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个人简介

Ph.D. (Doctor of Philosophy)

研究领域

Genomics Proteomics and Bioinformatics

Bioinformatics and Epigenetics Focus on Cancer and Neuroscience My overall research areas are in bioinformatics and epigenetics. I’m particularly interested in roles of epigenetic modifications in controlling processes in neuroscience and cancer. Here, I use epigenetics in the “modern” sense (some would say incorrect sense) to refer to modifications of DNA and histones to control gene expression. I’d add in transcription factors here, too, with the risk of diluting epigenetic to just mean “transcriptional regulation”. In recent times, it has become clear that these epigenetic modifications are a much more critical and flexible system than previously expected. Notably, even in adult cells, direct DNA methylation is subject to change to transduce signals. And in cancer, there is great excitement around targeting epigenetic modifications for therapy and differential diagnosis; in fact, some drugs targeted generally at epigenetic marks are FDA-approved and in current clinical usage. Technological changes (high density, high quality arrays with long probes, “next generation sequencing”, advances in chromatin immunoprecipitation protocols) have led an explosion in high quality, genome-scale data on epigenetic marks. Concomitant with these developments, nearly all (non-proprietary) datasets are available, after publication, via resources like NCBI GEO for public, unfettered access to data. All of these developments, coupled with the increase in other types of genome-scale data, has led to: (1) an acute need for high-quality analysis tools for individual datasets (2) also a need for tools to allow robust and extensible analysis across datasets using different experimental methodologies. Areas of Current Investigation (1) Epigenetic Modifications in Glioma Stem Cells. (2) Development of Novel Analysis Approaches for High-Throughput Chromatin Immunoprecipitation Experiments (3) Development of Novel Frameworks for Integrating Disparate Genome Scale Datasets (4) (in collaboration) Markers for outcomes of cervical cancer therapy; Analysis of transcriptional role of src-mutations in breast cancer

近期论文

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Bieda MC, Su H, MacIver MB (2008) Anesthetics exhibit selective effects on synaptic and tonic GABA-mediated inhibition. Anesth Analgesia in press Acevedo LG*, Bieda M*, Green R, Farnham PJ (2008) Analysis of the mechanisms mediating tumor-specific changes in gene expression in human liver tumors. Cancer Res 68:2641. * denotes co-first authors Johnson et al. (2008) Systematic evaluation of variability in ChIP-chip experiments using predefined DNA targets. Genome Res. 18: 393. Xu S, Bieda MC, Jin VX, Rabinovitch A, Farnham PJ (2007) A comprehensive ChIP–chip analysis of E2F1, E2F4, and E2F6 in normal and tumor cells reveals interchangeable roles of E2F family members. Genome Research 17:550. Yasui DH, Peddada S, Bieda M, Thatcher K, Vallero R, Farnham PJ, LaSalle J (2007) Integrated epigenomic analyses of neuronal MeCP2 reveal a role for long-range interaction with active genes. Proceedings of the National Academy of Science (USA) 104:19146. The ENCODE Project Consortium (2007) The ENCODE pilot project: Identification and analysis of functional elements in 1% of the human genome. Nature 447:799. Krig SR, Jin VX, Bieda MC, O’Geen H, Yaswen P, Green R, Farnham PJ (2007) Identification of genes directly regulated by the oncogene ZNF217 in ChIP-chip assays. Journal of Biological Chemistry 282:9703. Bieda M, Xu X, Singer M, Green R, Farnham PJ (2006) Unbiased location Analysis of E2F1-binding sites suggests a widespread role for E2F1 in the Human Genome. Genome Research, 16:595. Faculty of 1000 Biology: evaluations for Bieda M et al Genome Res 2006 May 16 (5) :595-605http://www.f1000biology.com/article/id/1029798/evaluation Bieda MC, Webb CT (2004) Distribution and patterns of CNSs in a Caenorhabditis gene family. published in SFI Working Papers Series available at:http://www.santafe.edu/research/publications/workingpapers/04-09-026.pdf Bieda MC, MacIver MB (2004) A major role for tonic GABAA conductances in anesthetic suppression of intrinsic neuronal excitability. Journal of Neurophysiology 2004 May 12 [Epub ahead of print] Bieda MC, Copenhagen DR (2004) N-type and L-type calcium channels mediate glycinergic synaptic inputs to retinal ganglion cells. Visual Neuroscience 21:545-550. Bieda MC, Copenhagen DR (2000) Inhibition is not required for the production of transient spiking responses from retinal ganglion cells. Visual Neuroscience 17:243-254. Bieda MC, Copenhagen DR (1999) Sodium action potentials are not required for light-evoked release of GABA or glycine from retinal amacrine cells. Journal of Neurophysiology 81:3092-3095. Dixon DB, Takahashi K-I, Bieda M, Copenhagen DR (1996) Quinine, intracellular pH and modulation of hemi-gap junctions in catfish horizontal cells. Vision Research 36:3925-3931. Rogawski MA, Yamaguichi S, Blake PA, Jones SM, Bieda MC, de Costa BR, Thurkauf A (1992) Anticonvulsant 1-Phenylcycloalkylamine analogs: uncompetitive NMDA antagonists with low motor toxicity. In: Multiple Sigma and PCP Receptor Ligands: Mechanisms for Neuromodulation and Neuroprotection? (Kamenka J-M, Domino EF, eds), pp 747-758. Ann Arbor, MI: NPP Books.

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