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Cellular Gene Expression (cellular + gene_expression)
Selected AbstractsActively regulating bioengineered tissue and organ formationORTHODONTICS & CRANIOFACIAL RESEARCH, Issue 3 2005DJ Mooney Structured Abstract Authors ,, Mooney DJ, Boontheekul T, Chen R, Leach K Objectives ,, Describe current and future approaches to tissue engineering, specifically in the area of bone regeneration. These approaches will allow one to actively regulate the cellular populations participating in this process. Design ,, Many approaches to actively regulate cellular phenotype are under exploration, and these typically exploit known signal transduction pathways via presentation of specific receptor-binding ligands, and may also deliver mechanical information via the physical bridge formed by the receptor-ligand interactions. Cellular gene expression may also be directly modulated utilizing gene therapy approaches to control tissue regeneration. Conclusions ,, Significant progress has been made to date in bone regeneration using inductive molecules and transplanted cells, and FDA approved therapies have resulted. While approaches to date have focused on delivery of single stimuli (e.g. one growth factor), future efforts will likely attempt to more closely mimic developmental processes by the delivery of multiple inputs to the cells in spatially and temporally regulated fashions. [source] Epigenetic gambling and epigenetic drift as an antagonistic pleiotropic mechanism of agingAGING CELL, Issue 6 2009George M. Martin Summary Generations of biogerontologists have been puzzled by the marked intraspecific variations in lifespan of their experimental model organisms despite all efforts to control both genotype and environment. The most cogent example comes from life table studies of wild-type Caenorhabditis elegans when grown in suspension cultures using axenic media. While nuclear and mitochondrial somatic mutations and ,thermodynamic noise' likely contribute to such lifespan variegations, I raise an additional hypothetical mechanism, one that may have evolved as a mechanism of phenotypic variation which could have preceded the evolution of meiotic recombination. I suggest that random changes in cellular gene expression (cellular epigenetic gambling or bet hedging) evolved as an adaptive mechanism to ensure survival of members of a group in the face of unpredictable environmental challenges. Once activated, it could lead to progressive epigenetic variegation (epigenetic drift) amongst all members of the group. Thus, while particular patterns of gene expression would be adaptive for a subset of reproductive individuals within a population early in life, once initiated, I predict that continued epigenetic drift will result in variable onsets and patterns of pathophysiology , perhaps yet another example of antagonistic pleiotropic gene action in the genesis of senescent phenotypes. The weakness of this hypothesis is that we do not currently have a plausible molecular mechanism for the putative genetic ,randomizer' of epigenetic expression, particularly one whose ,setting' may be responsive to the ecology in which a given species evolves. I offer experimental approaches, however, to search for the elusive epigenetic gambler(s). [source] Differentially expressed cellular genes following HBV: potential targets of anti-HBV drugs?JOURNAL OF VIRAL HEPATITIS, Issue 4 2005J. Yang Summary., The aim of the study was to screen for cellular genes that are differentially expressed following hepatitis B virus (HBV) infection, in an attempt to identify potential targets of anti-HBV drugs. An oligonucleotide microarray containing 231 virus-infection-associated genes was prepared. Differential gene expression in HepG2.2.15 cells compared to control with HepG2 cells was analysed by this in-house microarray. The change in gene expression in HepG2.2.15 cells treated by lamivudine on days 4 and 8 after exposure was also studied. Semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was used to comfirm the differentially expressed genes induced by HBV and lamivudine. There were 31 upregulated and four downregulated genes in HepG2.2.15 cells compared with the HepG2 control cells. Eleven genes were consistently altered by lamivudine at both time points. Of the 31 genes that were upregulated in HepG2.2.15 cells, there were seven genes which were downregulated by lamivudine. Of the four downregulated genes, there was one gene which was upregulated by lamivudine. Of the differentially expressed genes induced by HBV and lamivudine, the expression of five genes was confirmed by semi-quantitative RT-PCR. These results shed new light on the effects of HBV and lamivudine on cellular gene expression. Differentially expressed genes induced by HBV and lamivudine could potentially become new anti-HBV drug targets in novel therapies. [source] Modifications in the human T,cell proteome induced by intracellular HIV-1 Tat protein expressionPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue S1 2006Mayte Coiras Abstract The effects of the human immunodeficiency virus type,1 (HIV-1) Tat protein on cellular gene expression were analysed using a Jurkat cell line that was stably transfected with tat,gene in a doxycycline-repressible expression system. Expressed Tat protein (aa,1,101) was proved to present basically a nuclear localisation, and to be fully functional to induce HIV,LTR transactivation. Tat expression also resulted in protection from Tunicamycin-induced apoptosis as determined by DNA staining and TUNEL assays. We applied proteomics methods to investigate changes in differential protein expression in the transfected Jurkat-Tat cells. Protein identification was performed using 2-D DIGE followed by MS analysis. We identified the down-regulation of several cytoskeletal proteins such as actin, ,-tubulin, annexin,II, as well as gelsolin, cofilin and the Rac/Rho-GDI complex. Down-expression of these proteins could be involved in the survival of long-term reservoirs of HIV-infected CD4+ T,cells responsible for continuous viral production. In conclusion, in addition to its role in viral mRNA elongation, the proteomic approach has provided insight into the way that Tat modifies host cell gene expression. [source] | ||||||||||