Tibial muscular dystrophy (TMD) is a late onset, autosomal dominant distal myopathy that results from mutations in the two last domains of titin. The cascade of molecular events leading from the causative Titin mutations to the preterm death of muscle cells in TMD is largely unknown. To identify these components, we used gene expression profiling of muscle biopsies from TMD patients and healthy controls.
Gene expression profiling in tibial muscular dystrophy reveals unfolded protein response and altered autophagy.
Sex, Specimen part, Disease, Disease stage, Subject
View SamplesThe Pik3cd null females are subfertile and have less growing follicles than their heterozygous littermates in the ovary. These mice poorly respond to the exogenous gonadotropins and ovulate much less oocytes than controls. In addition, the estrodial stimulated GC proliferation in preantral follicles is also impaired in Pik3cd null ovaries. FSH and E2 dramatically activates PI3K/AKT pathway in GCs of wild type mice, but not in the Pik3cd null mice.
Phosphoinositide 3-kinase p110δ mediates estrogen- and FSH-stimulated ovarian follicle growth.
Sex, Age, Specimen part
View SamplesImpairments in certain cognitive processes (e.g., working memory) are typically most pronounced in schizophrenia (SZ), intermediate in bipolar disorder (BP) and least in major depressive disorder (MDD).
Transcriptome Alterations in Prefrontal Pyramidal Cells Distinguish Schizophrenia From Bipolar and Major Depressive Disorders.
Specimen part
View SamplesYEAST STRAIN:
Excess mannose limits the growth of phosphomannose isomerase PMI40 deletion strain of Saccharomyces cerevisiae.
No sample metadata fields
View SamplesAll experiment was done according to the Affymetrix manufacturers protocol. The resulting HGF gingiva expression profile(Hereditary gingival fibromatosis patient Gingiva replicate1 and replicate 2)was compared to normal gingiva control(Normal Gingiva replicate1 and replicate2). The data were collected and analyzed by GCOS 1.2 and GeneSpring 7.2 1-way T test.
A novel locus for maternally inherited human gingival fibromatosis at chromosome 11p15.
No sample metadata fields
View SamplesIn this study, we studied the genomic responses of the Insig and Scap deletion from perinatal lung.
Epithelial SCAP/INSIG/SREBP signaling regulates multiple biological processes during perinatal lung maturation.
Specimen part
View SamplesExpression profiling of 3T3-F442A adipocytes treated with growth hormone (GH, 500 nM) or vehicle (DMEM + 1% BSA) control for 30 min., 4 hr., or 48 hr in three independent experiments. Chronic GH treatment induces metabolic changes consistent with insulin resistance in 3T3-F442A adipocytes.
Profiles of growth hormone (GH)-regulated genes reveal time-dependent responses and identify a mechanism for regulation of activating transcription factor 3 by GH.
No sample metadata fields
View SamplesWe find significant evidence of the OVOL, AP1, STAT1, STAT3, and NFKB1 TFs having important roles in MET. We prioritize known gene/drug targets for follow-up in the clinic, and show that the AP1/MYC TF pair is a strong candidate for intervention. Overall design: Examination of the effects of OVOL1 and OVOL2 overexpression common to prostate cancer and breast cancer models.
A bioinformatics approach reveals novel interactions of the OVOL transcription factors in the regulation of epithelial - mesenchymal cell reprogramming and cancer progression.
No sample metadata fields
View SamplesExpression data from xenograft in BALB/c 6-wk-old nude mice with PC3 prostate cancer cells stably expressing PML or a vector control after treatment of the mice with palbociclib (100mg/kg/day diluted in sodium lactate 50mM pH4 given by gavage) during 5 consecutive days
A CDK4/6-Dependent Epigenetic Mechanism Protects Cancer Cells from PML-induced Senescence.
Specimen part, Cell line
View SamplesThe expression of the forkhead transcription factor CHES1, also known as FOXN3, is reduced in many types of cancers. In vitro, CHES1 expression suppresses cell proliferation in tumor cell lines but not in normal cells. Conversely shRNA-mediated depletion of CHES1 increases tumor cell proliferation.
CHES1/FOXN3 regulates cell proliferation by repressing PIM2 and protein biosynthesis.
Cell line
View Samples