Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR16232150_1.fastq.gz | Fastqsanger.gz | |||
| SRR16232150_2.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Gene expression levels were determined with control or MCT4 knockdown pancreatic cancer cells. MiaPaca2, Capan-2, and PL45 cells were transfected with non-specific or MCT4-specific RNAi. RNA was harvested at 72 hours post transfection and analyzed on Illumina microarrays.
2014-12-17 | E-GEOD-63231 | biostudies-arrayexpress
Project description:Monocarboxylate Transporter 4 (MCT4) is important for H+/lactate efflux from nucleus pulposus cells in the intervertebral disc of mice. We examined the transcriptomic profile of nucleus pulposus cells in wild-type and MCT4 global knock-out mice using microarrays.
2020-05-15 | GSE130561 | GEO
Project description:Alteromonas sp. genome sequencing
| PRJNA386068 | ENA
Project description:Ion balance is critical for membrane polarity, signaling and bioenergesis in cells. Here, we report that proton distribution resets metabolism and alters growth in hematopoietic cells. Multiple oncogenic mutations in acute myeloid leukemia utilize proton partitioning to enhance growth by epigenetically upregulating H+/lactate-co-transporter, MCT4, shuttling protons extracellularly to increase intracellular pH. Secondarily, activity of metabolic enzymes (hexokinase, pyruvate kinase and glucose-6-phosphate dehydrogenase) is increased, raising carbon flux through glycolysis and pentose phosphate pathway necessary for proliferation. MCT4-overexpression in normal hematopoietic stem and progenitor cells increases growth without malignant transformation. Yet, inhibiting MCT4 in AML decreases pHi and carbon flux that improves animal survival and, unexpectedly, elimination of leukemic initiating cells in vivo. AML with increased MCT4 expression have activating histone mark, H3K27ac, in MCT4 promoter where MLL-AF9 and BRD4 directly bind. These data demonstrate the sequential alteration of metabolism through epigenetic activation of proton regulator and point to cytoplasmic alkalization as a growth promoting strategy exploited by malignant cells. Inhibiting this process may diminish the competitive advantage of leukemia and potentially improve AML treatment.
2020-12-31 | GSE124696 | GEO
Project description:Prochlorococcus is found throughout the euphotic zone in the oligotrophic open ocean. Deep mixing and sinking in aggregates or while attached to particles can, however, transport cells below this sunlit zone, depriving them of light for extended periods of time and influencing their circulation via ocean currents. Viability of these cells over extended periods of darkness could shape the ecology and evolution of the Prochlorococcus collective. We have shown that when co-cultured with a heterotrophic microbe and subjected to repeated periods of extended darkness, Prochlorococcus cells develop a heritable dark-tolerant phenotype – through an apparent epigenetic mechanism – such that they survive longer periods of darkness. Here we examine this adaptation at the level of physiology and metabolism in co-cultures of dark-tolerant and parent strains of Prochlorococcus, each grown with the heterotroph Alteromonas under diel light:dark conditions. The relative abundance of Alteromonas is higher in dark-tolerant than parental co-cultures, while dark tolerant Prochlorococcus cells are also larger, contain less chlorophyll, and are less synchronized to the light:dark cycle. Meta-transcriptome analysis of the cultures further suggests that dark-tolerant co-cultures undergo a coupled shift in which Prochlorococcus uses more organic carbon and less photosynthesis, and Alteromonas uses more organic acids and fewer sugars. Collectively, the data suggest that dark adaptation involves a loosening of the coupling between Prochlorococcus metabolism and the light:dark cycle and a strengthening of the coupling between the carbon metabolism of Prochlorococcus and Alteromonas.
2024-04-23 | GSE264347 | GEO
Project description:We examine how the transcriptome of Prochlorococcus strain NATL2A changes in response to extended light deprivation, both when grown alone and in the presence of a naturally co-occurring heterotroph, Alteromonas macleodii MIT1002.
2018-05-01 | GSE93197 | GEO
Project description:Macrophage activation is a hallmark of atherosclerosis, accompanied by a switch in core metabolism from oxidative phosphorylation to glycolysis. The crosstalk between metabolic rewiring and epigenetic modifications in macrophages is worthy of further investigation. Here, we found that lactate efflux-associated monocarboxylate transporter 4 (MCT4)-mediated histone lactylation is closely related to atherosclerosis. Histone H3 lysine 18 lactylation dependent on MCT4 deficiency activated the transcription of anti-inflammatory genes and tricarboxylic acid cycle genes, resulting in the initiation of local repair and homeostasis. Strikingly, histone lactylation is characteristically involved in the stage-specific local repair process during M1 to M2 transformation, whereas histone methylation and acetylation are not. Gene manipulation and protein hydrolysis-targeted chimerism (PROTAC) technology were used to confirm that MCT4 deficiency favors ameliorating atherosclerosis. Therefore, our study shows that macrophage MCT4 deficiency, which links metabolic rewiring and epigenetic remodeling, plays a key role in training macrophages to become repair and homeostasis phenotypes.
2024-04-08 | GSE262808 | GEO
Project description:Alteromonas sp. chi3 Genome sequencing
| PRJNA891859 | ENA