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N.S. Chang

Research Institute

Laboratory of Molecular Immunology

Guthrie Medical Center

Sayre

USA

[email]@*.guthrie.org

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Affiliations

Research Institute, Laboratory of Molecular Immunology, Guthrie Medical Center, Sayre, USA. 1997 - 2003
Guthrie Research Institute, Guthrie Medical Center, 1 Guthrie Square, Sayre, USA. 2000

References

JNK1 physically interacts with WW domain-containing oxidoreductase (WOX1) and inhibits WOX1-mediated apoptosis. Chang, N.S., Doherty, J., Ensign, A. J. Biol. Chem. (2003) [Pubmed]
A potential role of p53 and WOX1 in mitochondrial apoptosis (review). Chang, N.S. Int. J. Mol. Med. (2002) [Pubmed]
The non-ankyrin C terminus of Ikappa Balpha physically interacts with p53 in vivo and dissociates in response to apoptotic stress, hypoxia, DNA damage, and transforming growth factor-beta 1-mediated growth suppression. Chang, N.S. J. Biol. Chem. (2002) [Pubmed]
Transforming growth factor-beta1 blocks the enhancement of tumor necrosis factor cytotoxicity by hyaluronidase Hyal-2 in L929 fibroblasts. Chang, N.S. BMC Cell Biol. (2002) [Pubmed]
Hyaluronidase induction of a WW domain-containing oxidoreductase that enhances tumor necrosis factor cytotoxicity. Chang, N.S., Pratt, N., Heath, J., Schultz, L., Sleve, D., Carey, G.B., Zevotek, N. J. Biol. Chem. (2001) [Pubmed]
Hyaluronidase activation of c-Jun N-terminal kinase is necessary for protection of L929 fibrosarcoma cells from staurosporine-mediated cell death. Chang, N.S. Biochem. Biophys. Res. Commun. (2001) [Pubmed]
TGF-beta-induced matrix proteins inhibit p42/44 MAPK and JNK activation and suppress TNF-mediated IkappaBalpha degradation and NF-kappaB nuclear translocation in L929 fibroblasts. Chang, N.S. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
Suppression of IkappaBalpha expression is necessary for c-Jun N-terminal kinase-mediated enhancement of Fas cytotoxicity. Chang, N.S., Schultz, L., Heath, J. Biochem. Biophys. Res. Commun. (2000) [Pubmed]
IkappaBalpha is essential for maintaining basal c-Jun N-terminal kinase (JNK) activation and regulating JNK-mediated resistance to tumor necrosis factor cytotoxicity in L929 cells. Chang, N.S. Biochem. Biophys. Res. Commun. (1999) [Pubmed]
p53 overexpression and downregulation of inter-alpha-inhibitor are associated with hyaluronidase enhancement of TNF cytotoxicity in L929 fibroblasts. Chang, N.S., Carey, G., Pratt, N., Chu, E., Ou, M. Cancer Lett. (1998) [Pubmed]
Cloning and characterization of a novel transforming growth factor-beta1-induced TIAF1 protein that inhibits tumor necrosis factor cytotoxicity. Chang, N.S., Mattison, J., Cao, H., Pratt, N., Zhao, Y., Lee, C. Biochem. Biophys. Res. Commun. (1998) [Pubmed]
Characterization of serum adhesive proteins that block tumor necrosis factor-mediated cell death. Chang, N.S., Joki, N., Mattison, J., Dinh, T., John, S. Cell Death Differ. (1997) [Pubmed]