Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic analysis of U-373MG exposed to synthetic ShK-like peptide from the Jellyfish

ABSTRACT: Jellyfish-derived ShK-like peptides are potent blockers of the voltage-gated potassium channel Kv1.3, which plays key roles in immune cell activation and glioblastoma cell physiology. In this study, we investigated the transcriptomic responses of U-373MG human glioblastoma cells exposed to two synthetic ShK-like peptides, NnK-1 (derived from Nemopilema nomurai) and CBRV1-10493 (derived from Carybdea brevipedalia), at 200 nM for 48 h (n = 3 per group). Since neither peptide affected cell viability at this concentration, 200 nM was selected as the treatment dose. Gene expression profiling was performed using QuantSeq 3' mRNA-Seq on an Illumina NextSeq 550 platform. Differentially expressed genes (DEGs) were identified using EdgeR with TMM+CPM normalization (fold change ≥ 1.5, p-value < 0.05). Exposure to NnK-1 resulted in 149 DEGs, with GO and IPA analyses indicating significant alterations in cell signaling and immune-related functions, including predicted inhibition of neuroinflammatory and immune response pathways associated with neurodegenerative diseases. Exposure to CBRV1-10493 identified 107 DEGs, with GO analysis revealing categories related to neurotransmission. These findings provide insights into the neuro-modulatory and immunological mechanisms of jellyfish ShK-like peptides in glioblastoma cells, and suggest their potential as candidates for therapeutic research in neurodegenerative and immune diseases.

ORGANISM(S): Homo sapiens

PROVIDER: GSE333392 | GEO | 2026/06/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Size matters: Biomolecular compositions of small and large extracellular vesicles in the urine of glioblastoma patients

Project description:Glioblastoma is a fatal and devastating primary brain tumour that poses significant challenges to accurate tumour monitoring and patient treatment. Substantial efforts are underway to develop accurate non-invasive liquid biopsy methods that can routinely assess glioblastoma markers in patient body fluids. We have recently shown that patient urine offers ready access to glioblastoma biomarkers within small extracellular vesicle populations (EVs; <200 nm membrane particles) and can accurately diagnose glioblastoma and reflect changes in glioblastoma pathophysiology. However, little is known about other urinary-EV populations in glioblastoma, and their capacity as biomarkers. In this study, we compared the biochemical properties of small (< 200 nm) and large (200-1000 nm) urinary-EVs using fourier-transform infrared spectroscopy and data independent acquisition mass spectrometry and identified significantly changing molecular distributions across the two EV populations in glioblastoma states. We also determined putative glioblastoma biomarkers associated with large urinary-EV biomarkers by ranking significant proteins with a logistic regression model. Our analysis revealed seven proteins capable of perfectly distinguishing all glioblastoma patients from healthy controls (AUC=1) and accurately classifying 96.7% of all cases as glioblastomas. Many significant large urinary-EV proteins also displayed consistent trends at different glioblastoma clinical timepoints, with protein abundance shifts post-surgery that return to pre-surgical levels at recurrence. Our findings demonstrate that both EV populations facilitate easy access to glioblastoma biomarkers for clinical diagnostics. Putative urinary-EV biomarkers described here merit further validation using comprehensive sets of longitudinal cohorts of glioblastoma urine.

2025-05-06 | PXD051553 | Pride

Regulatory RNA inhibition in human phagocytes using cell-penetrating PNA oligonucleotides

Project description:Here, we determined the ability of peptide nucleic acid (PNA) oligomers, coupled to different cell-penetrating peptides (CPPs), to interfere in regulatory RNA circuits of human blood-derived leukocytes. Using RNA-seq, FACS and confocal microscopy we identified octaarginin as a CPP enabling PNA delivery and sequence-dependent RNA inhibition in blood-derived myeloid cells at nanomolar concentration. At 200 nM, an R8-PNA targeting immune-regulatory microRNA-155 was delivered into nearly 100 % of human macrophages within 24 hours without apparent cytotoxicity, and globally de-repressed microRNA-155 target-mRNAs. This was not observed when coupling the PNA inhibitor to a K3 instead of the R8 peptide. We suggest that CPP choice is a fundamental success-determining factor for therapeutic RNA-inhibition in human myeloid leukocytes.

