Jinho Kim - Research
I am interested in how signaling networks evolved to invent new functions and how they are rewired in cancer cells to develop resistance to chemotherapeutic agents. To address these questions, I employ computational models of signaling networks and large-scale protein dynamics data.
Jinho Kim, PhD
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| Tyrosine signaling networks control various cellular functions such as cell-cell communication, proliferation, differentiation, and cell adhesion. We are exploring how tyrosine-signaling networks have been expanded, providing essential devices for the multicellular organism evolution. Since tyrosine signaling networks are highly related to multi-cellularity, we expect this research could provide insight into cancer development, which breaks and avoids the normal regulation of multicellular organisms. |
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Evolution of Tyrosine Signaling
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I aim to uncover critical driver networks of drug resistance, which is a major killer across numerous complex and infectious diseases. To elucidate mechanisms of resistance development against cancer therapies we are conducting an integrative network biology study employing several “omics” data, including exome sequencing and mass-spectrometry data. One of the specific goals of this research is to identify subnetworks responsible for the chemo-resistance. Reconstruction of signaling networks of the chemo-resistant cancer cell lines will provide essential information of how cancer cells gained abilities to multiply without proliferation signals and avoid death signals. |
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| Cell signaling networks are critical to understand almost any change to cellular phenotype and behavior. I aim to develop a network biology framework combining computational and experimental data starting from computational models of specificities of modular protein domains, which play a key role in cell signaling. These specificity models and protein dynamics data, for example from proteomics and phospho-proteomics, will provide essential information into how cell signaling networks operate to respond to various stimuli and be perturbed by disease causing mutations. |
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(Bakal, Science 2008)
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How did cell signaling networks evolve? This is a particularly interesting biological question and may provide insights into how cells work and become dysfunctional. We aim to explore how the Jun N-terminal Kinase (JNK) signaling network has evolved across 200M of years in closely related species. JNK controls several cellular processes including survival or death, proliferation, inflammation and stem cell differentiation. JNK is of high biomedical interest because its mutations have been implicated in different pathological conditions including cancer, diabetes and hepatitis. We are taking a systems level approach combining phospho-proteomics with computational and evolutionary biology, aiming to determine how signaling systems operates and evolve at the network level. |
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