Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Sensory neurons drive pancreatic cancer progression through glutamatergic cancer-neuron pseudo-synapses

ABSTRACT: The results provide significant insights into the role of Grin2D in regulating the secretion of neurotrophic factors that promote neuritogenesis. Transcriptomic analysis of orthotopically transplanted PDAC cancer cells with a knockout of the NMDA receptor subunit Grin2D, along with dorsal root ganglia (T8–T12) innervating the pancreas, strongly supports this conclusion. Furthermore, RNA-Seq analysis of tumor and ganglion biopsies from PDAC patients was performed to validate the identified gene candidates in a human context. This study tested the hypothesis that neuronal glutamate drives pancreatic cancer progression via glutamate-mediated GluN2D signaling at the cancer-neuron pseudo-synapses.

ORGANISM(S): Mus musculus

PROVIDER: GSE291933 | GEO | 2025/06/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Comparison of gene expression of L. reuteri ATCC 55730 at different growth phase in LDMIII medium

Project description:Comparison of gene expression between L. reuteri ATCC 55730 in LDMIII between early log phase (T8), late log phase (T12) or early stationary phase phase (T16) or late stationary phase (T24)

2011-01-15 | GSE24570 | GEO

Comparison of gene expression of L. reuteri ATCC PTA 6475 at different growth phase in a LDMIII

Project description:Comparison of gene expression between L. reuteri ATCC PTA 6475 in LDMIII between early log phase (T8), late log phase (T12) or early stationary phase phase (T16) or late stationary phase (T24)

2011-01-15 | GSE24415 | GEO

Comparison of gene expression of L. reuteri ATCC 55730 at different growth phase in LDMIII medium

2011-01-15 | E-GEOD-24570 | biostudies-arrayexpress

Comparison of gene expression of L. reuteri ATCC PTA 6475 at different growth phase in a LDMIII

2011-01-15 | E-GEOD-24415 | biostudies-arrayexpress

Sensory neurons drive pancreatic cancer progression through glutamatergic cancer-neuron pseudo-synapses

Project description:Sensory neurons drive pancreatic cancer progression through glutamatergic cancer-neuron pseudo-synapses

| PRJNA1235799 | ENA

The effect of different concentrations of ruminal VFAs on the circadian rhythm of gene expression in ovine ruminal epithelial cells using RNA-seq

Project description:This experiment aimed to investigate the effect of different concentrations of ruminal VFAs on the circadian rhythm of gene expression in ORECs of Grain-diet and Hay-diet groups. The ORECs treated with Grain-VFAs and Hay-VFAs were collected at six different timepoints (T0, T4, T8, T12, T16, and T20) for the circadian rhythm analysis using RNA sequencing.

2025-01-14 | GSE286932 | GEO

Metaplasticity at single glutamatergic synapses.

Project description:Optimal function of neuronal networks requires interplay between rapid forms of Hebbian plasticity and homeostatic mechanisms that adjust the threshold for plasticity, termed metaplasticity. Numerous forms of rapid synapse plasticity have been examined in detail. However, the rules that govern synaptic metaplasticity are much less clear. Here, we demonstrate a local subunit-specific switch in NMDA receptors that alternately primes or prevents potentiation at single synapses. Prolonged suppression of neurotransmitter release enhances NMDA receptor currents, increases the number of functional NMDA receptors containing NR2B, and augments calcium transients at single dendritic spines. This local switch in NMDA receptors requires spontaneous glutamate release but is independent of action potentials. Moreover, single inactivated synapses exhibit a lower induction threshold for both long-term synaptic potentiation and plasticity-induced spine growth. Thus, spontaneous glutamate release adjusts plasticity threshold at single synapses by local regulation of NMDA receptors, providing a novel spatially delimited form of synaptic metaplasticity.

| S-EPMC2911980 | biostudies-literature

The effect of ultrasound-guided erector spinae plane block in postoperative analgesia of patients undergoing abdominal surgery

Project description:Interventions: control group:None;experimental group:In patients with liver cancer, 0.5% ropivacaine T8 ESPB was 15ml on each side (25 cases).Colorectal cancer patients 0.5% ropivacaine T12 ESPB 15ml on each side (25 cases) Primary outcome(s): Pain score Study Design: Parallel

| 2681981 | ecrin-mdr-crc

Evolution of glutamatergic signaling and synapses.

Project description:Glutamate (Glu) is the primary excitatory transmitter in the mammalian brain. But, we know little about the evolutionary history of this adaptation, including the selection of l-glutamate as a signaling molecule in the first place. Here, we used comparative metabolomics and genomic data to reconstruct the genealogy of glutamatergic signaling. The origin of Glu-mediated communications might be traced to primordial nitrogen and carbon metabolic pathways. The versatile chemistry of L-Glu placed this molecule at the crossroad of cellular biochemistry as one of the most abundant metabolites. From there, innovations multiplied. Many stress factors or injuries could increase extracellular glutamate concentration, which led to the development of modular molecular systems for its rapid sensing in bacteria and archaea. More than 20 evolutionarily distinct families of ionotropic glutamate receptors (iGluRs) have been identified in eukaryotes. The domain compositions of iGluRs correlate with the origins of multicellularity in eukaryotes. Although L-Glu was recruited as a neuro-muscular transmitter in the early-branching metazoans, it was predominantly a non-neuronal messenger, with a possibility that glutamatergic synapses evolved more than once. Furthermore, the molecular secretory complexity of glutamatergic synapses in invertebrates (e.g., Aplysia) can exceed their vertebrate counterparts. Comparative genomics also revealed 15+ subfamilies of iGluRs across Metazoa. However, most of this ancestral diversity had been lost in the vertebrate lineage, preserving AMPA, Kainate, Delta, and NMDA receptors. The widespread expansion of glutamate synapses in the cortical areas might be associated with the enhanced metabolic demands of the complex brain and compartmentalization of Glu signaling within modular neuronal ensembles.

| S-EPMC9233959 | biostudies-literature

Glutamatergic neurons induce expression of functional glutamatergic synapses in primary myotubes.

Project description:BackgroundThe functioning of the nervous system depends upon the specificity of its synaptic contacts. The mechanisms triggering the expression of the appropriate receptors on postsynaptic membrane and the role of the presynaptic partner in the differentiation of postsynaptic structures are little known.Methods and findingsTo address these questions we cocultured murine primary muscle cells with several glutamatergic neurons, either cortical, cerebellar or hippocampal. Immunofluorescence and electrophysiology analyses revealed that functional excitatory synaptic contacts were formed between glutamatergic neurons and muscle cells. Moreover, immunoprecipitation and immunofluorescence experiments showed that typical anchoring proteins of central excitatory synapses coimmunoprecipitate and colocalize with rapsyn, the acetylcholine receptor anchoring protein at the neuromuscular junction.ConclusionsThese results support an important role of the presynaptic partner in the induction and differentiation of the postsynaptic structures.

| S-EPMC3276509 | biostudies-literature

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