Filters
Technology
Platform
GSE37667
Homo sapiens
27 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Although the specific functions of sleep have not been completely elucidated, the literature has suggested that sleep is essential for proper homeostasis. Sleep loss is associated with changes in behavioral, neurochemical, cellular, and metabolic function as well as impaired immune response. We evaluated the gene expression profiles of healthy male volunteers who underwent 60 hours of prolonged wakefulness (PW) followed by 12 hours of sleep recovery (SR) using high-resolution microarrays. Peripheral whole blood was collected at 8 am in the morning before the initiation of PW (baseline), after the second night of PW, and one night after SR. We identified over 500 genes that were differentially expressed. Notably, these genes were related to DNA damage and repair and stress response as well diverse immune system responses such as natural killer pathways including killer cell lectin-like receptors family, as well granzymes and T-cell receptors which play important roles in host defense. These results support the idea that sleep loss can lead to alterations in molecular processes that result in perturbation of cellular immunity, induction of inflammatory responses, and homeostatic imbalance. Moreover, expression of multiple genes was down-regulated following PW and up-regulated after SR compared to PW, suggesting an attempt of the body to re-establish internal homeostasis. In silico validation of alterations in the expression of CETN3, DNAJC and CEACAM genes, confirmed previous findings related to the molecular effects of sleep deprivation. Thus, the present findings confirm that the effects of sleep loss are not restricted to the brain and can occur intensely in peripheral tissues.
Publication Title
Whole blood genome-wide gene expression profile in males after prolonged wakefulness and sleep recovery.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 13 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Non-syndromic cleft lip/palate (NSCL/P) is a complex, frequent congenital malformation, determined by the interplay between genetic and environmental factors during embryonic development. Previous findings have appointed an aetiological overlap between NSCL/P and cancer, and alterations in similar biological pathways may underpin both conditions. Here, using a combination of transcriptomic profiling and functional approaches, we report that NSCL/P dental pulp stem cells exhibit dysregulation of a co-expressed gene network mainly associated with DNA double-strand break repair and cell cycle control (p = 2.88x10-2 5.02x10-9). This network included important genes for these cellular processes, such as BRCA1, RAD51, and MSH2, which are predicted to be regulated by transcription factor E2F1. Functional assays support these findings, revealing that NSCL/P cells accumulate DNA double-strand breaks upon exposure to H2O2. Furthermore, we show that E2f1, Brca1 and Rad51 involved in DNA repair are co-expressed in the developing embryonic orofacial primordia, and may act as a molecular hub playing a role in lip and palate morphogenesis. In conclusion, we show that cellular defences against DNA damage may take part in the pathogenesis of NSCL/P, in accordance with the hypothesis of aetiological overlap between this malformation and cancer. These results provide more information regarding the aetiology of NSCL/P and have the potential tocan potentially assist incontribute to the development of future preventive strategies.
Publication Title
Susceptibility to DNA damage as a molecular mechanism for non-syndromic cleft lip and palate.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 4 Downloadable Samples
Description
RNA was isolated from siCTRL, siNSUN2 and ALYREF-RIP HeLa cells, and multiple mouse tissues using the TRIzol (Invitrogen) reagent by following the company manual. Approximately 2.5 µg of total RNA was then used for library preparation using a TruSeq™ RNA Sample Prep Kit v2 (Illumina, San Diego, CA, USA) according to the manufacturer’s protocol.The libraries were sequenced using HiSeq3000 (Illumina) or HiSeq2500 in paired-read mode, creating reads with a length of 101 or 125 bp. Sequencing chemistry v2 or v4 (Illumina) was used. Overall design: Examination of gene expressive levels in siCTRL, siNSUN2 and ALYREF-RIP HeLa cells, and multiple mouse tissues
Publication Title
5-methylcytosine promotes mRNA export - NSUN2 as the methyltransferase and ALYREF as an m<sup>5</sup>C reader.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 35 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Modeling non-syndromic autism and the impact of TRPC6 disruption in human neurons.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 26 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
iPSC were obtained from DPC from TRPC6-mut patient, a idiopathic autistic patient and a control. Original DPC and iPSC obtained were submited to expression analysis in order to check if the expression pattern obtained for the iPSC cells were closer related to embyonic cells than to the original DPC
Publication Title
Modeling non-syndromic autism and the impact of TRPC6 disruption in human neurons.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 9 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
As TRPC6 channel induces CREB-mediated trancription, Dental pulp cells from TRPC6-mut patient and from 6 controls were analyzed in order to verify if the disruption of TRPC6 leads to transcriptional changes.
