Mitochondria are able to modulate cell state and fate during normal and pathophysiologic conditions through a nuclear mediated mechanism collectively termed as a retrograde response. Our previous studies in Drosophila have clearly established that progress through the cell cycle is precisely regulated by the intrinsic activity of the mitochondrion by specific signaling cascades mounted by the cell. As a means to further our understanding of how mitochondrial energy status affects nuclear control of basic cell decisions we have employed Affymetrix microarray-based transcriptional profiling of Drosophila S2 cells knocked down for the gene encoding subunit Va of the complex IV of the mitochondrial electron transport chain. The profiling data identifies up-regulation of glycolytic genes and metabolic studies confirm this increase in glycolysis. The transcriptional portrait which emerges implicates many signaling systems, including a p53 response, an insulin response, and up-regulation of conserved mitochondrial responses. This rich dataset provides many novel targets for further understanding the mechanism whereby the mitochondrion may direct cellular fate decisions. The data also provides a salient model of the shift of metabolism from a predominately oxidative state towards a predominately aerobic glycolytic state, and therefore provides a model of energy substrate management not unlike that found in cancer.
Expression profiling of attenuated mitochondrial function identifies retrograde signals in Drosophila.
Cell line
View SamplesThe heat-shock stress response was studied at the level of exons using Affymetrix Exon-array profiling for both sense and anti-sense transcripts. Sense transcript profiling was done as per the protocol of Affymetrix Exon 1.0 ST array and anti-sense transcript array profiling was done using a modified protocol (Xijin Ge et al., BMC Genomics. 2008 Jan 22;9:27).
Heat shock factor binding in Alu repeats expands its involvement in stress through an antisense mechanism.
Sex, Specimen part, Cell line
View SamplesThe repertoire of transcripts that are differentially regulated in response to Heat-shock were studied using Illumina WG-6 v2.0 BeadChip.
Heat shock factor binding in Alu repeats expands its involvement in stress through an antisense mechanism.
Sex, Specimen part, Cell line
View SamplesPrenatal alcohol exposure can cause long-lasting changes in functional and genetic programs of the brain, which may underlie behavioral alterations found in FASD.
Ethanol-related alterations in gene expression patterns in the developing murine hippocampus.
Specimen part
View SamplesA Transcriptomics Approach to Study the Biocompatibility and Finding out the Potential Applications of Magnetite (Fe3O4) Nanoparticles
Magnetite (Fe3O4) nanocrystals affect the expression of genes involved in the TGF-beta signalling pathway.
Cell line
View SamplesClinical application of induced pluripotent stem (iPS) cells is limited by low efficiency of iPS derivation, and protocols that permanently modify the genome to effect cellular reprogramming. Moreover, safe and effective means of directing the fate of patient-specific iPS cells towards clinically useful cell types are lacking. Here we describe a simple, non-mutagenic strategy for reprogramming cell fate based on administration of synthetic mRNA modified to overcome innate anti-viral responses. We show that this approach can reprogram multiple human cell types to pluripotency with efficiencies that greatly surpass established protocols. We further show that the same technology can be used to efficiently direct the differentiation of RNA-induced pluripotent stem (RiPS) cells into terminally differentiated myogenic cells. Our method represents a safe, efficient strategy for somatic cell reprogramming and directing cell fates that has broad applicability for basic research, disease modeling and regenerative medicine.
Highly efficient reprogramming to pluripotency and directed differentiation of human cells with synthetic modified mRNA.
Specimen part, Cell line
View SamplesCD47 is a ubiquitous cell surface receptor that limits cell clearance by phagocytes that express its counter-receptor signal-regulatory protein-a and directly regulates T cell immunity by interacting with its inhibitory ligand thrombospondin-1. Murine natural killer (NK) cells express higher levels of CD47 than other lymphocytes, but the role of CD47 in regulating NK cell homeostasis and immune function remains unclear. Cd47-/- mice exhibited depletion of NK precursors in bone marrow, but antisense Cd47 knockdown or gene disruption resulted in a dose dependent accumulation of immature and mature NK cells in spleen. Cd47-/- mice were impaired in controlling chronic Clone-13 lymphocytic choriomeningitis virus (LCMV) infection, which was associated with depletion of splenic NK cells and loss of effector cytokine and interferon response gene expression in Cd47-/- NK cells. These data identify CD47 as a cell-intrinsic and systemic regulator of NK cell homeostasis and NK cell responses to viral infection. Overall design: Examining natural killer (NK) cell intrinsic role of CD47 during viral infection.
CD47 Expression in Natural Killer Cells Regulates Homeostasis and Modulates Immune Response to Lymphocytic Choriomeningitis Virus.
Specimen part, Subject
View SamplesGoal of this study was to determine changes in transcription profile in mock versus G3P treated plants. Arabidopsis (Col-0 ecotype) plants were infiltrated with petiole exudate, with or without G3P, and distal leaves were sampled 24 h post treatments.
Glycerol-3-phosphate is a critical mobile inducer of systemic immunity in plants.
Specimen part
View SamplesIdentification of genes and pathways relevant to Cervical cancer pathogenesis. The study also aimed at identifying probable mechanistic differences in the low and high HOTAIR expressing cervical cancers patients .
Bridging Links between Long Noncoding RNA HOTAIR and HPV Oncoprotein E7 in Cervical Cancer Pathogenesis.
Age, Specimen part
View SamplesE-FABP expression in keratinocytes increase interferons, in particualur IFNlamda, expression, which activate P53, a critical tumor suppessor, to inhibit or prevent chemical-induced skin tumorigenesis.
Epidermal FABP Prevents Chemical-Induced Skin Tumorigenesis by Regulation of TPA-Induced IFN/p53/SOX2 Pathway in Keratinocytes.
Specimen part
View Samples