2021-03-01 | GSE152740 | GEO

Melatonin enhances function of porcine immature Sertoli cells via modulating gene expression and metabolism

Project description:<p>Melatonin (MT), a neurohormone synthesized and secreted primarily by the pineal gland, is of vital function to animal reproduction. However, the effect of MT treatment on porcine immature Sertoli cells (iSCs) remains unclear. Here, MT treatment (10 nM, 36 h) could elevate mitochondrial function and reduce oxidative stress, therefore inhibit apoptosis of porcine iSCs. Transcriptome profiling identified 39 differentially expressed genes (DEGs) (33 known and 6 novel) (MT vs Control), mainly involved in GO terms of steroid metabolic process, glutamine metabolic process, oxidoreductase activity and G protein coupled receptor binding, and KEGG pathways of steroid biogenesis, pyruvate metabolism, NF-kappa B and AMPK signal pathways. RT-qPCR validated 6 DEGs (Phgdh, Scd, Hmgcs1, Cytb, Pck2 and Sqle) induced by MT to be with the similar change trend to RNA-seq results. The protein level of HMGCS1 and the estradiol level were confirmed to be significantly decreased by MT (10 nM, 36 h) treatment of porcine iSCs. Inhibition of HMGCS1 in porcine iSCs could significantly reduce the level of estradiol. The levels of cholesterol content within cells and lactate in culture medium were unchanged by MT (10 nM, 36 h). 14 metabolites were significantly altered by MT (10 nM, 36 h) treatment of porcine iSCs. Which were involved in multiple vital metabolic pathways. Collectively, MT treatment of porcine iSCs could promote functions of porcine iSCs via modulating gene expression and metabolism.</p>

2025-01-06 | MTBLS11126 | MetaboLights

MHC-II peptidome of the CNS reveals endogenous guardian peptides

Project description:The central nervous system (CNS), despite the presence of strategically positioned anatomical barriers designed to protect it, is not entirely isolated from the immune system. In fact, it remains physically connected to and can be influenced by the peripheral immune system. How the CNS retains such responsiveness while maintaining “immune privilege” remains an outstanding conundrum. In searching for molecular cues that derive from the CNS and allow its direct communication with the immune system, we discovered a repertoire of CNS-derived endogenous guardian peptides presented on major histocompatibility complex (MHC) II molecules at the CNS borders. During homeostasis, a preponderance of these guardian peptides were found to be bound to MHC II molecules throughout the path of lymphatic drainage from the brain to its surrounding meninges and its draining cervical lymph nodes. With neuroinflammatory disease, however, the presentation of guardian peptides was diminished. Fascinatingly, boosting the presence of these guardian peptides reinforced a population of suppressor CD4+ T cells and significantly reduced CNS autoimmune disease. This unexpected discovery of CNS-derived autoimmune guardian peptides may be the molecular key adapting the CNS to receive information and to maintain continuous dialogue with the immune system while balancing overt autoreactivity. This sheds new light on how we conceptually think about and therapeutically target neuroinflammatory and neurodegenerative diseases.

2024-10-11 | GSE240691 | GEO

Chimeric RNA RRM2-C2orf48 plays an oncogenic role in the development of NNK-induced lung cancer

Project description:Chimeric RNAs have been used as biomarkers and therapeutic targets for multiple types of cancers. However, less attention has been paid to their mechanism of action in neoplasia. Here, we report that chimeric RNA RRM2-C2orf48 promotes 4-(methyl nitrosamine)-1-(3-pyridinyl)-1-butanone (NNK)-induced lung cancer. We found that RRM2-C2orf48 had higher expression levels in lung cancer cell lines and in lung cancer tissues from 74 patients than in normal cells and tissues, respectively. And its expression level was correlated with smoking. Next, we demonstrate that the expression level of RRM2-C2orf48 could increase after treatment with 200 mg/L NNK for 24 h. Overexpressing RRM2-C2orf48 accelerated the process of NNK-induced lung cancer and promoted cell growth. Meanwhile, suppressing RRM2-C2orf48 inhibited cell growth. Finally, we identified miR-219a-2-3p as a potential target of RRM2-C2orf48. In summary, RRM2-C2orf48 accelerated the process of NNK-induced lung cancer and miR-219a-2-3p may be involved in this process.

2022-11-19 | GSE217991 | GEO

Methylglyoxal activates the NRF2 pathway and impairs immune responses controlling the growth control of Mycobacterium tuberculosis (Mtb) in macrophages.

Project description:We compared the transcriptome profile of M. tuberculosis-infected murine bone marrow derived macrophages (BMM) treated or not with 200 uM methylglyoxal (MGO) and uninfected controls as described below. We found 3606 differentially expressed genes (DEGs) between uninfected and M. tuberculosis-infected BMM, being approximately half of these upregulated . 1699 DEGs were determined by comparing Mtb-MGO vs M. tuberculosis BMM, with 2/3 of these DEGs downregulated. Genes in the glyoxalate, glutathione and selenocompound metabolic KEEG pathways were increased comparing Mtb-MGO vs M. tuberculosis BMM. Instead genes involved in type I IFN responses, cytokine receptor and chemokine signalling gene ontology clusters (GO) were increased after infection with Mtb as compared to uninfected controls and decreased in Mtb-MGO vs M. tuberculosis BMM.

