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Search Results to Taeju Park

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One or more keywords matched the following properties of Park, Taeju

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research overview Dr. Park’s study is focused on two proteins – Crk and CrkL – that are reported to be elevated in several types of human cancer including glioblastoma (GBM) and correlated with poor prognosis. Tumor cell migration and invasion contribute to the spread of GBM to healthy brain tissues, leading to high recurrence rates. Dr. Park has demonstrated that Crk and CrkL play important roles in GBM cell migration and invasion. Dr. Park is also working on potential role of Crk and CrkL in diffuse intrinsic pontine glioma (DIPG) cell migration and invasion. In addition, Dr. Park is working to develop specific inhibitors of these proteins to block GBM and DIPG cell migration and invasion. In the lab, Dr. Park and his team take advantage of genetically engineered mouse models and the gene knockdown and overexpression technique to study tumorigenic functions of Crk and CrkL. They identified a protein that is activated by elevation of Crk and CrkL and binds to Crk and CrkL. The new malignant connection promotes tumor cell migration and invasion. Dr. Park’s goal is to develop drugs that specifically break down the aberrant protein-protein complex between Crk and CrkL and their binding partners. To test effects of chemical compounds on the binding of these proteins, Dr. Park developed in vitro assay systems and conducted a high-throughput screen. In partnership with the University of Kansas Cancer Center, the team has tested 200,000 chemical compounds and identified more than 600 potential candidate drugs. These compounds are undergoing rigorous post-screening validation using different biochemical experiments. They will continue to expand productive collaboration with KU core facilities to discover novel anticancer drugs. They are optimizing a new quadruple screening to discover inhibitors of both SH2 and SH3 domains of Crk and CrkL. The newly developed inhibitors will be used to advance studies of cancer and other human diseases in which Crk and CrkL play essential roles. Previously, Dr. Park generated mutant mice lacking both Crk and CrkL in the developing brain and demonstrated that Crk and CrkL play essential overlapping functions in neuronal migration during brain development. Recently, genomic analysis of a patient with a severe global developmental delay and ataxia identified two new mutations in Crk and another protein that may interact with Crk. His team generated two mutant mouse strains harboring the two mutations and plan to study individual and combined contributions of the two genes to brain development. These phenotyping results will provide essential knowledge for understanding both the underlying mechanism of the clinical deficits and the signaling pathways in brain development, therefore laying the foundation for developing therapeutic interventions.

One or more keywords matched the following items that are connected to Park, Taeju

Item TypeName
Concept Membrane Proteins
Concept Muscle Proteins
Concept Nerve Tissue Proteins
Concept Nuclear Proteins
Concept Proteins
Concept Recombinant Fusion Proteins
Concept Extracellular Matrix Proteins
Concept Oncogene Proteins v-fos
Concept GTP-Binding Proteins
Concept Tumor Suppressor Proteins
Concept Adaptor Proteins, Vesicular Transport
Concept Adaptor Proteins, Signal Transducing
Concept Green Fluorescent Proteins
Concept Proto-Oncogene Proteins c-crk
Concept Apoptosis Regulatory Proteins
Concept Proto-Oncogene Proteins c-akt
Academic Article Fibroblast Growth Requires CT10 Regulator of Kinase (Crk) and Crk-like (CrkL).
Academic Article Crk proteins transduce FGF signaling to promote lens fiber cell elongation.
Academic Article CRK proteins selectively regulate T cell migration into inflamed tissues.
Academic Article Crk and CrkL are required for cell transformation by v-fos and v-ras.
Academic Article Neurobiology: Reelin mediates form and function.
Academic Article Dendritic planarity of Purkinje cells is independent of Reelin signaling.
Academic Article Crk1/2 and CrkL form a hetero-oligomer and functionally complement each other during podocyte morphogenesis.
Academic Article Essential roles of Crk and CrkL in fibroblast structure and motility.
Academic Article Phospholipase C-delta1 is activated by capacitative calcium entry that follows phospholipase C-beta activation upon bradykinin stimulation.
Academic Article Rapid and simple measurement of serotonin N-acetyltransferase activity by liquid biphasic diffusion assay.
Academic Article Inhibition of ubiquitin ligase Siah-1A by disabled-1.
Academic Article Cardiovascular and craniofacial defects in Crk-null mice.
Academic Article Crk and Crk-like play essential overlapping roles downstream of disabled-1 in the Reelin pathway.
Academic Article Dok-7 regulates neuromuscular synapse formation by recruiting Crk and Crk-L.
Academic Article The adaptor protein CRK is a pro-apoptotic transducer of endoplasmic reticulum stress.
Academic Article Crk1/2-dependent signaling is necessary for podocyte foot process spreading in mouse models of glomerular disease.
Academic Article Cyclic AMP-independent inhibition of voltage-sensitive calcium channels by forskolin in PC12 cells.
Academic Article Inhibition of voltage-sensitive calcium channels by the A2A adenosine receptor in PC12 cells.
Academic Article Crk Adaptor Proteins Regulate NK Cell Expansion and Differentiation during Mouse Cytomegalovirus Infection.
Grant "Requirement of CT10 regulator of kinase (Crk) and Crk-like (CrkL) in glioblastoma growth"
Academic Article Requirement for Crk and CrkL during postnatal lens development.
Academic Article Quantitative assessment of glioblastoma phenotypes in?vitro establishes cell migration as a robust readout of Crk and CrkL activity.
Academic Article Crk and CrkL as Therapeutic Targets for Cancer Treatment.
Academic Article Crk and Crkl have shared functions in neural crest cells for cardiac outflow tract septation and vascular smooth muscle differentiation.
Academic Article Use of phosphotyrosine-containing peptides to target SH2 domains: Antagonist peptides of the Crk/CrkL-p130Cas axis.

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