Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A sexually dimorphic "pre-stressed" translational signature in CA3 pyramidal neurons of BDNF Val66Met mice

ABSTRACT: BDNF Val66Met mice, a model that is genetically susceptible to stress, recapitulated the translational effects of acute stress in the absence of applied stressors. However, unstressed heterozygous BDNF Val66Met mice did not display activation of immediate early genes, indicating a “pre-stressed” translational phenotype.

ORGANISM(S): Mus musculus

PROVIDER: GSE100579 | GEO | 2017/06/28

SECONDARY ACCESSION(S): PRJNA392171

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

A sexually dimorphic pre-stressed translational signature in CA3 pyramidal neurons of BDNF Val66Met mice.

Project description: Not available

| S-EPMC5634406 | biostudies-literature

Sexually dimorphic BDNF signaling directs sensory innervation of the mammary gland.

Project description: Not available

| S-EPMC3826154 | biostudies-literature

Muscle-generated BDNF is a sexually dimorphic myokine that controls metabolic flexibility.

Project description: Not available

| S-EPMC7219567 | biostudies-literature

Translational profiling of stress-induced neuroplasticity in the CA3 pyramidal neurons of BDNF Val66Met mice.

Project description: Not available

| S-EPMC5468507 | biostudies-literature

BDNF stimulation of protein synthesis in cortical neurons requires the eIF4E kinase Mnk1

Project description:Although the Mnks have been known for >15 years, their roles in the regulation of protein synthesis have remained obscure. Here we explore how BDNF stimulates protein synthesis in cortical neurons. Using a combination of pharmacological and genetic approaches, we show that this effect depends on MEK/ERK signaling and on the downstream kinase, Mnk1, which phosphorylates eIF4E. Translation initiation is mediated by the interaction of eIF4E with the m7GTP cap of mRNA and with eIF4G. The latter interaction is inhibited by the interactions of eIF4E with partner proteins such as CYFIP1, which together with its partner, FMRP acts as a translational repressor. We find that BDNF induces the release of CYFIP1 from eIF4E, and that this depends on Mnk1. Finally, using a novel combination of BONCAT and SILAC, we identify the a subset of proteins whose synthesis is upregulated by BDNF signalling via Mnk1 in neurons. The This subset of Mnk1-sensitive proteins are enriched for functions involved in neurotransmission and synaptic plasticity. Additionally, we find significant overlap between our subset of Mnk1 Mnk1-sensitive proteins and proteins encoded by known FMRP-binding mRNAs. Taken together, our data implicate Mnk1 as a key component of BDNF-mediated translational regulation in neurons.

2014-11-06 | PXD001074 | Pride

Attenuated upregulation of GABAergic markers in response to BDNF in neurons lacking Xbp1

Project description:XBP1 is a transcription factor that is induced by unconventional splicing associated with endoplasmic reticulum stress and plays a role in development of liver and plasma cells. We previously reported that brain derived neurotrophic factor (BDNF) leads to splicing of XBP1 mRNA in neurites, and that XBP1 is required for BDNF-induced neurite extension and branching. To search for the molecular mechanisms of how XBP1 plays a role in neural development, comprehensive gene expression analysis was performed in primary telencephalic neurons obtained from Xbp1 knockout mice at embryonic day 12.5. By searching for the genes induced by BDNF in wild type neurons but this induction was reduced in Xbp1 knockout mice, we found that upregulation of three GABAergic markers, somatostatin (Sst), neuropeptide Y (Npy), and calbindin (Calb1), were compromised in Xbp1 knockout neurons. Attenuated induction of Npy and Calb1 was confirmed by quantitative RT-PCR. In neurons lacking in Xbp1, upregulation of GABAergic markers was attenuated. Impaired BDNF-induced neurite extension in Xbp1 knockout neurons might be mediated by disturbed BDNF-induced differentiation of GABAergic interneurons. Keywords: time-cource, genetic modification

2008-09-25 | GSE11322 | GEO

the expression of BDNF and the levels of this neurotrophin influence the behavioural response in Zebrafish

Project description:Experimental evidence suggests that environmental stress conditions can alter the expression of BDNF and the levels of this neurotrophin influence the behavioural response in mammalian models. Recently it has been demonstrated that the exposure to 34° C for 21 days alters the brain proteome and behaviour in zebrafish. The aim of this work was to investigate the role of BDNF in the nervous system of adult zebrafish under control and heat treatment conditions. For this purpose, wild type (WT), heterozygous BDNF+/- (HT) and knock out BDNF-/- (KO) zebrafish were kept for 21 days at 26° C or 34° C and then euthanized for brain analysis or subjected to behavioural tests (Y-maze test, novel tank test, light and dark test, social preference test, mirror biting test) used for assessing behavioural aspects such as boldness, anxiety, social preference, aggressivity, interest for the novel environment and exploration. RTqPCR analysis showed the reduction of gene expression of BDNF and its receptors after heat treatment. Moreover, proteomic analysis and behavioural tests showed genotype- and temperature-dependent effects on brain proteome and behaviour of zebrafish.

2022-06-09 | PXD030733 | Pride

Maternal obesity alters brain derived neurotrophic factor (BDNF) signaling in the placenta in a sexually dimorphic manner.

Project description: Not available

| S-EPMC5193148 | biostudies-literature

Defining the Caprin-1 interactome in unstressed and stressed conditions

Project description:IP-MS was utilized to identify Caprin-1 protein-protein interactions in stress and unstressed conditions.

2021-05-07 | PXD023271 | Pride

A novel intergenic enhancer that regulates Bdnf expression in developing cortical neurons

Project description:Brain-derived Neurotrophic Factor (BDNF) promotes neuronal differentiation and survival and is implicated in the pathogenesis of many neurological disorders. Here, we identified a novel intergenic enhancer located 170 kb from the Bdnf gene, which promotes the expression of Bdnf transcript variants during mouse neuronal differentiation and activity. Following Bdnf activation, enhancer-promoter contacts increase, and the region moves away from the repressive nuclear periphery. Bdnf enhancer activity is necessary for neuronal clustering and dendritogenesis in vitro, and for cortical development in vivo. Our findings provide the first evidence of a regulatory mechanism whereby the activation of a distal enhancer promotes Bdnf expression during brain development.

2023-01-04 | GSE190306 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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