Pluripotency-associated transcription factor Foxd3 is required for maintaining pluripotent cells. However, the molecular mechanisms underlying its function are largely unknown. Here, we report that Foxd3 maintains the ESC identity through counteracting differentiation induction of Calcienurin-NFAT signaling.
Foxd3 suppresses NFAT-mediated differentiation to maintain self-renewal of embryonic stem cells.
Specimen part, Cell line, Treatment
View SamplesWe generated three kinds of genetically identical mouse reprogrammed cells: induced pluripotent stem cells (iPSCs), nuclear transfer embryonic stem cells (ntESCs) and iPSC-nt-ESCs that are established after successively reprogramming of iPSCs by nuclear transfer (NT). NtESCs show better developmental potential than iPSCs, whereas iPSC-nt-ESCs display worse developmental potential than iPSCs.
No associated publication
Sex, Specimen part, Cell line
View SamplesNEDD9 is important for lung cancer metastasis. However, the detailed mechanism remains elusive. Using the microarray data generated with human lung cancer cell lines with either NEDD9 overexpression or NEDD9 knockdown, we plan to idnetify important signal pathways regulated by NEDD9. This may explain how NEDD9 excutes its function in lung cancer.
NEDD9 promotes lung cancer metastasis through epithelial-mesenchymal transition.
Specimen part, Cell line
View SamplesThe intestinal epithelial barrier plays a critical role in the mucosal immunity. However, it remains largely unknown how the epithelial barrier is maintained after damage. Here we show that FGF2 synergizes with IL-17A to induce genes for repairing of damaged epithelium. Deficiency of FGF2 or IL-17A resulted in impaired epithelial proliferation, increased pro-inflammatory microbiota outgrowth, and consequently worse pathology in a DSS-induced colitis model.
Growth Factor FGF2 Cooperates with Interleukin-17 to Repair Intestinal Epithelial Damage.
Specimen part
View SamplesAlthough a wide range of interactions between BRs and auxin have been recognized, knowledge about the direct molecular mechanism of interaction between them in specific physiological processes is very limited. In this study we found that auxin resisitent mutant msg2/iaa19 and arf7 were also resisitant to the BR effect on morphogenensis of dark-grown Arabidosis seedlings. Moreover, BR signaling transcription factor BZR1 can directly bind to promoter regions of IAA19 and ARF7.
Brassinosteroids regulate the differential growth of Arabidopsis hypocotyls through auxin signaling components IAA19 and ARF7.
Specimen part, Treatment
View SamplesThe young panicles 2 cm length were used for expression analysis in well watered control and drought stressed treatment. The panicle samples from biological replicates of six rice varieties were obtained in three independent experiments. The expression profiles were generated using Affymetrix rice genome arrays.
Comparative Analysis of Expression Profiles of Panicle Development among Tolerant and Sensitive Rice in Response to Drought Stress.
Specimen part, Treatment
View SamplesWe use genetic manipulations of regulators representing different pathways to examine whether transcriptomes progressively resemble dietary restriction when multiple regulators are perturbed.
A Systems Approach to Reverse Engineer Lifespan Extension by Dietary Restriction.
Specimen part
View SamplesUnraveling the mechanisms underlying early neural differentiation of ESCs is crucial to the cell-based therapies of neurodegenerate diseases. Neural fate acquisition is proposed to be controlled by a default mechanism, for which the molecular regulation is not well understood. In this study, we investigated the functional roles of Mediator Med23 in pluripotency and lineage commitment of embryonic stem cells (ESCs). Unexpectedly we found that, despite the largely unchanged pluripotency and self-renewal of ESCs, Med23-depletion rendered the cells prone to neural differentiation in different differentiation assays. Knockdown of other Mediator subunit, Med1 or Med15, did not alter the neural differentiation of ESCs; and Med15 knockdown selectively inhibited endoderm differentiation, suggesting the specificity of cell fate control by distinctive Mediator subunits. Gene profiling revealed that Med23-depletion attenuated the BMP signaling in ESCs. Mechanistically, MED23 modulated Bmp4 expression by controlling the activity of ETS1 that is involved in the Bmp4 promoter-enhancer communication. Interestingly, Med23 knockdown in zebrafish embryos also enhanced the neural development at early embryogenesis, which could be reversible by coinjection of bmp4 mRNA. Taken together, our study reveals an intrinsic, restrictive role of MED23 in early neural development, thus providing new molecular insights for neural fate determination.
Mediator Med23 deficiency enhances neural differentiation of murine embryonic stem cells through modulating BMP signaling.
No sample metadata fields
View SamplesDietary restriction (DR) is the most powerful natural means to extend lifespan. Here we obtain temporally resolved transcriptomes during calorie restriction and intermittent fasting in Caenorhabditis elegans, and find that early and late responses involve metabolism and cell cycle/DNA damage, respectively.
A Systems Approach to Reverse Engineer Lifespan Extension by Dietary Restriction.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A Systems Approach to Reverse Engineer Lifespan Extension by Dietary Restriction.
No sample metadata fields
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