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J. L. Yang
·¨¹Å¹a±Ð±Â


Professor Ph.D., Michigan State University

Molecular Oncology; DNA Repair and Mutagenesis
email:jlyang@life.nthu.edu.tw
phone (886) 3-574-2756 or
(886) 3-5715131 # 3487
fax (886) 3-5717237

 
   
 

Research Interest: 
1. Role of mitogen-activated protein kinases in DNA-damage-response network (cell-cycle arrest, DNA-damage detection and repair, and apoptosis) elicited by carcinogenic metals, including lead, arsenic, cadmium, and chromium.
2. Degradation/stabilization of cell cycle controlling proteins following carcinogenic metals.

Selected Publications: 

  1. Wang CY, Wang YT, Tzeng DW, and YangJL (2009)Lead acetate induces EGFR activation upstream of SFK and PKCa linkage to the Ras/Raf-1/ERK signaling. Toxicol Appl Pharmacol (in press)


  2. Li JP, Wang CY, Tang, YA, Lin YW, and Yang JL(2008) Role of extracellular signal-regulated kinase (ERK) signaling in nucleotide excision repair and genotoxicity in response to As(III) and Pb(II). Pure Appl Chem 80: 2735-2750


  3. Wang CY, Lin YW, and YangJL (2008) Activation of protein kinase Ca signaling prevents cytotoxicity and mutagenicity following lead acetate in CL3 human lung cancer cells. Toxicology 250: 55-61


  4. Li JP, and Yang JL* (2007) Cyclin B1 proteolysis via p38 MAPK signaling participates in G2 checkpoint elicited by arsenite. J Cell Physiol 212: 481-488


  5. Lin YW, and Yang JL* (2006) Cooperation of ERK and SCFSkp2 for MKP-1 destruction provides a positive feedback regulation of proliferating signaling. J Biol Chem 281: 915-926


  6. Li JP, Lin JC, and Yang JL* (2006) ERK activation in arsenite-treated G1-enriched CL3 cells contributes to survival, DNA repair inhibition, and micronucleus formation. Toxicol Sci 89: 164-172


  7. Hsiue GH, Wang CH, Lo CL, Wang CH, Li JP, and Yang JL (2006) Environmental-sensitive micelles based on poly(2-ethyl-2-oxazoline)-b- poly(l-lactide) diblock copolymer for application in drug delivery. Int J Pharm 317:69-75


  8. Ko JC, WangYT, and Yang JL* (2004) Dual and opposing roles of ERK in regulating G1 and S-G2/M delays in A549 cells caused by hyperoxia. Exp Cell Res 297: 472-483


  9. Lin YW, Chuang SM, Yang JL* (2003) ERK1/2 achieves sustained activation by stimulating MAPK phosphatase-1 degradation via the ubiquitin-proteasome pathway. J Biol Chem 278: 21534-21541


  10. Lin YW, Chuang SM, Yang JL* (2003)Persistent activation of ERK1/2 by lead acetate increases nucleotide excision repair synthesis and confers anti-cytotoxicity and anti-mutagenicity. Carcinogenesis 24: 53-61


  11. Chuang SM, Wang IC, Hwua YS,Yang JL* (2003) Short-term depletion of catalase suppresses cadmium-elicited c-Jun N-terminal kinase activation and apoptosis: role of protein phosphatases. Carcinogenesis 24: 7-15


  12. Yang JL*, Chuang SM(2001) Comparison of roles of three mitogen-activated protein kinases induced by chromium(VI) and cadmium in non-small-cell lung carcinoma cells.Mol Cell Biochem 222: 85-95


  13. Chao JI, Yang JL* (2001) Alteration of cadmium-induced mutational spectrum by catalase depletion in Chinese hamster ovary-K1 cells. Mutat. Res.498: 7-18



  14. Chao JI, Yang JL* (2001) Opposite roles of ERK and p38 mitogen-activated protein kinases in cadmium-induced genotoxicity and mitotic arrest. Chem. Res. Toxicol. 14: 1193-1202



  15. Chuang SM, Liou GY, Yang JL* (2000) Activation of JNK, p38 and ERK mitogen-activated protein kinases by chromium(VI) is mediated through oxidative stress but does not affect cytotoxicity. Carcinogenesis 21: 1491-1500



  16. Chuang SM, Wang IC, Yang JL* (2000) Roles of JNK, p38 and ERK mitogen-activated protein kinases in the growth inhibition and apoptosis induced by cadmium. Carcinogenesis 21: 1423-1432.



 
 
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