Chi‐Yun Wang

ORCID: 0000-0003-0317-5378
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Bone Tissue Engineering Materials
  • Electrospun Nanofibers in Biomedical Applications
  • Immune Response and Inflammation
  • Graphene and Nanomaterials Applications
  • Orthopaedic implants and arthroplasty
  • Microplastics and Plastic Pollution
  • PI3K/AKT/mTOR signaling in cancer
  • Facial Trauma and Fracture Management
  • Cancer, Hypoxia, and Metabolism
  • S100 Proteins and Annexins
  • Radio Frequency Integrated Circuit Design
  • Cell death mechanisms and regulation
  • Membrane Separation Technologies
  • Autophagy in Disease and Therapy
  • Ubiquitin and proteasome pathways
  • Macrophage Migration Inhibitory Factor
  • Galectins and Cancer Biology
  • Titanium Alloys Microstructure and Properties
  • Immune Cell Function and Interaction
  • Metabolism, Diabetes, and Cancer
  • biodegradable polymer synthesis and properties
  • Protein Tyrosine Phosphatases
  • interferon and immune responses
  • Bone Metabolism and Diseases
  • Cellular transport and secretion

Ming Chi University of Technology
2020-2025

Chang Gung Memorial Hospital
2019-2025

Wake Forest University
2017-2025

University at Albany, State University of New York
2023

National Taiwan University
2020-2023

The University of Texas MD Anderson Cancer Center
2015-2020

Memorial Hospital of South Bend
2020

MediaTek (Taiwan)
2017-2019

MediaTek (China)
2014-2016

National Cheng Kung University
2008-2014

Abstract PI3K/Akt signaling is activated in cancers and governs tumor initiation progression, but how Akt under diverse stresses poorly understood. Here we identify AMPK as an essential regulator for activation by various stresses. Surprisingly, also growth factor EGF through Ca2+/Calmodulin-dependent kinase EGF-mediated biological functions. phosphorylates Skp2 at S256 promotes the integrity E3 ligase activity of SCF complex leading to K63-linked ubiquitination subsequent oncogenic...

10.1038/s41467-018-07188-9 article EN cc-by Nature Communications 2018-11-05

A titer for homologous viral neutralization activity (> 1:19,683) was observed after a 3.5-year immunization period with an octameric, branching peptide representing the principal neutralizing determinant (PND) of human immunodeficiency virus-1 IIIB envelope protein. Booster immunizations elicited persistent and potent antibodies in guinea pigs, exceeding responses produced by conventional bovine serum albumin conjugate 100-fold. Peptide length, central presentation conserved sequence,...

10.1126/science.1925584 article EN Science 1991-10-11

Summary The inflammatory effects of glycogen synthase kinase‐3 (GSK‐3) have been identified; however, the potential mechanism is still controversial. In this study, we investigated GSK‐3‐mediated interleukin‐10 (IL‐10) inhibition on lipopolysaccharide (LPS)‐induced inflammation. Treatment with GSK‐3 inhibitor significantly blocked LPS‐induced nitric oxide (NO) production as well inducible NO (iNOS) expression in BV2 murine microglial cells and primary rat microglia‐enriched cultures. Using...

10.1111/j.1365-2567.2008.02959.x article EN Immunology 2009-08-04

Anesthetic propofol has immunomodulatory effects, particularly in the area of anti-inflammation. Bacterial endotoxin lipopolysaccharide (LPS) induces inflammation through toll-like receptor (TLR) 4 signaling. We investigated molecular actions against LPS/TLR4-induced inflammatory activation murine RAW264.7 macrophages.Non-cytotoxic levels reduced LPS-induced inducible nitric oxide synthase (iNOS) and NO as determined by western blotting Griess reaction, respectively. Propofol also production...

10.1371/journal.pone.0017598 article EN cc-by PLoS ONE 2011-03-08

Autophagy is regulated for IFN-gamma-mediated antimicrobial efficacy; however, its molecular effects IFN-gamma signaling are largely unknown. Here, we show that autophagy facilitates IFN-gamma-activated Jak2-STAT1. induces in wild-type but not protein 5 (Atg5(-/-))-deficient mouse embryonic fibroblasts (MEFs), and, autophagy-dependently, IFN regulatory factor 1 and cellular inflammatory responses. Pharmacologically inhibiting using 3-methyladenine, a known inhibitor of class III...

