Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PTBP2 knock-down RNA-seq from human iPSC-neurons

ABSTRACT: PTBP2 knock-down RNA-seq from human iPSC-neurons

PROVIDER: PRJNA851735 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

PTBP2 knock-down RNA-seq from human iPSC-neurons

Project description:To determine targets of PTBP2-dependent alternative splicing, we depleted PTBP2 in human neurons derived from induced-pluripotent stem cells (iPSC-neurons) using an LNA gapmer and performed RNA-seq on untreated, negative control-treated, and knock-down samples.

2023-05-08 | GSE206660 | GEO

PTBP2 eCLIP from human iPSC-neurons and human cortex (Brodmann area 4) [CLIP-seq]

Project description:To determine direct targets of PTBP2-dependent alternative splicing, we performed CLIP-seq analysis of PTBP2 binding in both human cortical tissue and human neurons derived from induced-pluripotent stem cells (iPSC-neurons), and we combine this with splicing analysis following PTBP2 depletion in iPSC-neurons.

2023-04-13 | GSE206650 | GEO

SPARC knock down

Project description:SPARC knock down

| PRJNA327124 | ENA

FGFR3 knock-down

Project description:FGFR3 knock-down

| PRJNA330963 | ENA

PTBP2 eCLIP from human iPSC-neurons and human cortex (Brodmann area 4) [CLIP-seq]

Project description:PTBP2 eCLIP from human iPSC-neurons and human cortex (Brodmann area 4) [CLIP-seq]

| PRJNA851722 | ENA

Transcriptomic analysis of ATP6V1A knock-down and amyloid beta-treated neurons

Project description:Transcriptomic analysis of ATP6V1A knock-down and amyloid beta-treated neurons

| PRJNA527281 | ENA

Transcriptomic analysis of ATP6V1A knock-down and amyloid beta-treated neurons

Project description:ATP6V1A plays a unique role in synapse function in neurons and we found decreased neuronal activity in ATP6V1A-deficient neurons. To characterize the molecular pathways regulated by ATP6V1A under both normal and stressed conditions, we generated hiPSC-derived NGN2-neurons with reduced ATP6V1A expression by CRISPRi knock-down (KD) and performed RNA-seq analysis on the wild-type and KD neurons which were subject to amyloid-beta or vehicle treatment. A number of gene ontology (GO)/pathways were identified in KD neurons without amyloid-beta treatment (proton transporting V-ATPase complex, phagosome acidification and trivalent inorganic cation transport were down-regulated, and mitochondrial protein complex up-regulated), while KD in amyloid-beta treated cells specifically resulted in down-regulation of cell adhesion, synapse assembly and structure/activity and up-regulation of UPR and ER stress response.

2020-10-30 | GSE128367 | GEO

Human Clariom D Transcriptome profiling of microRNA-mediated neuronal reprogramming with PTBP2 knockdown

Project description:To identify PTBP2 targets important for neural fate acqusition, miR-9/9*-124-mediated direct conversion of human fibroblasts into neurons was employed. We showed that PTBP2 is important for the successful acquisition of neuronal fate and profiled fibroblasts and reprogrammed neurons with and without PTBP2 knockdown to identify neuronal-associated PTBP2 targets during reprogramming.

2021-05-25 | GSE120918 | GEO

CRISPR/Cas9 knock down line

Project description:CRISPR/Cas9 knock down line

| PRJNA521684 | ENA

Microarray analysis of alternative splicing in PTBP2 knockout mouse brain

Project description:The splicing regulator PTBP2 controls a program of embryonic splicing required for neuronal maturation. The splicing regulatory proteins PTBP1 and PTBP2 show distinct temporal expression profiles in the developing brain. Neuronal progenitor cells predominantly express PTBP1, whereas developing neurons express high levels of PTBP2, which are subsequently reduced late in neuronal maturation. We show here that PTBP2 and the program of splicing it controls are essential to proper neuronal maturation and survival. To investigate its in vivo function, we generated conditional PTBP2 null alleles in mice. Loss of PTBP2 in neuronal progenitor cells leads to neonatal death without gross defects in brain architecture. Mice with specific depletion of PTBP2 in the cortex and forebrain are viable. However over the first three postnatal weeks, when the normal cortex expands and develops mature circuits, the PTBP2 null cortices degenerate. We find that PTBP2-/- neurons cultured from embryonic brain show the same initial viability as wild type cells with proper early marker expression and neurite outgrowth. Strikingly, between 10 and 20 days in culture PTBP2 null neurons undergo a catastrophic failure to mature and die. To assess the target transcripts leading to these phenotypes, we examined the genomewide splicing changes in the PTBP2 null brains. This identified a large number of mis-regulated exons that share a temporal pattern of regulation; in the absence of PTBP2 many isoforms normally found in adults are precociously expressed in the developing brain. Transcripts following this pattern encode essential neuronal proteins affecting neurite growth, pre- and post-synaptic assembly, and synaptic transmission. Our results define a new genetic regulatory program essential for neuronal survival and maturation, where PTBP2 acts to temporarily repress expression of protein isoforms until the final maturation of the neuron.

2013-12-01 | GSE51738 | 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