Publication Title
Modeling non-syndromic autism and the impact of TRPC6 disruption in human neurons.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 33 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Over expression of PDGF-C in mouse liver resulted in the progression of hepatic fibrosis, steatosis and the development of HCC; this mouse model closely resembles the human HCC that is frequently associated with hepatic fibrosis.
Publication Title
Acyclic retinoid targets platelet-derived growth factor signaling in the prevention of hepatic fibrosis and hepatocellular carcinoma development.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 5 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
The discreteness of cell fates is an inherent and fundamental feature of multicellular organisms. Here we show that cross-antagonistic mechanisms of actions of MyoD and PPARg, which are the master regulators of muscle and adipose differentiation, respectively, confer the robustness to the integrity of cell differentiation. Simultaneous expression of MyoD and PPARg in mesenchymal stem/stromal cells led to the generation of a mixture of multinucleated myotubes and lipid-filled adipocytes. Interestingly, hybrid cells, i.e., lipid-filled myotubes, were not generated, suggesting that these differentiation programs are mutually exclusive. Mechanistically, while exogenously expressed MyoD was rapidly degraded in adipocytes through ubiquitin-proteasome pathways, exogenously expressed PPARg was not down-regulated in myotubes. In PPARg-expressing myotubes, PPARg-dependent histone hyperacetylation was inhibited in a subset of adipogenic gene loci, including that of C/EBPa, an essential effector of PPARg. Thus, the cross-repressive interactions between MyoD- and PPARg-induced differentiation programs ensure the discrete cell fate decisions.
Publication Title
Antagonism between the master regulators of differentiation ensures the discreteness and robustness of cell fates.
Sample Metadata Fields
Cell line, Treatment
View Samples- Xenopus laevis
- 4 Downloadable Samples
- Affymetrix Xenopus laevis Genome Array (xenopuslaevis)
Description
A balance between cell survival and apoptosis is essential for animal development. Although proper development involves multiple interactions between germ layers, little is known about the intercellular and intertissue signaling pathways that promote cell survival in neighboring or distant germ layers . We show that serum- and glucocorticoid-inducible kinase 1 (SGK1) promoted ectodermal cell survival during early Xenopus embryogenesis through a non-cell-autonomous mechanism. Dorsal depletion of SGK1 in Xenopus embryos resulted in shortened axes and reduced head structures with defective eyes, and ventral depletion led to defective tail morphologies. Although the gene encoding SGK1 was mainly expressed in the endoderm and dorsal mesoderm, knockdown of SGK1 caused excessive apoptosis in the ectoderm. SGK1-depleted ectodermal explants showed little or no apoptosis, suggesting non-cell-autonomous effects of SGK1 on ectodermal cells. Microarray analysis revealed that SGK1 knockdown increased the expression of genes encoding FADD and caspase-10, components of the death-inducing signaling complex (DISC). Inhibition of DISC function suppressed excessive apoptosis in SGK1-knockdown embryos. SGK1 acted through the transcription factor nuclear factor kappaB to stimulate production of bone morphogenetic protein 7 (BMP7), and overexpression of BMP7 in SGK1-knockdown embryos reduced the abundance of DISC components. We show that phosphoinositide 3-kinase (PI3K) functioned upstream of SGK1, thus revealing an endodermal and mesodermal pathway from PI3K to SGK1 to NF-kappaB that produces BMP7, which provides a survival signal to the ectoderm by decreasing DISC function.
Publication Title
The kinase SGK1 in the endoderm and mesoderm promotes ectodermal survival by down-regulating components of the death-inducing signaling complex.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Rattus norvegicus
- 3 Downloadable Samples
- Illumina HiSeq 2000
Description
Applied de novo assembly, both protein coding and non-coding RNAs were profiled in AFB1 induced HCC and AFB1 resistant liver sample. Compared with normal liver, the perturbation on transcriptome was revealed in multiple aspects, implying the potential mechanism of toxic resistance. Overall design: All rats were randomly divided into control and treated groups according to their weight. Then AFB1 was injected intraperitoneally to treated group in customized schedule. Biopsy was applied every 10 weeks on both groups. Tissues from rats died of HCC were reserved. All rats were sacrificed at 70th week. According to whether tumor formed, liver tissues from animals in treated group were further divided into AFB1 induced tumor sample and AFB1 resistant sample. Both samples were stored for later transcriptome analysis, as well as the normal sample from control group. RNA profiles of all 3 samples were generated by deep sequencing, using Illumina HiSeq2000 platform.
Publication Title
Distinct response of the hepatic transcriptome to Aflatoxin B1 induced hepatocellular carcinogenesis and resistance in rats.
Sample Metadata Fields
No sample metadata fields
View Samples