Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

PhosphoRiboTrap sequencing data of chemogenetic MCH neuron activation

ABSTRACT: PhosphoRiboTrap sequencing data of chemogenetic MCH neuron activation

PROVIDER: PRJNA609068 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11193429_1.fastq.gz	Fastqsanger.gz
	SRR11193429_2.fastq.gz	Fastqsanger.gz
	SRR11193430_1.fastq.gz	Fastqsanger.gz
	SRR11193430_2.fastq.gz	Fastqsanger.gz
	SRR11193431_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 44

Similar Datasets

PhosphoRiboTrap sequencing data of chemogenetic MCH neuron activation

Project description:We report phosphoRiboTrap experiments result which aim to explore the nature of the cell types in the Median Eminence (ME) regulated as a consequene of chemogenetic MCH neuron activation. Control and MCH-hM3Dq mice were 12 hrs-fasted and i.p. injected with CNO (3 mg/kg), Arcuate (ARC) and median eminence expat were extracted for preciptation of S6-marked ribosomes from both groups of mice. Extracted RNA from Immunoprecipitated ribosomes (IP) and total tissue (ARC+ME) from each mouse were subjected to deep mRNA sequencing. By analyzing the overlap of genes enriched in the IP/Input of MCH neuron activated mice with previously identified cell types using single cell mRNA sequencing of cells in the mediobasal hypothalamus (Campbell et al., 2017), we identified gene clusters which were activated upon MCH neuron activation.

2020-05-07 | GSE146019 | GEO

Single nucleus sequecing data of MCH neurons [scRNA-seq]

Project description:In order to understand heterogeneity of MCH neurons, by using MCH-Cre dependent ZsGreen (fl/fl) reporter mice, we isolated nuclear from 16 hypothalami of 16 mice at the age of 16-18weeks. Through flow cytometry, we were able to distinguish ZsGreen positive nuclei, and collected puried MCH nuclei in suspension. Those nuclei suspension were subjected to single cell sequence by 10x™ GemCode™ Technology for further single nuleus mRNA analysis and unravel subclusters of MCH neurons

2020-05-07 | GSE146020 | GEO

Genes that were altered after chemogenetic activation of endogenous oxytocin in the dorsal horn

Project description:Purpose: RNAseq analysis was carried out to investigate the alterd genes by chemogenetic activation of endogenous oxytocin in the superficial layer (laminae I-II) and deep layer (laminae III-VI) of the dorsal horn. Methods: At 120 min after the s.c. administration of Saline or CNO (1 mg/kg) (n=3, each), adult male oxytocin-hM3Dq-mCherry transgenic rats were decapitated immediately without being anesthetized. Spinal cords specimens including laminae I-II and III-VI were collected separately. Results: 254 genes in the laminae I-II, and 191 genes in the laminae III-VI of the dorsal horn were significantly altered after chemogenetic activation of endogenous oxytocin.

2022-09-07 | GSE210528 | GEO

A chemogenetic screen for neuro-immune interactions in the gut: Trpv1+ nociceptor neurons control T regulatory cells

Project description:Neuroimmune crosstalk is critical for intestinal and tissue homeostasis. Yet the role of molecularly distinct subsets of gut-innervating neurons in regulating the activity of gut immunocytes, and the mechanisms of this neuroimmune signaling remain unclear. Here, we performed a chemogenetic and flow cytometry-based analysis of mice targeting eight different peripheral neuron subsets to assess how gut immunocytes are altered following neural activation. We found that distinct neurons modulated discreet anatomical populations of immunocytes in the gut in ileum, cecum, and colon. Nos1+ neuron activation decreased the percentage of RORg+ ileal conventional CD4+ T cells, whereas ChAT+ neuron activation decreased ileal neutrophils. Trpv1+ neuron activation displayed the most robust immunomodulatory phenotype, causing downregulation of RORg+ T regulatory cells in the colon and cecum. The immune cells exhibited decreased proliferation, enhanced cell stress, and altered cell activation markers. Further genetic and pharmacological approaches showed that spinal afferent Trpv1+ neurons specifically decreased Treg cells by signaling via the neuropeptide CGRP. Our study provided a comprehensive understanding of neuro-immune interactions, revealing a role for mechanisms by which Trpv1+ neurons regulate gut Treg cells.