2024-07-20 | GSE271061 | GEO

Identification of natriuretic peptide receptor A (NPR-A) expression signatures in podocytes in vivo reveals baseline control of protective pathways including Protein S

Project description:Natriuretic peptide receptor-A (NPR-A) is the principal receptor for the natriuretic peptides ANP and BNP. Targeted deletion of NPR-A in mouse glomerular podocytes significantly enhances renal injury in vivo in the DOCA-salt experimental model. It was therefore hypothesized that natriuretic peptides exert a direct protective effect on glomerular barrier integrity through activation of NPR-A and modulation of gene expression patterns in podocytes. RNA-seq analysis revealed a total of 158 DEGs with 81 downregulated DEGs and 77 upregulated DEGs in Npr1 deficient podocytes. Among the downregulated genes were protein S and semaphorin 3G, which are known to have a protective effect in podocytes. Protein S was also expressed in and secreted from isolated human glomeruli. GO enrichment analysis revealed that the upregulated DEGs in NPR-A deficient podocytes were associated with cell migration and motility. In line, BNP significantly decreased podocyte outgrowth from cultured glomeruli.

2024-10-02 | GSE249221 | GEO

Endogenous self-peptides guard CNS immune privilege

Project description:The central nervous system (CNS), despite the presence of strategically positioned anatomical barriers designed to protect it, is not entirely isolated from the immune system1,2. In fact, it remains physically connected to and can be influenced by the peripheral immune system. How the CNS retains such responsiveness while maintaining an immunologically unique status remains an outstanding conundrum. In searching for molecular cues that derive from the CNS and allow its direct communication with the immune system, we discovered a repertoire of CNS-derived endogenous regulatory self-peptides presented on major histocompatibility complex (MHC) II molecules at the CNS borders. During homeostasis, a preponderance of these regulatory self-peptides were found to be bound to MHC II molecules throughout the path of lymphatic drainage from the brain to its surrounding meninges and its draining cervical lymph nodes. With neuroinflammatory disease, however, the presentation of regulatory self-peptides diminished. Upon boosting the presentation of these regulatory self-peptides, a population of suppressor CD4+ T cells could be expanded, controlling CNS autoimmunity in a CTLA-4 and TGF dependent manner. This unexpected discovery of CNS-derived autoimmune self-peptides may be the molecular key adapting the CNS to maintain continuous dialogue with the immune system while balancing overt autoreactivity. This sheds new light on how we conceptually think about and therapeutically target neuroinflammatory and neurodegenerative diseases.

2024-10-11 | GSE272901 | GEO

Endogenous self-peptides guard CNS immune privilege [TCR-seq]

Project description:The central nervous system (CNS), despite the presence of strategically positioned anatomical barriers designed to protect it, is not entirely isolated from the immune system1,2. In fact, it remains physically connected to and can be influenced by the peripheral immune system. How the CNS retains such responsiveness while maintaining an immunologically unique status remains an outstanding conundrum. In searching for molecular cues that derive from the CNS and allow its direct communication with the immune system, we discovered a repertoire of CNS-derived endogenous regulatory self-peptides presented on major histocompatibility complex (MHC) II molecules at the CNS borders. During homeostasis, a preponderance of these regulatory self-peptides were found to be bound to MHC II molecules throughout the path of lymphatic drainage from the brain to its surrounding meninges and its draining cervical lymph nodes. With neuroinflammatory disease, however, the presentation of regulatory self-peptides diminished. Upon boosting the presentation of these regulatory self-peptides, a population of suppressor CD4+ T cells could be expanded, controlling CNS autoimmunity in a CTLA-4 and TGF dependent manner. This unexpected discovery of CNS-derived autoimmune self-peptides may be the molecular key adapting the CNS to maintain continuous dialogue with the immune system while balancing overt autoreactivity. This sheds new light on how we conceptually think about and therapeutically target neuroinflammatory and neurodegenerative diseases.

2024-10-11 | GSE276987 | GEO

Endogenous self-peptides guard CNS immune privilege [TCR_Dura-dCLN]

Project description:The central nervous system (CNS), despite the presence of strategically positioned anatomical barriers designed to protect it, is not entirely isolated from the immune system1,2. In fact, it remains physically connected to and can be influenced by the peripheral immune system. How the CNS retains such responsiveness while maintaining an immunologically unique status remains an outstanding conundrum. In searching for molecular cues that derive from the CNS and allow its direct communication with the immune system, we discovered a repertoire of CNS-derived endogenous regulatory self-peptides presented on major histocompatibility complex (MHC) II molecules at the CNS borders. During homeostasis, a preponderance of these regulatory self-peptides were found to be bound to MHC II molecules throughout the path of lymphatic drainage from the brain to its surrounding meninges and its draining cervical lymph nodes. With neuroinflammatory disease, however, the presentation of regulatory self-peptides diminished. Upon boosting the presentation of these regulatory self-peptides, a population of suppressor CD4+ T cells could be expanded, controlling CNS autoimmunity in a CTLA-4 and TGF dependent manner. This unexpected discovery of CNS-derived autoimmune self-peptides may be the molecular key adapting the CNS to maintain continuous dialogue with the immune system while balancing overt autoreactivity. This sheds new light on how we conceptually think about and therapeutically target neuroinflammatory and neurodegenerative diseases.

2024-10-11 | GSE273051 | 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