This SuperSeries is composed of the SubSeries listed below.
Induction of Expandable Tissue-Specific Stem/Progenitor Cells through Transient Expression of YAP/TAZ.
Specimen part
View SamplesTo investigate the role of YAP/TAZ as factors able to convert differentiated cells into stem cells of the same tissue, we compared the expression profiles of pancreatic organoids (yDucts) obtained by doxycycline-inducible expression of YAP in pancreatic acini with original acini and native ducts (Ducts).
Induction of Expandable Tissue-Specific Stem/Progenitor Cells through Transient Expression of YAP/TAZ.
Specimen part
View SamplesTo investigate the role of YAP/TAZ as factors able to convert differentiated cells into stem cells of the same tissue, we compared the expression profiles of mammary organoids (yOrg) obtained by doxycycline-inducible expression of YAP in luminal differentiated mammary cells with original luminal differentiated mammary cells (Lum) and organoids from native mammary stem cells (Org).
Induction of Expandable Tissue-Specific Stem/Progenitor Cells through Transient Expression of YAP/TAZ.
Specimen part
View SamplesTo investigate the role of YAP/TAZ as factors able to convert differentiated cells into stem cells of the same tissue, we compared the expression profiles of neural stem cells (NSCs) obtained by doxycycline-inducible expression of YAP (yNSCs) in neurons with original neurons and neural stem cells (NSCs) treated in the same way.
Induction of Expandable Tissue-Specific Stem/Progenitor Cells through Transient Expression of YAP/TAZ.
Specimen part
View SamplesTo investigate the role of YAP/TAZ as b-catenin inhibitors, we compared the expression profiles of Rex1GFPd2 ES cells transfected with siControl#1, siControl#2, siYAP/TAZ#1, siYAP/TAZ#2 and cultured in 2i medium or PD-only medium
YAP/TAZ incorporation in the β-catenin destruction complex orchestrates the Wnt response.
Specimen part
View SamplesBlood from subjects with cardioembolic stroke and controls was collected, and the RNA extracted was interrogated and whole genome U133 Affymetrix Arrays. Twenty-three control samples and sixty-nine cardioembolic stroke samples were assayed.
Gene expression in peripheral immune cells following cardioembolic stroke is sexually dimorphic.
Specimen part, Subject
View SamplesNotch signaling is widely implicated in mouse mammary gland development and tumorigenesis. To investigate the effects of acute activation of Notch signaling in the mammary epithelial compartment, we generated bi-transgenic MMTV-rtTA; TetO-NICD1 (MTB/TICNX) mice that conditionally express a constitutively active NOTCH1 intracellular domain (NICD1) construct in the mammary epithelium upon doxycycline administration.
Notch promotes recurrence of dormant tumor cells following HER2/neu-targeted therapy.
Sex, Age, Specimen part, Treatment, Time
View SamplesPotassium is one of the essential macronutrients required for plant growth and development. It plays a major role in different physiological processes like cell elongation, stomatal movement, turgor regulation, osmotic adjustment, and signal transduction by acting as a major osmolyte and component of the ionic environment in the cytosol and subcellular organelles.
Gene expression analysis of rice seedling under potassium deprivation reveals major changes in metabolism and signaling components.
Specimen part, Treatment, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Knockout of G protein β5 impairs brain development and causes multiple neurologic abnormalities in mice.
Specimen part
View SamplesGb5 is a divergent, evolutionarily-conserved, member of the heterotrimeric G protein b subunit family that is expressed principally in brain and neuronal tissue. Among Gb isoforms, Gb5 is unique in its ability to heterodimerize with members of the R7 subfamily of the regulator of G protein signaling (RGS) proteins that contain G protein-g like (GGL) domains. Previous studies employing Gb5 knockout mice have shown that Gb5 is an essential stabilizer of GGL domain-containing RGS proteins and regulates the deactivation of retinal phototransduction and the proper functioning of retinal bipolar cells. The purpose of this study is to better understand the functions of Gb5 in the brain outside the visual system by employing molecular biology, immunohistochemistry and confocal imaging technologies. We show here that mice lacking Gb5 have a markedly abnormal neurologic phenotype that includes neurobehavioral developmental delay, wide-based gait, motor learning and coordination deficiencies, and hyperactivity. Using immunohistochemical analysis and a green fluorescent reporter of Purkinje cell maturation we show that the phenotype of Gb5-deficient mice includes, in part, delayed development of the cerebellar cortex, an abnormality that likely contributes to the neurobehavioral phenotype. Multiple neuronally-expressed genes are dysregulated in non-cerebellar portion of Gb5 KO mice.
Knockout of G protein β5 impairs brain development and causes multiple neurologic abnormalities in mice.
Specimen part
View Samples