10.1074/jbc.m110.133355 article EN cc-by Journal of Biological Chemistry 2010-07-01

Glycogen synthase kinase-3beta (GSK-3beta)-modulated IFN-gamma-induced inflammation has been reported; however, the mechanism that activates GSK-3beta and effects of activation remain unclear. Inhibiting decreased inflammation. IFN-gamma treatment rapidly activated via neutral sphingomyelinase- okadaic acid-sensitive phosphatase-regulated dephosphorylation at Ser(9), proline-rich tyrosine kinase 2 (Pyk2)-regulated phosphorylation Tyr(216). Pyk2 was through phosphatidylcholine-specific...

10.4049/jimmunol.0804033 article EN The Journal of Immunology 2009-06-20

Excessive inflammation and apoptosis are pathological features of endotoxaemic acute renal failure. Activation glycogen synthase kinase-3 (GSK-3) is involved in apoptosis. We investigated the effects inhibiting GSK-3 on lipopolysaccharide (LPS)-induced failure, nuclear factor-kappaB (NF-kappaB), apoptosis.The with inhibitors, including lithium chloride (LiCl) 6-bromo-indirubin-3'-oxime (BIO), LPS-treated (15 mg x kg(-1)) C3H/HeN mice (LiCl, 40 kg(-1) BIO, 2 (1 microg mL(-1)) epithelial cells...

10.1111/j.1476-5381.2009.00284.x article EN British Journal of Pharmacology 2009-06-05

Glycogen synthase kinase (GSK)-3β may modulate endoplasmic reticulum (ER) stress-induced apoptosis; however, the mechanism remains unclear. Our data showed that human monocytic leukemia/lymphoma U937 and acute myeloid leukemia HL-60, but not chronic K562, cells were susceptible to apoptosis induced by ER stressor tunicamycin, a protein glycosylation inhibitor. Tunicamycin caused early activation of caspase-2, -3, -4, -8, followed apoptosis, whereas caspase-9 was slowly activated. Inhibiting...

10.1124/jpet.108.148122 article EN Journal of Pharmacology and Experimental Therapeutics 2009-02-02

Abstract Dynamic changes in histone modifications under various physiological cues play important roles gene transcription and cancer. Identification of new marks critical for cancer development is particular importance. Here we show that, a glucose-dependent manner, E3 ubiquitin ligase NEDD4 ubiquitinates H3 on lysine 23/36/37 residues, which specifically recruits acetyltransferase GCN5 subsequent acetylation. Genome-wide analysis chromatin immunoprecipitation followed by sequencing reveals...

10.1038/ncomms14799 article EN cc-by Nature Communications 2017-03-16

Abstract Annexin A2 (p36) is usually present together with its natural ligand p11 as a heterotetramer complex, which has multiple biological functions depending on cellular localization. However, the detailed mechanism of annexin translocation and physiological role in inflammation remain unclear. Here, we show that IFN‐γ stimulation enhances surface lung epithelial cells. While total protein remains unchanged, expression upregulated via IFN‐γ‐activated JAK2/STAT1 signal pathway. Notably,...

10.1002/jcp.23026 article EN Journal of Cellular Physiology 2011-09-19

Inactivation of glycogen synthase kinase (GSK)-3 has been implicated in cancer progression. Previously, we showed an abundance inactive GSK-3 the human chronic myeloid leukemia (CML) cell line. CML is a hematopoietic malignancy caused by oncogenic Bcr-Abl tyrosine kinase. In signaling, role not well defined. Here, report that enforced expression constitutively active reduced proliferation and increased inhibition-induced apoptosis nearly 1-fold. inhibition activated GSK-3-dependent...

10.1096/fj.10-180190 article EN The FASEB Journal 2011-06-24

Oncogenic activation accompanied by escape from immune surveillance, such as IFN-γ resistance, is critical for cancer cell growth and survival. In this study, we investigated the crosstalk signaling between resistance of hyperproliferation in gastric cells. inhibited MKN45 cells but not hyperproliferating AGS did respond to because a decrease STAT1 due dysfunctional receptors. Signaling PI3K/AKT, well MEK/ERK, was required hyperproliferation; notably, PI3K/AKT alone mediated resistance....

10.1016/j.imbio.2012.01.001 article EN cc-by-nc-nd Immunobiology 2012-01-05
Coming Soon ...