER: PRJNA719238 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14130413_1.fastq.gz	Fastqsanger.gz
	SRR14130413_2.fastq.gz	Fastqsanger.gz
	SRR14130414_1.fastq.gz	Fastqsanger.gz
	SRR14130414_2.fastq.gz	Fastqsanger.gz
	SRR14130415_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Single-cell transcriptome analysis of Myt1l mutant mouse cortices at birth.

Project description:We examined the effect of Myt1l deficiency in the cortices of mice at birth on the single cell level. Homozygous Myt1l deficiency resulted in postnatal lethality, and mutant mice presented increased expression of non-neuronal genes in neurons.

2023-02-14 | GSE171326 | GEO

Bulk transcriptome analysis of Myt1l mutant mouse cortices across development.

Project description:We examined the effect of Myt1l deficiency in the cortices of mice during developement. Homozygous Myt1l deficiency resulted in postnatal lethality, and mutant mice presented gene expression changes associated with developmental delays and resembled changes observed in autism spectrum disorder patients.

2023-02-14 | GSE171325 | GEO

Bulk transcriptome analysis of Myt1l mutant mouse cortices across development.

Project description:Bulk transcriptome analysis of Myt1l mutant mouse cortices across development.

| PRJNA719237 | ENA

CUT&RUN analysis of MYT1L binding in mouse cortices across development.

Project description:We examined MYT1L binding in the genome within cortices of mice during developement.

2023-02-14 | GSE217553 | GEO

Bulk transcriptome analysis of Myt1l mutant mouse neuron primary cultures.

Project description:We examined the effect of Myt1l deficiency in the neurons of mice. Homozygous Myt1l deficiency resulted in postnatal lethality, and mutant mice presented gene expression changes associated with developmental delays and resembled changes observed in autism spectrum disorder patients.

2023-02-14 | GSE217554 | GEO

MYT1L haploinsufficiency in human neurons and mice causes autism-associated phenotypes that can be reversed by genetic and pharmacologic intervention

Project description:MYT1L is an autism spectrum disorder (ASD)-associated transcription factor that is expressed in virtually all neurons throughout life. How MYT1L mutations cause neurological phenotypes and whether they can be targeted remains enigmatic. Here, we examine the effects of MYT1L deficiency in human neurons and mice. Mutant mice exhibit neurodevelopmental delays with thinner cortices, behavioural phenotypes, and gene expression changes that resemble those of ASD patients. MYT1L target genes, including WNT and NOTCH, are activated upon MYT1L depletion and their chemical inhibition can rescue delayed neurogenesis in vitro. MYT1L deficiency also causes upregulation of the main cardiac sodium channel, SCN5A, and neuronal hyperactivity, which could be restored by shRNA-mediated knockdown of SCN5A or MYT1L overexpression in postmitotic neurons. Acute application of the sodium channel blocker, lamotrigine, also rescued electrophysiologic defects in vitro and behaviour phenotypes in vivo. Hence, MYT1L mutation causes both developmental and postmitotic neurological defects. However, acute intervention can normalise resulting electrophysiological and behavioural phenotypes in adulthood.

2023-02-20 | PXD037867 | Pride

CUT&RUN analysis of MYT1L binding in mouse cortices across development.

Project description:CUT&RUN analysis of MYT1L binding in mouse cortices across development.

| PRJNA899526 | ENA

Bulk transcriptome analysis of conditional MYT1L-mutant ESC-derived human induced neurons.

Project description:We examined the effect of heterozygous MYT1L deficiency in human induced neurons. Increased expression of genes with MYT1L binding motifs and activation of non-neuronal genes were observed in human neurons along with deregulation of autism-associated risk genes upon depletion of MYT1L.

2023-02-14 | GSE171324 | GEO

Bulk transcriptome analysis of Myt1l mutant mouse neuron primary cultures.

Project description:Bulk transcriptome analysis of Myt1l mutant mouse neuron primary cultures.

| PRJNA899527 | ENA

Bulk transcriptome analysis of conditional MYT1L-mutant ESC-derived human induced neurons following Wnt and/or Notch inhibitor treatment.

Project description:We examined the effect of Wnt and/or Notch inhibition in the context of heterozygous MYT1L deficiency in human induced neurons. Increased expression of genes with MYT1L binding motifs and activation of non-neuronal genes were observed in human neurons along with deregulation of autism-associated risk genes upon depletion of MYT1L.

2023-02-14 | GSE217555 | 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