MicroRNA regulates protein expression of cells by repressing translation of specific target messenger transcripts. Loss of the neuron specific microRNA miR-128 in Dopamine D1-receptor expressing neurons in the murine striatum (D1-MSNs) lead to increased neuronal excitability, locomotor hyperactivity and fatal epilepsy.
MicroRNA-128 governs neuronal excitability and motor behavior in mice.
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View SamplesCongenital malformations in facial bones significantly impact the overall representation of the face. Establishing correlations between gene expression and morphogenesis of craniofacial structures may lead to new discoveries of molecular mechanisms of craniofacial development. Thus in the present investigation, we will generate gene expression profiles of facial bones at embryo stage 14.5 to establish their roles in regulating craniofacial development.
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Specimen part
View SamplesCongenital malformations in facial bones significantly impact the overall representation of face. Establishing a correlations between gene expression and morphogenesis of craniofacial structures may lead to new discoveries of molecular mechanisms of craniofacial development. Thus in the present investiation we will generate gene expression profile of different facial bones at different time intrevals over a period of 5 years to establish their roles in regulating craniofacial development
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Specimen part
View SamplesTo characterize genes, pathways, and transcriptional regulators enriched in the mouse cornea, we compared the expression profiles of whole mouse cornea, bladder, esophagus, lung, proximal small intestine, skin, stomach, and trachea.
The Ets transcription factor EHF as a regulator of cornea epithelial cell identity.
Specimen part
View SamplesHair follicles undergo recurrent cycling of controlled growth (anagen), regression (catagen), and relative quiescence (telogen) with a defined periodicity. Taking a genomics approach to study gene expression during synchronized mouse hair follicle cycling, we discovered that, in addition to circadian fluctuation, CLOCK-regulated genes are also modulated in phase with the hair growth cycle. During telogen and early anagen, circadian clock genes are prominently expressed in the secondary hair germ, which contains precursor cells for the growing follicle. Analysis of Clock and Bmal1 mutant mice reveals a delay in anagen progression, and the secondary hair germ cells show decreased levels of phosphorylated Rb and lack mitotic cells, suggesting that circadian clock genes regulate anagen progression via their effect on the cell cycle. Consistent with a block at the G1 phase of the cell cycle, we show a significant upregulation of p21 in Bmal1 mutant skin. While circadian clock mechanisms have been implicated in a variety of diurnal biological processes, our findings indicate that circadian clock genes may be utilized to modulate the progression of non-diurnal cyclic processes.
Circadian clock genes contribute to the regulation of hair follicle cycling.
Sex
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View SamplesCongenital malformations in facial bones significantly impact the overall representation of the face. Establishing correlations between gene expression and morphogenesis of craniofacial structures may lead to new discoveries of molecular mechanisms of craniofacial development. Thus in the present investigation, we will generate gene expression profiles of facial bones at embryo stage 14.5 to establish their roles in regulating craniofacial development.
No associated publication
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
Specimen part
View SamplesWe wished to examine the genes regulated by FoxD3 in pigment cells to gain understanding in how FoxD3 represses melanoblast specification in the neural crest. For technical reasons, we could not use neural crest cells, so we used melanoma cells, since they are derived from neural crest cells. To this end, we transfected B16-F10 mouse melanoma cells with constructs expressing FoxD3, or FoxD3-VP16, in which the C-terminal portion of FoxD3 (which contains the transcriptional repression domain) has been replaced by the VP16 transcriptional activation domain.
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View SamplesWe investigated Smad4-mediated TGF-beta signaling in the development of occipital somite-derived myogenic progenitors during tongue morphogenesis by comparing the transcriptomes of tongue derived from Myf5-Cre;Smad4flox/flox mutant and Myf5-Cre;Smad4flox/+ control mice at day E13.5. Based on gene expression profiles and functional studies, we elucidated the influences Smad4 activity and TGF-beta signaling have on the gene expression profiles underlying tongue development. The data are consistent with the hypothesis that TGF-beta-Smad4-FGF6 signaling cascade plays a crucial role in myogenic cell fate determination and lineage progression during tongue myogenesis.
A TGFβ-Smad4-Fgf6 signaling cascade controls myogenic differentiation and myoblast fusion during tongue development.
Specimen part
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