A systematic survey of the transcriptional status of individual segments of the developing chick hindbrain (r1-5) and the adjacent region of the embryonic midbrain (m) during the HH11 stage of chick development
Transcriptomic analysis of midbrain and individual hindbrain rhombomeres in the chick embryo.
Specimen part
View SamplesFew families of signaling factors have been implicated in the control of development. Here we identify the neuropeptides nociceptin and somatostatin, a neurotransmitter and neuroendocrine hormone, as a class of developmental signals in chick and zebrafish. We show that signals from the anterior mesendoderm are required for the formation of anterior placode progenitors with one of the signals being somatostatin. Somatostatin controls ectodermal expression of nociceptin and both peptides regulate Pax6 in lens and olfactory progenitors. Consequently, loss of somatostatin and nociceptin signaling leads to severe reduction of lens formation. Our findings not only uncover these neuropeptides as developmental signals, but also identify a long-sought-after mechanism that initiates Pax6 in placode progenitors and may explain the ancient evolutionary origin of neuropeptides, pre-dating a complex nervous system.
Neuropeptides: developmental signals in placode progenitor formation.
Specimen part
View SamplesA microarray analysis (MA) on the F4/80+ CD11b+ macrophages (population P5) isolated from a pool of ipsilateral L4/L5 DRG in spared nerve injured WT and miR-21 cKO
Exosomal cargo including microRNA regulates sensory neuron to macrophage communication after nerve trauma.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Reconstruction of phrenic neuron identity in embryonic stem cell-derived motor neurons.
Specimen part
View SamplesExpression response after induction of putative phrenic neuronal determinants in ES cell-derived motor neurons was compared to a pre-determined list of genes over-expressed in FACS-sorted primary.
Reconstruction of phrenic neuron identity in embryonic stem cell-derived motor neurons.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transcriptome and metabolome analysis of liver and kidneys of rats chronically fed NK603 Roundup-tolerant genetically modified maize.
Sex, Specimen part
View SamplesAnalysis of interferon-stimulated genes (ISGs) in various primary cells and immortalized cell lines, following type 1 interferon (IFN) treatment. Some cell types become resistant to HIV-1 infection following type 1 interferon treatment (such as macrophages, THP-1, PMA-THP-1, U87-MG cells and to a lesser extent, primary CD4+ T cells) while others either become only partially resistant (e.g., HT1080, PMA-U937) or remain permissive (e.g., CEM, CEM-SS, Jurkat T cell lines and U937); for more information see (Goujon and Malim, Journal of Virology 2010) and (Goujon and Schaller et al., Retrovirology 2013). We hypothesized that the anti-HIV-1 ISGs are differentially induced and expressed in restrictive cells compared to permissive cells and performed a whole genome analysis following type 1 IFN treatment in cell types exhibiting different HIV-1 resistance phenotypes.
Human MX2 is an interferon-induced post-entry inhibitor of HIV-1 infection.
Cell line, Treatment, Subject
View SamplesTissue-specific comparison of gene expression levels in T65H translocation mice, either with or without uniparental duplications of Chrs 7 & 11. Identification of highly differentially expressed transcripts.
Chromosome-wide identification of novel imprinted genes using microarrays and uniparental disomies.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Transcriptome profile analysis reflects rat liver and kidney damage following chronic ultra-low dose Roundup exposure.
Sex, Specimen part
View SamplesCachexia, described as a syndrome of weight loss, muscle wasting, fat loss and insulin resistance has been described in patients with chronic liver disease. Whereas extensive work is being done to delineate these molecular pathways in adult patients with chronic liver or other disease, very little is known about these pathways in children with chronic liver disease.
No associated publication
Specimen part, Disease, Subject
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