Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomic analysis indicates that Cav-1 regulates mitochondria and cellular metabolism pathways in hippocampal NSPCs

ABSTRACT: To investigate the mechanisms underlying Cav-1 regulation of NSPCs, we used quantitative proteomics to assess protein alterations in response to Cav-1 deletion in primary hippocampal NSPCs. Due to our findings that Cav-1 deletion in NSPCs reduces proliferation, we hypothesized that Cav-1 regulates proteins and pathways involved cell cycle dynamics and proliferation.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Stephanie Cologna

PROVIDER: MSV000090289 | MassIVE |

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Similar Datasets

Gene expression in the hippocampal DG in WT and Cav3.1KO mice

Project description:Low-threshold voltage gated T-type calcium channels are characterized by unique electrophysiological features with the fast inactivation and slow deactivation kinetics. Previous reports suggest that T-type calcium channels may be involved in the adult hippocampal neurogenesis, however, function of T-type calcium channels in newly generated cells is still uncertain. We demonstrated that Cav3.1 is predominantly localized in the NPCs in mouse SGZ, and that deletion of Cav3.1 attenuates proliferation and survival in 5-bromo-2'-deoxyuridine (BrdU)-labeled new born cells in the hippocampal DG. To reveal mechanism underlying impaired adult hippocampal neurogenesis in Cav3.1 KO mice, gene expression in the hippocampal DG is compared between WT and Cav3.1 KO mice. We here defined several altered genes related with cell apoptosis, proliferation and neuronal differentiation in Cav3.1 KO mice.

2021-09-15 | GSE158131 | GEO

miR-17-92 cluster regulates adult hippocampal neurogenesis, anxiety and depression

Project description:Emerging evidence has shown that noncoding RNAs, particularly microRNAs (miRNAs), contribute to the pathogenesis of mood and anxiety disorders, although the molecular mechanisms are poorly understood. Here we show altered levels of miR-17-92 in adult hippocampal neural progenitors have a significant impact in neurogenesis and anxiety- and depression-related behaviors in mice. miR-17-92 deletion in adult neural progenitors causes a decrease, while its overexpression an increase of neurogenesis in the dentate gyrus, through regulating genes in the glucocorticoid pathway, especially serum- and glucocorticoid-inducible protein kinase-1 (Sgk1). miR-17-92 knockout mice show anxiety- and depression-like behaviors, whereas miR-17-92 overexpressing mice exhibit anxiolytic and antidepression-like behaviors. Furthermore, we show that miR-17-92 expression in the adult mouse hippocampus responds to chronic stress, and miR-17-92 rescues proliferation defects, induced by corticosterone, in hippocampal neural progenitors. Our study uncovers a crucial role for miR-17-92 in adult neural progenitors to regulate neurogenesis and anxiety- and depression-like behaviors.

2016-12-09 | GSE83636 | GEO

Kat2a regulates hippocampal memory formation

Project description:Kat2a regulates hippocampal memory formation

| PRJNA231958 | ENA

GSAP regulates mitochondrial function through Mitochondria-associated ER membrane in the pathogenesis of Alzheimer’s disease

Project description:Gamma-secretase activating protein (GSAP) plays an important role in regulating gamma-secretase activity and specificity, which contributes to the pathogenesis of Alzheimer’s disease (AD) and Down syndrome. GSAP is expressed in a variety of cell types in the bain. To elucidate the molecular function of GSAP across different cell types in the brain, we performed single nuclei RNA sequencing (sn-RNAseq) on hippocampal tissues obtained from wildtype (WT) and GSAP knockout (GKO) mice. To further investigate the pathogenic function of GSAP in the AD progression, we also determined effects of GSAP gene deletion in the J20 AD mouse model through sn-RNAseq on hippocampal tissues obtained from J20;WT and J20;GKO mice.

2021-05-27 | GSE157985 | GEO

Mediator Med23 regulates adult hippocampal neurogenesis

Project description:Mediator Med23 regulates adult hippocampal neurogenesis

| PRJNA638362 | ENA

Mediator Med23 regulates adult hippocampal neurogenesis

Project description:we provide evidence that Med23 is involved in the regulation of adult hippocampal neurogenesis in mouse. Med23-deficient NSCs in the SGZ display faster self-renewal activity possibly by reducing cell cycle length, but neuroblasts, immature and mature new-born neurons are reduced.

2020-06-10 | GSE152113 | GEO

Acetyl CoA metabolism by ACSS2 regulates neuronal histone acetylation and hippocampal memory [RNA-seq In Vivo]

Project description:Metabolic production of acetyl-CoA has been linked to histone acetylation and gene regulation, however the mechanisms are largely unknown. We show that the metabolic enzyme acetyl-CoA synthetase 2 (ACSS2) is a critical and direct regulator of histone acetylation in neurons and of mammalian spatial object memory. We observe increased nuclear ACSS2 in differentiating neurons in vitro. Genome-wide, ACSS2 binding corresponds with increased histone acetylation and gene expression of key neuronal genes. These data indicate that ACSS2 functions as a chromatin-bound co-activator to increase local concentrations of acetyl-CoA and to locally promote histone acetylation for transcription of neuron-specific genes. Remarkably, in vivo attenuation of hippocampal ACSS2 expression in adult mice impairs long-term spatial memory, a cognitive process reliant on histone acetylation. ACSS2 reduction in hippocampus also leads to a defect in upregulation of key neuronal genes involved in memory, and these hippocampal genes are pre-bound by ACSS2. These results reveal a unique connection between cellular metabolism, gene regulation, and neural plasticity, establishing a link between generation of acetyl-CoA “on-site” at chromatin of critical neuronal genes.

2017-05-01 | GSE90855 | GEO

Acetyl CoA metabolism by ACSS2 regulates neuronal histone acetylation and hippocampal memory [RNA-seq In Vitro]

2017-05-01 | GSE90854 | GEO

Acetyl CoA metabolism by ACSS2 regulates neuronal histone acetylation and hippocampal memory [in vivo ChIP-seq]

2017-05-01 | GSE90853 | GEO

A fatty acid oxidation-dependent metabolic shift regulates adult neural stem cell quiescence

Project description:Adult hippocampal neurogenesis is important for certain forms of cognition and failing neurogenesis has been implicated in neuropsychiatric diseases. The neurogenic capacity of hippocampal neural stem/progenitor cells (NSPCs) depends on a balance between quiescent and proliferative states. However, how this balance is regulated remains poorly understood. Here we show that the rate of fatty acid oxidation (FAO) defines quiescence vs. proliferation in NSPCs. Quiescent NSPCs show high levels of carnitine palmitoyltransferase 1a (Cpt1a)-dependent FAO, which is downregulated in proliferating NSPCs. Pharmacological inhibition and conditional deletion of Cpt1a in vitro and in vivo leads to altered NSPC behavior, showing that Cpt1a-dependent FAO is required for stem cell maintenance and proper neurogenesis. Strikingly, experimental manipulation of malonyl-CoA, the metabolite that regulates levels of FAO, is sufficient to induce exit from quiescence and to enhance NSPC proliferation. Thus, the data presented here identify a shift in FAO metabolism that governs NSPC behavior and suggest an instructive role for fatty acid metabolism in regulating NSPC activity.

2019-11-15 | PXD005598 | Pride

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