Saet-Byel Jung

ORCID: 0000-0001-5747-087X
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About
Contact & Profiles
Research Areas
  • GDF15 and Related Biomarkers
  • Adipose Tissue and Metabolism
  • Chronic Myeloid Leukemia Treatments
  • Tuberculosis Research and Epidemiology
  • Adipokines, Inflammation, and Metabolic Diseases
  • Myeloproliferative Neoplasms: Diagnosis and Treatment
  • Diet and metabolism studies
  • Mycobacterium research and diagnosis
  • Regulation of Appetite and Obesity
  • Immune cells in cancer
  • Nutrition and Health in Aging
  • Immune Response and Inflammation
  • Muscle Physiology and Disorders
  • Kruppel-like factors research

Chungnam National University
2007-2021

University of Pittsburgh Medical Center
2010

University of Pittsburgh
2010

Case Western Reserve University
2010

University School
2010

Reduced mitochondrial electron transport chain activity promotes longevity and improves energy homeostasis via cell-autonomous –non-autonomous factors in multiple model systems. This mitohormetic effect is thought to involve the unfolded protein response (UPRmt), an adaptive stress-response pathway activated by proteotoxic stress. Using mice with skeletal muscle–specific deficiency of Crif1 (muscle-specific knockout [MKO]), integral large mitoribosomal subunit (39S), we identified growth...

10.1083/jcb.201607110 article EN cc-by-nc-sa The Journal of Cell Biology 2016-12-16

Oxidative functions of adipose tissue macrophages control the polarization M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function causes systemic insulin resistance in vivo is not clear. Here, we show that mice with mitochondrial phosphorylation (OxPhos) due to myeloid-specific deletion CR6-interacting factor 1 (Crif1), an essential mitoribosomal involved biogenesis OxPhos subunits, have inflammation. Macrophage GDF15 expression impaired function, induced upon...

10.1038/s41467-018-03998-z article EN cc-by Nature Communications 2018-04-13

To evaluate if p53 decreases Kruppel-Like Factor 2 (KLF2) expression and determine whether p53-mediated suppression of KLF2 plays a role in p53-induced endothelial dysfunction.Endothelial mediates endothelium-dependent vascular homeostasis by differentially regulating genes, leading to an anti-inflammatory antithrombotic surface with normal vasodilatory function. In contrast, the tumor suppressor leads inflammatory gene impairs vasodilatation, thus promoting dysfunction. The effect on was...

10.1161/atvbaha.110.215061 article EN Arteriosclerosis Thrombosis and Vascular Biology 2010-10-15

In this study, we investigated the role of toll-like receptor (TLR) and mitogen-activated protein kinase (MAPK) pathways involved in tumor necrosis factor (TNF)-α interleukin (IL)-6 expression after stimulation with purified derivatives (PPD) or native 38-kDa antigen (Ag) Mycobacterium tuberculosis H37Rv human primary monocytes. Both PPD Ag significantly induced TNF-α IL-6 MAPK [extracellular signal-regulated (ERK) 1/2 p38] are rapidly phosphorylated monocytes stimulated Ag. p38 ERK...

10.4167/jbv.2007.37.1.11 article EN cc-by-nc Journal of Bacteriology and Virology 2007-01-01
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