Sec15 Controls STAT3 Traffic Direction to Modulate Hematopoietic Stem Cell Fate
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1184176 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To advance the development of our gene expression approach in uncovering regulatory pathways, we utilized whole-genome microarray expression profiling as a discovery platform to identify genes that could illuminate the role of the Sec15 gene. Liver tissues from Sec15 knockout and control mice were collected at six weeks of age to perform comparative analyses. This approach aimed to identify key gene expression changes linked to Sec15 deficiency
2024-11-14 | GSE281520 | GEO
Project description:RNA pol II Dynamics Modulate Co-transcriptional Chromatin Modification, CTD phosphorylation and transcriptional direction
| PRJNA382974 | ENA
Project description:Metabolic reprogramming is an active regulator of stem cell fate choices, and successful stem cell differentiation in different compartments requires the induction of oxidative phosphorylation. However, the mechanisms that promote mitochondrial respiration during stem cell differentiation are poorly understood. Here we demonstrate that Stat3 promotes muscle stem cell myogenic lineage progression by stimulating mitochondrial respiration. We identify Fam3a, a cytokine-like protein, as a major Stat3 downstream effector in muscle stem cells. We demonstrate that Fam3a is required for muscle stem cell commitment and skeletal muscle development. We show that myogenic cells secrete Fam3a, and exposure of Stat3-ablated muscle stem cells to recombinant Fam3a in vitro and in vivo rescues their defects in mitochondrial respiration and myogenic commitment. Together, these findings indicate that Fam3a is a Stat3-regulated secreted factor that promotes muscle stem cell oxidative metabolism and differentiation, and suggests that Fam3a is a potential tool to modulate cell fate choices.
2019-03-19 | GSE128527 | GEO
Project description:Translational control is a widespread mode of gene regulation in organisms ranging from bacteria to mammals. Computational models posit that translational control of protein expression during elongation is exerted through a traffic jam of multiple ribosomes at ribosome pause sites on mRNAs. Yet neither the in vivo frequency of ribosome traffic jams nor the contribution of such traffic jams to protein expression has been measured in any organism. Here we show that upon starvation for single amino acids in the bacterium Escherichia coli, ribosome traffic jams are pervasive across the transcriptome, but they occur at only a subset of codons cognate to the limiting amino acid, and their severity is determined by the translation efficiency of mRNAs. Surprisingly, a computational model based on the observed traffic jams at ribosome pause sites is quantitatively inconsistent with measured protein synthesis rates. By comparison, a model incorporating abortion of protein synthesis at ribosome pause sites in addition to ribosome traffic jams predicts protein synthesis rate with higher accuracy. Consistent with the latter model, a significant fraction of the nascent polypeptides at ribosome pause sites is degraded through the activity of the transfer-messenger RNA during amino acid starvation in E. coli. Our work provides a minimal, experimentally-constrained model for predicting protein expression from ribosome dynamics, and it suggests the existence of a trade-off between the cellular translational capacity and the processivity of protein synthesis in vivo. 6 samples for ribosome profiling and 5 samples for total mRNA profiling
2014-05-15 | E-GEOD-51052 | biostudies-arrayexpress
Project description:Many patients have cancers that have increased activity of a protein called STAT3 that contributes critically to the development and growth of their cancer. Despite our knowledge of STAT3’s importance to cancer, scientists and doctors have not developed a drug that targets it and that patients can take to treat their cancer more effectively than treatments that are now available. Tvardi Therapeutics, Incorporated has developed a compound, TTI-101, which can be given by mouth and acts as a direct inhibitor of STAT3. Administration of TTI-101 to mice demonstrated that it blocked growth of cancers of the breast, head and neck, lung, and liver and it was safe when administered at high doses to mice, rats, and dogs. In this application, Tvardi is proposing to further develop TTI-101 for treatment of solid tumors for which the prognosis is dismal. The investigators will determine how safe it is when administered to patients with cancer, determine whether an adequate dose can be administered to patients with cancer that will block STAT3 in their cancer, and determine whether treatment with TTI-101 leads to reduced growth of their cancer.
| 2247646 | ecrin-mdr-crc
Project description:Seeds in the experimental group were exposed to 48 h of traffic noise recorded in a highly congested area of the city, while the control group was kept under background white noise. While traffic noise exposure made no effects on seed germination, noise treatment significantly increased the growth of seedlings by 39%. By employing RNA-sequencing profiling, we further investigated the noise-induced molecular changes in the A. thaliana seedlings. The aberrant expression of 690 genes was detected in the noise-exposed seedlings.
2023-10-15 | GSE240794 | GEO
Project description:Timeline RNAseq of fibroblast to neuron direction conversion
| PRJEB32551 | ENA
Project description:Mass spectrometry analysis of proteins interacting with STAT3¬Flag was performed. STAT3-Flag was transiently expressed in HeLa cells and the interactome of STAT3-Flag was studied in lysosomal extracts. proteins co-¬immunoprecipitating with STAT3--Flag identified eight subunits of the vacuolar H+-¬ ATPase (V-¬ATPase) as potential STAT3 binding partners. Validation experiments were performed by antibody pull-down of STAT3.
2018-08-29 | PXD006788 | Pride
Project description:Traffic-related air pollution has been a common public health problem, which is associated with central nervous system dysfunction according to large-scale epidemiological studies. Current studies are mostly limited to artificial laboratory exposure environments and specific genetic mechanisms remain unclear. In the spring, we transported the aged mice from the laboratory to the 1-meter-high dry platform in the campus and tunnel at the same time. Aged mice were exposed form 7 am to 7 pm each day for 2, 4 and 12 weeks, respectively. Compared with the control group (in campus), the memory function of mice in the exposure group (in tunnel) was significantly impaired in Morris water maze. Traffic-related air pollution exposure increased the number of activated microglia in the hippocampal DG and CA1, and up-regulated mRNA expression of inflammatory factors IL-18, IL-1β, IL-6 and TNF-α. By screening the risk genes of Alzheimer’s disease, we found the mRNA and protein levels of ABCA7 were down-regulated and those of PYK2 were up-regulated in the dorsolateral prefrontal cortex (dPFC) of aged mice. The DNA methylation ratio increased in four CpG sites of abca7 promoter region and decreased in one CpG site of pyk2 promoter region, which were consistent with the altered expression of ABCA7 and PYK2. In conclusion, exposure to the real traffic environment impaired memory function and enhanced neuroinflammation of aged mice, which could be relevant to the alteration of ABCA7 and PYK2 gene expression. Our work provided a new and promising understanding of the pathological mechanisms of cognitive impairment caused by traffic-related air pollution.
2022-07-16 | GSE208109 | GEO
Project description:Cohesin-mediated loop extrusion is blocked at specific cis-elements, including CTCF sites, producing patterns of loops and domain boundaries along chromosomes. Here, we explore such cis-elements, and their role in gene regulation. We find that transcription termination sites of active genes form cohesin- and RNA polymerase II-dependent domain boundaries that do not accumulate cohesin. At these sites, cohesin is first stalled and then rapidly unloaded. Start sites of transcriptionally active genes form cohesin-bound boundaries, as shown before, but are cohesin-independent. Together with cohesin loading possibly at enhancers, these sites create a pattern of cohesin traffic that guides enhancer-promoter interactions. Disturbing this traffic pattern, by removing CTCF, renders cells sensitive to knock-out of genes involved in transcription initiation, such as the SAGA complexes, and RNA processing such DEAD/H-Box RNA helicases. Without CTCF, these factors are less efficiently recruited to active promoters.
2022-08-15 | GSE180657 | GEO