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Ching-Chow Chen

Researcher at National Taiwan University

Publications -  89
Citations -  9913

Ching-Chow Chen is an academic researcher from National Taiwan University. The author has contributed to research in topics: Protein kinase C & Histone deacetylase. The author has an hindex of 40, co-authored 88 publications receiving 8624 citations.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal Article

p38 but Not p44/42 Mitogen-Activated Protein Kinase Is Required for Nitric Oxide Synthase Induction Mediated by Lipopolysaccharide in RAW 264.7 Macrophages

TL;DR: The role of mitogen-activated protein kinases (MAPK) p44/42 and p38 in the lipopolysaccharide (LPS)-induced nitric oxide (NO) production in RAW 264.7 macrophages was studied further.
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Akt phosphorylation of p300 at Ser-1834 is essential for its histone acetyltransferase and transcriptional activity.

TL;DR: It is shown that Akt is activated and translocated to the nucleus in response to tumor necrosis factor alpha and acetylation is attributed to the Akt-enhanced intrinsic histone acetyltransferase activity of p300 and its association with another HAT, p/CAF.
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Flavonoids Inhibit Tumor Necrosis Factor-α-Induced Up-Regulation of Intercellular Adhesion Molecule-1 (ICAM-1) in Respiratory Epithelial Cells through Activator Protein-1 and Nuclear Factor-κB: Structure-Activity Relationships

TL;DR: The results suggested that AP-1 seems to play a more significant role than NF-kappaB in the flavonoid-induced ICAM-1 inhibition, and the inhibitory effects of apigenin and luteolin on IC AM-1 expression are mediated by the sequential attenuation of the three MAPKs activities, the c-fos and c-jun mRNA expressions, the AP- 1 transcriptional activity.
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Endoplasmic reticulum stress stimulates the expression of cyclooxygenase-2 through activation of NF-κB and pp38 mitogen-activated protein kinase

TL;DR: ER stress due either to expression of viral surface proteins or drugs can stimulate the expression of COX-2 through the NF-κB and pp38 kinase pathways, providing important insights into cellular carcinogenesis associated with latent endoplasmic reticulum stress.