A5035400785- Autophagy in Disease and Therapy
- Parkinson's Disease Mechanisms and Treatments
- Neurobiology and Insect Physiology Research
- Protein Kinase Regulation and GTPase Signaling
- Nuclear Receptors and Signaling
- Ubiquitin and proteasome pathways
- PI3K/AKT/mTOR signaling in cancer
- Mitochondrial Function and Pathology
- Invertebrate Immune Response Mechanisms
- Cytokine Signaling Pathways and Interactions
- Metabolism, Diabetes, and Cancer
- Hippo pathway signaling and YAP/TAZ
- interferon and immune responses
- Cancer-related Molecular Pathways
- Pancreatic function and diabetes
- FOXO transcription factor regulation
- Signaling Pathways in Disease
- Insect Resistance and Genetics
- Microtubule and mitosis dynamics
- Insect behavior and control techniques
- Developmental Biology and Gene Regulation
- ATP Synthase and ATPases Research
- Cell death mechanisms and regulation
- Aquaculture disease management and microbiota
- Plant Molecular Biology Research
Seoul National University
2016-2025
Institute of Molecular Biology and Genetics
2010-2015
Creative Research
2006-2015
Korea Advanced Institute of Science and Technology
2002-2012
Chungnam National University
2000-2005
Korea Institute of Science and Technology
2002-2003
Pukyong National University
2001
Harvard University
1991-1997
Merck & Co., Inc., Rahway, NJ, USA (United States)
1994
Boston University
1992
Recent studies have indicated that serine phosphorylation regulates the activities of STAT1 and STAT3. However, kinase(s) responsible role in STAT function remain unresolved. In present studies, we examined growth factor-dependent We provide vitro vivo evidence ERK family mitogen-activated protein (MAP) kinases, but not JNK or p38, specifically phosphorylate STAT3 at 727 response to factors. Evidence for additional mitogen-regulated is also provided. a relatively poor substrate all MAP...
Significance VDAC1 transports ions and small molecules at the mitochondrial outer membrane. In this study, we discover that Parkin, a frequently mutated Parkinson disease protein, ubiquitinates in two different manners, poly- monoubiquitination. Interestingly, defective polyubiquitination hinders Parkin-mediated mitophagy, but monoubiquitination induces apoptosis. When deficient with is expressed mammalian cells fruit fly, observe increased calcium influx apoptosis typical vivo phenotypes...
Parkin, an E3 ubiquitin ligase, has been found to be responsible for autosomal recessive juvenile parkinsonism characterized primarily by selective loss of dopaminergic neurons with subsequent defects in movements. However, the molecular mechanisms underlying this neuron remain elusive. Here, we Drosophila parkin loss-of-function mutants, which exhibit shrinkage decreased tyrosine hydroxylase level and impaired locomotion. The behavioral defect mutant flies was partially restored...
Mutations in parkin and LRRK2 together account for the majority of familial Parkinson's disease (PD) cases. Interestingly, recent evidence implicates involvement mitochondrial homeostasis. Supporting this, we show here by means Drosophila model system that, like parkin, mutations induce pathology flies when expressed their flight muscles, toxic effects which can be rescued coexpression. When specifically fly dopaminergic neurons, mutant results appearance significantly enlarged mitochondria,...
Mitophagy has been implicated in mitochondrial quality control and various human diseases. However, the study of vivo mitophagy remains limited. We previously explored using a transgenic mouse expressing mitochondria-targeted fluorescent protein Keima (mt-Keima). Here, we generated mt-Keima Drosophila to extend our efforts vivo. A series experiments confirmed that can be faithfully quantitatively measured Drosophila. also showed alterations upon environmental genetic perturbation Analysis...
Parkinson’s disease (PD) is a progressive neurodegenerative disorder. However, cell type–dependent transcriptional regulatory programs responsible for PD pathogenesis remain elusive. Here, we establish transcriptomic and epigenomic landscapes of the substantia nigra by profiling 113,207 nuclei obtained from healthy controls patients with PD. Our multiomics data integration provides type annotation 128,724 cis-regulatory elements (cREs) uncovers type–specific dysregulations in cREs strong...
Activation of phosphatidylinositol 3-kinase (PI3K) and activation the 70/85-kDa S6 protein kinases (αII αI isoforms, referred to collectively as pp70S6k) have been independently linked regulation cell proliferation. We demonstrate that these lie on same signalling pathway PI3K mediates pp70 by cytokine interleukin-2 (IL-2). also show pp70S6k can be blocked at different points along using specific inhibitors T-cell Inhibition activity with structurally unrelated but highly (wortmannin or...