The mechanistic target of rapamycin complex 1 (mTORC1) regulates beta cell growth and mass; yet it remains unclear whether it also directs beta cell functional maturation. To understand the global molecular basis of the phenotype caused by the loss of Raptor in beta cells, we isolated pancreatic islets from 8-week-old RapKO and WT mice. We compared gene-expression profile by Affymetrix microarray of islets, which revealed that a number of mRNAs were dys-regulated in Raptor-deficient islets.
No associated publication
Sex, Specimen part
View SamplesTrophoblast lineages, as the precursor of placenta, are essential for post-implantation embryo survival. However, the regulatory networks for trophoblast development remains incompletely understood. Here, we identified CITED1 as a regulator to induce trophoblast-like differentiation from mESCs. Overexpression of CITED1 in ESCs prompted differentiation towards trophoblast accompanying with elevated expression of trophoblast marker genes. To evaluate the ability of CITED1 to induce trophoblast differentiation at a genome-wide scale, we compared the global transcriptional profiles between CITED1 overexpressing cells and control ESCs by Affymetrix microarray analysis at day 1 and day 2 after transfection.
No associated publication
Specimen part, Cell line
View SamplesThe protein level of OCT4, a core pluripotency transcriptional factor, is vital for embryonic stem cell (ESC) maintenance, differentiation and somatic cell reprogramming. Although OCT4 protein is regulated at multiple scales, the role and regulatory mechanisms of OCT4 ubiquitination in reprogramming remains elusive. We identified the five lysine residues as ubiquitination sites on OCT4, and found that destruction of the ubiquitination can enhance OCT4 activity in reprogramming.
No associated publication
Specimen part
View SamplesInduced pluripotent stem (iPS) cells were produced from reprogramming of somatic cells, and they are shown to possess pluripotent properties similar to embryonic stem (ES) cells. Here we used microarrays to detail the global expression pattern among the ES cells and iPS cells, as well as the original mouse embryo fibroblast (MEF), to identify important players involved in the reprogramming process.
iPS cells produce viable mice through tetraploid complementation.
Specimen part, Cell line
View SamplesWe found miR-125a was a key regulator that stabilizes the commitment and immunoregulatory capacity of Treg cells.To gain insights into the general functional features of miR-125a-deficient Treg cells, we performed a genome-wide gene array analysis on Treg population isolated from the spleens of 6 to 8-week-old miR-125a-deficient and WT mice
No associated publication
Specimen part
View SamplesGerm free (GF) and conventionalized (CONV-D) wild-type C57Bl/6 male mice in the CARB-fed, 24h fasted, and 30d trained states; plus GF and CONV-D CARB-fed Ppara-/- mice. CARB-fed indicates a standard polysaccharide-rich mouse chow diet.
No associated publication
Sex, Specimen part
View SamplesSusceptible and Resistant mouse strain, e.g. DBA/2J and C57BL/6J respectively, were inoculated with a highly pathogenic H5N1 influenza A virus (A/Hong Kong/213/2003) for 72 hours.
Host genetic variation affects resistance to infection with a highly pathogenic H5N1 influenza A virus in mice.
Sex
View SamplesThis SuperSeries is composed of the SubSeries listed below.
CHOP induces activating transcription factor 5 (ATF5) to trigger apoptosis in response to perturbations in protein homeostasis.
Specimen part, Treatment
View SamplesDisruption of protein folding in the endoplasmic reticulum triggers the Unfolded Protein Response (UPR), a transcriptional and translational control network designed to restore protein homeostasis. Central to the UPR is PERK phosphorylation of the alpha subunit of eIF2 (eIF2~P), which represses global translation coincident with preferential translation of mRNAs, such as ATF4 and CHOP, that serve to implement the UPR transcriptional regulation. In this study, we used sucrose gradient ultracentrifugation and a genome-wide microarray approach to measure changes in mRNA translation during ER stress. Our analysis suggests that translational efficiencies vary across a broad range during ER stress, with the majority of transcripts being either repressed or resistant to eIF2~P, while a notable cohort of key regulators are subject to preferential translation. From this latter group, we identify IBTKa as being subject to both translation and transcriptional induction during eIF2~P in both cell lines and a mouse model of ER stress. Translational regulation of IBTKalpha mRNA involves the stress-induced relief of two inhibitory uORFs in the 5'-leader of the transcript. Depletion of IBTKalpha by shRNA reduced viability of cultured cells coincident with increased caspase 3/7 cleavage, suggesting that IBTKalpha is a key regulator in determining cell fate during the UPR.
Selective mRNA translation during eIF2 phosphorylation induces expression of IBTKα.
Specimen part
View SamplesAnalysis of gene expression in lungs of C57BL/6J mice that develop chronic airway disease phenotypes after a single Sendai virus infection, compared with mice treated with UV-inactivated virus.
Persistent activation of an innate immune response translates respiratory viral infection into chronic lung disease.
Sex, Time
View Samples