Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1327138 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Viruses associated with Daphnia mendotae (Arthropoda Cladocera)
| PRJNA182249 | ENA
Project description:Recent pre-clinical data provide strong evidence that short-term starvation before the administration of cytostatic drugs for the chemotherapy of solid tumors leads to significantly higher efficacy and lower toxicity levels. However, these findings have so far not been validated in patients. The aim of this trial is to provide first clinical evidence regarding the impact of pre-chemotherapeutic short-term starvation on response to therapy (primary endpoint). Additionally, progression-free survival, adverse events, and overall survival will be monitored (secondary endpoints). In perspective, short-term starvation before chemotherapy could represent a simple and secure way to improve both efficacy and tolerance of chemotherapies at low cost.
| 2202552 | ecrin-mdr-crc
Project description:1. Quantitative Proteomic Analysis of Isolated Mitochondria. Each group has three replicates: Glc group: Glucose starvation group.
GlcFH group: FH activity inhibition combined with glucose starvation group.
2. Quantitative proteomics analysis was performed to assess intracellular protein disulfide bond levels. The experiment included the following groups, each with three replicates:UOK group: UOK262 cells under glucose starvation; UOKFH group: UOK262 cells overexpressing FH under glucose starvation. V786O group: 786-O cells under glucose starvation; XCT786O group: 786-O cells overexpressing XCT under glucose starvation.
3. Quantitative Proteomics Analysis of Cellular Protein Expression Differences, Each group has three replicates: Glcn group: glucose starvation group. Glcp group: glucose sufficiency group
2025-02-16 | MSV000097130 | MassIVE
Project description:"Starving cancer to death" is pursued for cancer therapy. An intriguing regime is to inhibit glucose transporter GLUT1 in cancer cells. But past attempts are challenged by that cancer cells can somehow tolerate starvation. In addition, during cancer progression, cancer cells may suffer from insufficient nutrient supply, for example due to insufficient angiogenesis. So uncovering mechanism of starvation resistance shall not only shed insight into cancer progression but also benefit cancer therapy. TFE3 is known as a transcription factor capable of activating autophagic genes. Physiological TFE3 activity is regulated by phosphorylation-triggered translocation, which is sensitive to nutrient status. We recently reported TFE3 constitutively localizes to cell nucleus in kidney cancer, promoting cell proliferation even under replete condition. But whether and how TFE3 affects kidney cancer cell sensitivity to starvation is unclear. In this study, we find TFE3 promotes kidney cancer cell resistance to glucose starvation. We show starvation triggers TFE3 protein stabilization through increasing its O-GlcNAcylation. Furthermore, through unbiased functional genomic study, we identify genes sensitive to TFE3 protein level, including SLC36A1, a lysosomal amino acid transporter. We find SLC36A1 is overexpressed in kidney cancer, promotes mTOR activity and kidney cancer cell proliferation. Importantly, SLC36A1 level is directly upregulated by TFE3 upon starvation, which enhances cellular resistance to starvation. Suppressing TFE3 or SLC36A1 significantly increased cellular sensitivity to GLUT1 inhibitor in kidney cancers. Collectively, we uncover a TFE3-SLC36A1 axis that responds to starvation and enhances starvation tolerance in kidney cancer.
2024-03-29 | GSE246789 | GEO
Project description:Pi availability is a significant limiting factor for plant growth in both natural and agricultural systems. To cope with such limiting conditions, plants have adapted developmental and biochemical strategies to enhance Pi acquisition and to avoid starvation. A myriad of genes that are involved in the regulation and display of these strategies have been identified. However, the possible epigenetic components regulating the phosphate starvation responses have not been thoroughly investigated. DNA methylation is a major epigenetic mark involved in diverse biological processes and it may play a critical role in Pi starvation stress adaptation, also changes in DNA methylation can lead to a unique gene expression pattern in response to specific developmental and environmental conditions. Here in we demonstrate that non-CpG DNA methylation is required for proper expression of a number of Pi-limitation responsive genes in Arabidopsis thaliana and results in altered morphologic and physiologic phosphate starvation responses.Our data suggest that DNA methylation is involved in the modulation of Pi starvation responses via the transcriptional regulation of a set of phosphate-starvation responsive genes. Analysis of 8 different treatments, 2 different Organs (Root and Shoot), 2 different Phosphate treatments (High Pi, Low Pi), 2 different Times (Short Term, Long Term), 2 biological replicates for treatment
2015-12-31 | E-GEOD-72770 | biostudies-arrayexpress