Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Neddylation Signaling Inactivation by Tetracaine Hydrochloride Suppresses Cell Proliferation and Vemurafenib-resistance of Melanoma

ABSTRACT: Neddylation Signaling Inactivation by Tetracaine Hydrochloride Suppresses Cell Proliferation and Vemurafenib-resistance of Melanoma

PROVIDER: PRJNA1142019 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Neddylation Signaling Inactivation by Tetracaine Hydrochloride Suppresses Cell Proliferation and Vemurafenib-resistance of Melanoma

Project description:This study aimed to investigate the transcriptomic changes in A375 cells upon treatment with 400μM tetracaine hydrochloride (TTC) for 24 hours. RNA-seq data were generated from TTC-treated and untreated control A375 cells to identify differentially expressed genes and pathways involved in the cellular response to TTC exposure. The findings may provide insights into the molecular mechanisms underlying the effects of TTC on A375 cells.

2024-09-25 | GSE273497 | GEO

Expression data from BRAFV600E A375 melanoma cells treated with vehicle or vemurafenib

2014-05-20 | GSE42872 | GEO

Vemurafenib, Cetuximab, and Irinotecan Hydrochloride in Treating Patients With Solid Tumors That Are Metastatic or That Cannot Be Removed by Surgery

Project description:This phase I trial studies the side effects and best dose of vemurafenib when given together with cetuximab and irinotecan hydrochloride in treating patients with solid tumors that have spread to other parts of the body or cannot be removed by surgery. Vemurafenib and irinotecan hydrochloride may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Immunotherapy with monoclonal antibodies, such as cetuximab, may help the body’s immune system attack the cancer, and may interfere with the ability of tumor cells to grow and spread. Giving vemurafenib with cetuximab and irinotecan hydrochloride may be a better treatment for solid tumors.

| 2139759 | ecrin-mdr-crc

Expression data from BRAFV600E A375 melanoma cells treated with vehicle or vemurafenib

Project description:Vemurafenib is a BRAF inhibitor with specificity for the most common BRAF mutant encountered in melanomas (BRAFV600E). Vemurafenib suppresses the proliferation of BRAF mutant human melanoma cells by suppressing downstream activation of the MEK/ERK mitogen activated protein kinases. We used microarrays to examine the transcriptional response of a vemurafenib-sensitive BRAFV600E human melanoma cell line (A375) to vemurafenib in order to further delineate the mechanisms by which BRAFV600E drives cell proliferation and energy metabolism in human melanoma. BRAFV600E A375 human melanoma cells were treated with vehicle (0.1% DMSO) or 10 uM vemurafenib for 24 h after which total RNA was extracted. Cells were prepared and RNA was extracted in 3 separate batches (three different cell stocks on three separate days) providing three independent replicates (n=3). Paired replicates (prepared from the same stock of cells on the same day) are denoted by A, B and C.

2014-05-20 | E-GEOD-42872 | biostudies-arrayexpress

Vemurafenib induces a noncanonical senescence-associated secretory phenotype in melanoma cells which promotes vemurafenib resistance

Project description:To explore the characteristics of senescent melanoma cells induced by vemurafenib or cisplatin, melanoma A375 cells were treated with vemurafenib and cisplatin, respectively. The senescent phenotypes were verified by β-gal staining, EdU assay, cell morphology and the senescence-related pathways. RNA-seq was performed to explore the differentially expressed genes in the senescent cells induced by vemurafenib or cisplatin.

2023-07-07 | GSE209769 | GEO

Targeting neddylation is a novel therapeutic strategy for lupus by reconstructing double negative T cell homeostasis

Project description:Systemic lupus erythematosus (SLE) is an autoimmune disorder with systemic inflammation, autoantibody accumulation and organ damage. The abnormalities of double-negative (DN) T cells are considered as an important commander of SLE. Neddylation, an important type of protein post-translational modification (PTM), has been well-proved to regulate T cell-mediated immune response. However, the function of neddylation in SLE remains largely unexplored. Here, we reported that neddylation inactivation with MLN4924 or genetic abrogation of Ube2m in T cells prevented SLE development for decreased DN T cell accumulation. Further investigations revealed that inactivation of neddylation blocked Bim ubiquitination degradation and maintained Bim level in DN T cells, contributing to the apoptosis of the accumulated DN T cells for Fas mutation. Then double knockout (KO) lupus-prone mice (Ube2m-/-Bim-/-lpr) were generated and results showed that loss of Bim interrupted the improvement of DN T cell apoptosis and the consequential relieved lupus symptoms for Ube2m KO. Our findings identified that neddylation inactivation promoted Bim-mediated apoptosis of DN T cells and prevented lupus progress. Clinically, we also found the percentages of DN T cells were improved accompanied with reduced apoptosis of DN T cells in SLE patients. Moreover, the neddylation of Cullin1 was higher while Bim level was decreased in SLE patients compared with healthy control. Meantime, the inhibition of neddylation induced Bim-dependent apoptosis of DN T cells isolated from SLE patients. Together, these findings provide the first evidence of the neddylation role in lupus development, suggesting a novel therapeutic strategy for lupus.

2024-01-26 | PXD045686 | Pride

CDK7 inhibition suppresses Castration-Resistant Prostate Cancer through MED1 inactivation

Project description:CDK7 inhibition suppresses Castration-Resistant Prostate Cancer through MED1 inactivation

| PRJNA515688 | ENA

S1406 Phase II Study of Irinotecan and Cetuximab With or Without Vemurafenib in BRAF Mutant Metastatic Colorectal Cancer

Project description:This randomized phase II trial studies how well irinotecan hydrochloride and cetuximab with or without vemurafenib works in treating patients with colorectal cancer that has spread to nearby tissue or lymph nodes, that has spread to other places in the body, or cannot be removed by surgery. Irinotecan hydrochloride and vemurafenib may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Monoclonal antibodies, such as cetuximab, may block the ability of tumor cells to grow and spread. It is not yet known whether irinotecan hydrochloride and cetuximab are more effective with or without vemurafenib in treating colorectal cancer.

| 2168626 | ecrin-mdr-crc

Anylasis of the diatom Phaeodactylum tricornutum under 64-75-5,Tetracycline hydrochloride stress

Project description:Anylasis of the diatom Phaeodactylum tricornutum under 64-75-5,Tetracycline hydrochloride stress

2023-11-10 | GSE218473 | GEO

Neddylation orchestrates the complex transcriptional and post-transcriptional program that drives axonal myelination

Project description:Myelination is essential for neuronal function and health. In peripheral nerves, >100 causative mutations have been identified that cause Charcot-Marie-Tooth disease, a disorder that can affect myelin sheaths. Among these, a number of mutations are related to essential targets of the post-translation modification neddylation, although how these lead to myelin defects is unclear. Here, we demonstrate that inhibiting neddylation leads to a striking absence of peripheral myelin and axonal loss both in developing and regenerating mouse nerves. Importantly, our data indicate that neddylation exerts a global influence on the complex transcriptional and post-transcriptional program by simultaneously regulating the expression and function of multiple essential myelination signals, including the master transcription factor EGR2 and the negative regulators c-Jun and Sox2, and inducing global secondary changes in downstream pathways, including the mTOR and YAP/TAZ signalling pathways. This places neddylation as a critical regulator of myelination and delineates the potential pathogenic mechanisms involved in CMT mutations related to neddylation.

2024-03-06 | GSE241269 | 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