The short chain fatty acid (SCFA) receptor (free fatty acid receptor-3; FFAR3) is expressed in pancreatic beta cells; however, its role in insulin secretion is not clearly defined. Here, we examined the role of FFAR3 in insulin secretion. Using islets from global knockout FFAR3 (Ffar3-/-) mice, we explored the role of FFAR3 and ligand-induced FFAR3 signaling on glucose stimulated insulin secretion. RNA sequencing was also performed to gain greater insight into the impact of FFAR3 deletion on the islet transcriptome. First exploring insulin secretion, it was determined that Ffar3-/- islets secrete more insulin in a glucose-dependent manner as compared to wildtype (WT) islets. Next, exploring its primary endogenous ligand, propionate, and a specific agonist for FFAR3, signaling by FFAR3 inhibited glucose-dependent insulin secretion, which occurred through a Gai/o pathway. To help understand these results, transcriptome analyses by RNA-sequencing of Ffar3-/- and WT islets observed multiple genes with well known roles in islet biology to be altered by genetic knockout of FFAR3. Our data shows that FFAR3 signaling mediates glucose stimulated insulin secretion through Gai/o sensitive pathway. Future studies are needed to more rigorously define the role of FFAR3 by in vivo approaches. Overall design: Analysis of total RNA from 3 biological replicates of pancreatic islets isolated from free fatty acid receptor 3 knockout (Ffar3 KO) and wildtype (Ffar3 WT) male mice
FFAR3 modulates insulin secretion and global gene expression in mouse islets.
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View SamplesWe profiled the skeletal muscle transcriptome between wild type and aB-crystallin/HspB2 knock mice exposed to normal chow and high fat diets to examine the role of aB-crystallin/HspB2 in diet induced obesity. Combined with metabolic profiling of the mice, these data reveal that aB-crystallin/HspB2 is involved in the genesis of insulin resistance on a high fat diet, and we provide extensive RNA profiling to illuminate potential mechanistic insights into the muscle-specific role of aB-crystallin/HspB2. Overall design: Hind limb muscle mRNA profiles of wild type and aB-crystallin/HspB2 knock mice exposed to either normal chow or high fat diets using RNAseq analysis
αB-crystallin and HspB2 deficiency is protective from diet-induced glucose intolerance.
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View SamplesThe purpose of this study was to deteremine gene expression changes in when HMCES is inactivated. We found very few changes. Overall design: Compare wild type and HMCES knockout U2OS cancer cells using RNA-seq.
HMCES Maintains Genome Integrity by Shielding Abasic Sites in Single-Strand DNA.
Specimen part, Cell line, Subject
View SamplesLMO2 is a component of multisubunit DNA-binding transcription factor complexes that regulate gene expression in hematopoietic stem and progenitor cell development. Enforced expression of LMO2 causes leukemia by inducing hematopoietic stem cell-like features in T-cell progenitor cells, but the biochemical mechanisms of LMO2 function have not been fully elucidated. In this study we systematically dissected the LMO2/LDB1 binding interface to investigate the role of this interaction in T-cell leukemia. Alanine scanning mutagenesis of the LIM interaction domain of LDB1 revealed a discrete motif R320LITR required for LMO2 binding. Most strikingly, co-expression of full length, wild type LDB1 increased LMO2 steady state abundance, whereas co-expression of mutant proteins deficient in LMO2 binding compromised LMO2 stability. These mutant LDB1 proteins also exerted dominant negative effects on growth and transcription in diverse leukemic cell lines. Raw gene expression data on HSB-2 cells is presented here. Overall design: RNAseq were performed on HSB cell lines to examine their expression patterns
LMO2 Oncoprotein Stability in T-Cell Leukemia Requires Direct LDB1 Binding.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Stability of gene expression in human T cells in different gravity environments is clustered in chromosomal region 11p15.4.
Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Dynamic gene expression response to altered gravity in human T cells.
Cell line
View SamplesWe investigated differentially regulated genes in human Jurkat T lymphocytic cells in 20s and 5min microgravity and in hypergravity and compared expression profiles to identify potential gravity-regulated genes and adaptation processes.
Dynamic gene expression response to altered gravity in human T cells.
Cell line
View SamplesWe investigated differentially regulated and stably expressed genes in human Jurkat T lymphocytic cells in 5min simulated microgravity and hypergravity and compared expression profiles to identify gravity-regulated and unaffected genes as well as adaptation processes.
Stability of gene expression in human T cells in different gravity environments is clustered in chromosomal region 11p15.4.
Cell line
View SamplesWe investigated differentially regulated genes in human Jurkat T lymphocytic cells in 20s and 5min microgravity and in hypergravity and compared expression profiles to identify potential gravity-regulated genes and adaptation processes.
Dynamic gene expression response to altered gravity in human T cells.
Cell line
View SamplesWe report downstream gene expression changes in stem cells of the adult mouse hair follicle upon conditional ablating of the transcription factor Forkhead Box C1 transcription factor (FOXC1). Hair follicles undergo cycles of rest (telogen; Tel) and regeneration (anagen; Ana). As such, we performed our analysis on these two different stages of hair follicles. Overall design: mRNA-sequencing of WT vs. Foxc1-conditional or inducible KO (Foxc1-cKO or iKO) hair follicle stem cells (HFSCs) purified from mouse dorsal back skin by flow-activated cell sorting (FACS).
FOXC1 maintains the hair follicle stem cell niche and governs stem cell quiescence to preserve long-term tissue-regenerating potential.
Specimen part, Cell line, Subject
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