ADHD is the most common neurobehavioral disorder in school-aged children. In addition to genetic factors, environmental influences or gene x environmental interactions also play an important role in ADHD. One example of a well studied environmental risk factor for ADHD is exposure to polychlorinated biphenyls (PCBs). In this study, we investigated whether the well-established genetic model of ADHD based on the Spontaneously Hypertensive Rat (SHR) and a well established PCB-based model of ADHD exhibited similar molecular changes in brain circuits involved in ADHD. The brains from 28 male rats (8 SHR, 8 Sprague-Dawley (SD) controls, 8 Wistar-Kyoto (WKY) controls, and 4 PCB-exposed SD rats) were harvested at postnatal day 55-65 and RNA was isolated from six brain regions of interest. The RNA was analyzed for differences in expression of a set of 308 probe sets interrogating 218 unique genes considered highly relevant to ADHD or epigenetic gene regulation using the Rat RAE 230 2.0 GeneChip (Affymetrix). Selected observations were confirmed by real time quantitative RT-PCR. The results show that the expression levels of genes Gnal, COMT, Adrbk1, Ntrk2, Hk1, Syt11 and Csnk1a1 were altered in both the SHR rats and the PCB-exposed SD rats. Arrb2, Stx12, Aqp6, Syt1, Ddc and Pgk1 expression levels were changed only in the PCB-exposed SD rats. Genes with altered expression only in the SHRs included Oprm1, Calcyon, Calmodulin, Lhx1 and Hes6.The epigenetic genes Crebbp, Mecp2 and Hdac5 are significantly altered in both models. The data provide strong evidence that genes and environment can affect different set of genes in two different models of ADHD and yet result in the similar disease-like symptoms.
A comparison of molecular alterations in environmental and genetic rat models of ADHD: a pilot study.
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View SamplesThis study examined the expression profile of medullary carcioma of the colon compared to adjacent histologically normal colonic mucosa.
Medullary carcinoma of the colon: a distinct morphology reveals a distinctive immunoregulatory microenvironment.
Specimen part, Disease, Disease stage
View SamplesInsect hemocytes mediate important cellular immune responses including phagocytosis and encapsulation, and also secrete immune factors such as opsonins, melanization factors, and antimicrobial peptides. In Anopheles, they contribute to the defense against malaria parasite invasion during the early sporogonic cycle. We used microarrays to identify transcripts that are specific or enriched in circulating hemocytes compared to either neuronal or to the rest of the body.
Discovery of Plasmodium modulators by genome-wide analysis of circulating hemocytes in Anopheles gambiae.
Specimen part, Treatment
View SamplesInsect hemocytes mediate important cellular immune responses including phagocytosis and encapsulation, and also secrete immune factors such as opsonins, melanization factors, and antimicrobial peptides. In Anopheles, they contribute to the defense against malaria parasite invasion during the early sporogonic cycle.
Discovery of Plasmodium modulators by genome-wide analysis of circulating hemocytes in Anopheles gambiae.
Specimen part
View SamplesThe disrupted genetic mechanisms underlying neural abnormalities in Autism Spectrum Disorder remain mostly unknown and speculative. No biological marker nor genetic signature is currently available to assist with early diagnosis.
Prediction of autism by translation and immune/inflammation coexpressed genes in toddlers from pediatric community practices.
Sex, Specimen part
View SamplesSky1 is a Saccharomyces cerevisiae rich serine-arginine (SR) protein-specific kinase and its enzymatic activity is essential in the cytotoxicity caused by cisplatin, although the molecular mechanisms supporting this function are not understood. We present a transcriptome analysis discriminating between RNA changes induced by cisplatin which are dependent or independent of the Sky1 function.
Sky1 regulates the expression of sulfur metabolism genes in response to cisplatin.
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View SamplesRNASeq data from WT, Zmym2 knockout- and Zmym2 overexpressing- E14tg2a mouse embryonic stem cells Overall design: RNASeq of ESCs in medium containing Serum and Leukaemia Inhibitory Factor (LIF)
ZMYM2 inhibits NANOG-mediated reprogramming.
Subject
View SamplesThe effect of the overexpression of a stabilized version of the transcription factor RELATED TO APETALA2.12 (RAP2.12) on the transcriptome of Arabidopsis rosettes was investigated. To this purpose, 4-week old rosette of wild-type and 35S:13RAP2.12 plants were compared. Samples were composed of pools of 3 plants.
Age-dependent regulation of ERF-VII transcription factor activity in Arabidopsis thaliana.
Age, Specimen part
View SamplesWe reprogrammed human CD34+ cells from cord blood using a lentiviral vector encoding OCT4, SOX2 and KLF4.We collected RNA from parental CD34+ cells (3samples), reprogramming timepoints (9 timepoints), iPS clones derived from this experiment (6 clones), and human ES cell lines (9 samples). All samples were sequenced at 100bp reads. Overall design: Endogenous retroelement expression during reprogramming
Loss of transcriptional control over endogenous retroelements during reprogramming to pluripotency.
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View SamplesThe gene regulatory network in naïve mouse embryonic stem cells (ESCs) must be reconfigured for lineage competence. Tcf3 enables rewiring to formative pluripotency by repressing components of the ESC transcription factor circuitry. However, elimination of Tcf3 only delays, and does not prevent, state transition. Here we delineate distinct contributions of the Ets-family transcription factor Etv5 and the repressor Rbpj. Downstream of Erk1/2 signalling, Etv5 activates enhancers for formative pluripotency. Concomitant up-regulation of Rbpj ensures irreversible exit from the naïve state by extinguishing reversal factors, Nanog and Tbx3. Triple deletion of Etv5, Rbpj and Tcf3 incapacitates ESCs, such that they remain undifferentiated and locked in self-renewal even in the presence of differentiation stimuli. Thus, pluripotency progression is driven hierarchically by two repressors, that respectively dissolve and extinguish the naive network, and an initiator that commissions the formative network. Similar tripartite action may be a general mechanism for efficient cell transitions. Overall design: RNA-seq analysis of parental Rex1-GFPd2 ES cells (RGd2), and deletion mutants generated in this background (Etv5-KO, RbpJ-KO, Etv5-RpbJ-dKO, Etv5-RbpJ-Tcf3-tKO) cultured in 2i, N2B27 or supplemented with Chiron, 3 biological replicates per condition.
Complementary Activity of ETV5, RBPJ, and TCF3 Drives Formative Transition from Naive Pluripotency.
Subject
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