Sentences with phrase «gene expression programs as»

We use the fission yeast, Schizosaccharomyces pombe, to study the dynamic changes and plasticity of gene expression programs as a function of cell proliferation, quiescence and ageing, and the effect of various genetic and environmental perturbations.

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As a Howard Hughes Medical Institute investigator and biochemistry professor at Stanford, Pat led a team that developed the first methods for analyzing, visualizing and interpreting global gene expression programs.

«Telomerase is a unique protein - RNA complex where the protein subunit uses its RNA component as a template to add identical fragments of DNA to the end of chromosomes,» said Emmanuel Skordalakes, Ph.D., associate professor in the Gene Expression and Regulation program of Wistar's NCI - designated Cancer Center.

The goal of the NIH program, as described on its website, is «to understand the principles behind the three - dimensional organization of the nucleus in space and time (the fourth dimension), the role nuclear organization plays in gene expression and cellular function, and how changes in the nuclear organization affect normal development as well as various diseases.»

What's really impressive about Babar's accomplishment is that he did the work for both papers — one on the role of a population of stem cells in lung cancer development (published in Cell) the other on gene expression in group A Streptococcus (published in PNAS)-- as a participant in summer undergraduate research programs.

«RNAi therapies are a unique approach to cancer treatment as they have the potential to «turn off» the genes» coding for proteins involved in cancer cell division,» said Ramesh K. Ramanathan, M.D., medical director of the Virginia G. Piper Cancer Center Clinical Trials Program at Scottsdale Healthcare and deputy director of the Clinical Translational Research Division of the Translational Genomics Research Institute (TGen) in Phoenix, Ariz. «Using a lipid nanoparticle, the RNAi drug can be delivered to a cancer cell to block the expression of specific proteins involved in tumor growth.»

Now researchers at UC San Francisco have taken the first step toward a comprehensive atlas of gene expression in cells across the developing human brain, making available new insights into how specific cells and gene networks contribute to building this most complex of organs, and serving as a resource for researchers around the world to study the interplay between these genetic programs and neurodevelopmental disorders such as autism, intellectual disability and schizophrenia.

Transcriptome studies such as the National Institute of Health's Genotype - Tissue Expression (GTEx) program aim to overcome this limitation by studying gene expression levels and regulation mechanisms and their relationship with diseases, instead of only DNAExpression (GTEx) program aim to overcome this limitation by studying gene expression levels and regulation mechanisms and their relationship with diseases, instead of only DNAexpression levels and regulation mechanisms and their relationship with diseases, instead of only DNA sequence.

This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.

Maria Mavrikaki, PhD, has been awarded the Eleanor and Miles Shore Harvard Medical School Fellowship, established as part of a cooperative program between Harvard Medical School and McLean Hospital, to support her research on the effects of stress - and sex - regulated microRNAs on gene expression.

Recent theorizing within this tradition suggests that these shifts may be manifested in changes in the relative frequency of particular cell types in blood (Irwin and Cole, 2011) as well as in the epigenetic programming and gene expression of such cells (Miller et al., 2011a).