Anatoly Kiyatkin, Ph.D.

Contact Dr. Kiyatkin

1020 Locust Street
Jefferson Alumni Hall, Suite 269
Philadelphia, PA 19107

(215) 503-4794

Medical School
Ph.D., Moscow Institute of Physics and Technology, Biophysics, 1986

University Appointment
Research Assistant Professor

Research and Clinical Interests
Research interests are focused on the experimental and computational analyses of growth factor and hormone receptor signaling networks. We apply a cross-disciplinary approach that combines experimental studies, nonlinear systems analysis and interactive computational models to achieve a qualitative understanding of integrated signaling responses in normal and malignant cells. Currently our projects encompass: studies of the crosstalk between epidermal growth factor and prolactin-mediated signaling in breast cancer cells; molecular mechanisms and components controlling an alternative MEK-independent route of ERK activation in ER-positive breast cancer cells and the effects of ethanol on this compensatory circuit; system-level research of deregulated invasion and metastasis of squamous carcinoma cells. Through a combination of network analysis, mathematical modeling and experimentation, we plan to identify key switches that promote carcinogenesis and develop novel strategies to effectively treat human cancers with molecular therapeutics.

Publications

Most recent Peer-reviewed Publications

1. Immunogenicity, efficacy, safety, and mechanism of action of epitope vaccine (Lu AF20513) for alzheimer's disease: Prelude to a clinical trial
2. Emergence of bimodal cell population responses from the interplay between analog single-cell signaling and protein expression noise
3. Cross-talk between mitogenic Ras/MAPK and survival PI3K/Akt pathways: A fine balance
4. Prolactin-stimulated activation of ERK1/2 mitogen-activated protein kinases is controlled by PI3-kinase/Rac/PAK signaling pathway in breast cancer cells
5. PI3K/Akt-sensitive MEK-independent compensatory circuit of ERK activation in ER-positive PI3K-mutant T47D breast cancer cells
6. Molecular dynamics simulations reveal that Tyr-317 phosphorylation reduces Shc binding affinity for phosphotyrosyl residues of epidermal growth factor receptor
7. Multistrip western blotting to increase quantitative data output.
8. Systems-level interactions between insulin-EGF networks amplify mitogenic signaling
9. Detection of the active components of calf thymus nuclear proteins (TNP), histones that are binding with high affinity to HIV-1 envelope proteins and CD4 molecules
10. Experimental investigation and probabilistic modeling of switch-like signal transduction systems
11. Anti-Aβ1-11 antibody binds to different β-amyloid species, inhibits fibril formation, and disaggregates preformed fibrils but not the most toxic oligomers
12. Scaffolding protein Grb2-associated binder 1 sustains epidermal growth factor-induced mitogenic and survival signaling by multiple positive feedback loops
13. Inferring dynamic architecture of cellular networks using time series of gene expression, protein and metabolite data
14. Signal processing at the Ras circuit: what shapes Ras activation patterns?
15. Tyr-317 Phosphorylation Increases Shc Structural Rigidity and Reduces Coupling of Domain Motions Remote from the Phosphorylation Site as Revealed by Molecular Dynamics Simulations
16. Immunization with a plant-produced colorectal cancer antigen
17. Erratum: Untangling the wires: A strategy to trace functional interactions in signaling and gene networks (Proceedings of the National Academy of Sciences of the United States of America (October 1, 2002) 99:20 (12841-12846))
18. Untangling the wires: A strategy to trace functional interactions in signaling and gene networks
19. Temperature dependence of the epidermal growth factor receptor signaling network can be accounted for by a kinetic model
20. Crystallographic structure and functional interpretation of the cytoplasmic domain of erythrocyte membrane band 3

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