2024-04-01 | GSE240982 | GEO

Transcriptome Analysis of Ciliary-Dependent MCH Signaling in Differentiating 3T3-L1 Preadipocytes

Project description:We sequenced total 12 samples: 3 samples at day 0 without Insulin induction, 3 samples at day 0 with MCH treatment, 3 samples at day 2 after insulin induction, 3 samples at day 2 after insulin inducation and MCH treatment.

2021-03-01 | GSE145452 | GEO

Sleep-active hypothalamic MCH-system modulates hippocampal synaptic plasticity and is vulnerable in early Alzheimer’s Disease

Project description:In Alzheimer’s disease (AD), pathophysiological changes in the hippocampus cause deficits in episodic memory formation, leading to cognitive impairment. Hippocampal hyperactivity and decreased sleep quality are associated with early AD, but their basis is poorly understood. We find that homeostatic mechanisms transiently counteract increased excitatory drive of hippocampal CA1 neurons in AppNL-G-F mice, but fail to stabilize it at control levels. Spatial transcriptomics (ST) analysis identifies the Pmch gene encoding Melanin-Concentrating Hormone (MCH) as part of the adaptive response in AppNL-G-F mice. Hypothalamic MCH peptide is produced in sleep-active lateral hypothalamic neurons that project to CA1 and modulate memory. We show that MCH downregulates synaptic transmission and modulates firing rate homeostasis in hippocampal neurons. Moreover, MCH reverses the increased excitatory drive of CA1 neurons in AppNL-G-F mice. Consistent with our finding that a reduced fraction of MCH-neurons is active in AppNL-G-F mice, these animals spend less time in rapid eye movement (REM) sleep. In addition, MCH-axons projecting to CA1 become progressively impaired in both AppNL-G-F mice and AD patients. Our findings identify the MCH-system as vulnerable in early AD and suggest that impaired MCH-system function contributes to aberrant excitatory drive and sleep defects, which can compromise hippocampal-dependent functions.

2023-09-07 | GSE225181 | GEO

Effects of optogenetic and chemogenetic LC activation on the hippocampal transcriptome

Project description:The locus coeruleus noradrenergic (LC-NA) system plays an important role in organizing a physiological response to acute stress. However, if and how the LC affects stress-mediated transcriptomic changes in the brain is still barely understood. Here, we extensively characterize LC mediated transcriptomic response during acute stress in the hippocampus. Combining for the first time bulk mRNA-sequencing and selective chemogenetic and optogenetic manipulations of the LC-NA system

2023-02-02 | GSE218313 | GEO

LEP-MCH conditioned childhood obesity

Project description:LEP-MCH conditioned childhood obesity

| PRJEB50693 | ENA

Krencik NPCs, iAstros, Chemogenetic iAstros, OptoNeurons

Project description:Krencik NPCs, iAstros, Chemogenetic iAstros, OptoNeurons

| PRJNA777567 | ENA

MeCP2 binds to mCH as neurons mature, influencing transcription and onset of Rett syndrome [ChIP-Seq]

Project description:The postnatal neurodevelopmental disorder Rett syndrome (RTT) is caused by mutations in the gene encoding Methyl-CpG-binding Protein 2 (MeCP2). Despite decades of research, it remains unclear how MeCP2 actually regulates transcription or why RTT features appear only 6-18 months after birth. We examined MeCP2 binding to methylated cytosine in the CH context (mCH, where H = A, C, or T) in the adult mouse brain and found that MeCP2 binds these mCH sites, influencing nucleosome positioning and transcription. Strikingly, this pattern is unique to the mature nervous system, as it requires the increase in mCH after birth to reveal differences in MeCP2 binding to mCG, mCH, and non-methylated DNA elements. This study provides insight into the molecular mechanism governing MeCP2 targeting and how this targeting might contribute to the delayed onset of RTT symptoms. MeCP2 ChIP-Seq were conducted from ~ 7-week-old hypothalamus tissues from Mecp2-/y; MECP2-EGFP mice.

2015-04-15 | E-GEOD-66868 | biostudies-arrayexpress

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