Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Serca2b inhibition aids T cell activation and selectively promotes tumor cell death

ABSTRACT: Serca2b inhibition aids T cell activation and selectively promotes tumor cell death

PROVIDER: PRJNA675875 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Serca2b inhibition aids T cell activation and selectively promotes tumor cell death

Project description:We found that T cells and tumor cells are differentially dependent on Atp2a2 for their survival. In fact, Atp2a2 KO T cells have increased function, whereas Atp2a2 KO tumor cells die. Thapsigargin is a drug that targets the protein product of Atp2a2: Serca2b. We found that in tumor cells, the SAGA complex transmits TG signals to induce tumor cell death, principally via Ccdc101.

2023-11-10 | GSE161209 | GEO

Inhibition of YTHDF2 triggers proteotoxic cell death in MYC-driven breast cancer

Project description:Inhibition of YTHDF2 triggers proteotoxic cell death in MYC-driven breast cancer

| PRJNA564948 | ENA

JAK inhibition selectively suppresses melanoma lacking IFN-γ pathway

Project description:JAK inhibition selectively suppresses melanoma lacking IFN-γ pathway

| PRJNA828250 | ENA

Pyrimidine de novo synthesis inhibition selectively blocks effector but not memory T-cell development.

Project description:Pyrimidine de novo synthesis inhibition selectively blocks effector but not memory T-cell development.

| PRJNA824308 | ENA

Multicenter AIDS Cohort Study

Project description:Multicenter AIDS Cohort Study

| PRJNA671262 | ENA

Multicenter AIDS Cohort Study

Project description:Multicenter AIDS Cohort Study

| PRJNA671263 | ENA

Inhibition of histone H3K27 demethylases inactivates brachyury (TBXT) and promotes chordoma cell death

Project description:Inhibition of histone H3K27 demethylases inactivates brachyury (TBXT) and promotes chordoma cell death

| PRJNA492132 | ENA

AIDS-related Kaposi's sarcoma

Project description:Kaposi's Sarcoma (KS) is a proliferation of aberrant vascular structures lined by spindle cells, and is caused by a gammaherpes virus (HHV8/KSHV). Its course is aggravated by co-infection with HIV-1, where the timing of infection with HIV-1 and HHV8 is important for the clinical outcome. METHODS: In order to better understand the pathogenesis of KS, we have analysed tissue from two AIDS-KS lesions, and from normal skin by serial analysis of gene expression (SAGE). Semi-quantitative RT-PCR was then used to validate the results. RESULTS: The expression profile of AIDS-related KS (AIDS-KS) reflects an active process in the skin. Transcripts of HHV8 were found to be very low, and HIV-1 mRNA was not detected by SAGE, although it could be found using RT-PCR. Comparing the expression profile of AIDS-KS tissue with publicly available SAGE libraries suggested that AIDS-KS mRNA levels are most similar to those in an artificially mixed library of endothelial cells and leukocytes, in line with the description of KS lesions as containing spindle cells with endothelial characteristics, and an inflammatory infiltrate. At least 64 transcripts were found to be significantly elevated, and 28 were statistically downregulated in AIDS-KS compared to normal skin. Five of the upregulated mRNAs, including Tie 1 and sialoadhesin/CD169, were confirmed by semi-quantitative PCR to be elevated in additional AIDS-KS biopsies. Antibodies to sialoadhesin/CD169, a known marker of activated macrophages, were shown to specifically label tumour macrophages. CONCLUSION: The expression profile of AIDS-KS showed 64 genes to be significantly upregulated, and 28 genes downregulated, compared with normal skin. One of the genes with increased expression was sialoadhesin (CD169). Antibodies to sialoadhesin/CD169 specifically labelled tumour-associated macrophages, suggesting that macrophages present in AIDS-KS lesions belong to a subset of human CD169+ macrophages. Keywords: other

2003-07-16 | GSE514 | GEO

dAdo regulates plant cell death

Project description:dAdo regulates plant cell death

| PRJNA862371 | ENA

LSD1 inhibition induces differentiation and cell death in Merkel cell carcinoma

Project description:Merkel cell carcinoma (MCC) is a highly aggressive, neuroendocrine skin cancer that lacks actionable mutations, which could be utilized for targeted therapies. Epigenetic regulators governing cell identity may represent unexplored therapeutic entry points. Here, we targeted epigenetic regulators in a pharmacological screen and discovered that the lysine-specific histone demethylase 1A (LSD1/KDM1A) is required for MCC growth in vitro and in vivo. We show that LSD1 inhibition in MCC disrupts the LSD1-CoREST complex leading to displacement and degradation of HMG20B (BRAF35), a poorly characterized complex member that is essential for MCC proliferation. Inhibition of LSD1 causes derepression of transcriptional master regulators of the neuronal lineage, activates a gene expression signature resembling normal Merkel cells, and induces cell cycle arrest and cell death. Our study unveils the importance of LSD1 for proliferation and maintaining cell identity in MCC. There is growing evidence that cancer cells exploit cellular plasticity and dedifferentiation programs to evade destruction by the immune system. The combination of LSD1 inhibitors with checkpoint inhibitors may thus represent a promising treatment strategy for MCC patients.

2020-11-03 | PXD020590 | Pride

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