Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
5R01CA066746-02
Application #
2110204
Study Section
Pathology B Study Section (PTHB)
Project Start
1995-04-01
Project End
2000-01-31
Budget Start
1996-02-01
Budget End
1997-01-31
Support Year
2
Fiscal Year
1996
Total Cost
Indirect Cost

  Institution

Name
University of California Los Angeles
Department
Surgery
Type
Schools of Medicine
DUNS #
119132785
City
Los Angeles
State
CA
Country
United States
Zip Code
90095

  Publications

Calhoun, Colonya C; Lu, Ying-Chun; Song, Jun et al. (2009) Knockdown endogenous CypA with siRNA in U2OS cells results in disruption of F-actin structure and alters tumor phenotype. Mol Cell Biochem 320:35-43
Lu, Ying-Chun; Song, Jun; Cho, Hee-Yeon et al. (2006) Cyclophilin a protects Peg3 from hypermethylation and inactive histone modification. J Biol Chem 281:39081-7
Song, Jun; Pang, Shen; Lu, Yingchun et al. (2004) Gene silencing in androgen-responsive prostate cancer cells from the tissue-specific prostate-specific antigen promoter. Cancer Res 64:7661-3
Song, Jun; Pang, Shen; Lu, Yingchun et al. (2004) Poly(U) and polyadenylation termination signals are interchangeable for terminating the expression of shRNA from a pol II promoter. Biochem Biophys Res Commun 323:573-8
Song, Jun; Lu, Ying-Chun; Yokoyama, Kazunari et al. (2004) Cyclophilin A is required for retinoic acid-induced neuronal differentiation in p19 cells. J Biol Chem 279:24414-9
Chiu, Robert; Rey, Osvaldo; Zheng, Jun-Qi et al. (2003) Effects of altered expression and localization of cyclophilin A on differentiation of p19 embryonic carcinoma cells. Cell Mol Neurobiol 23:929-43
Cui, Yukun; Mirkia, Kirash; Florence Fu, Yu-Hsieh et al. (2002) Interaction of the retinoblastoma gene product, RB, with cyclophilin A negatively affects cyclosporin-inhibited NFAT signaling. J Cell Biochem 86:630-41
Zhou, H; Lin, A; Gu, Z et al. (2000) 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced c-Jun N-terminal kinase (JNK) phosphatase renders immortalized or transformed epithelial cells refractory to TPA-inducible JNK activity. J Biol Chem 275:22868-75
Nishitani, J; Nishinaka, T; Cheng, C H et al. (1999) Recruitment of the retinoblastoma protein to c-Jun enhances transcription activity mediated through the AP-1 binding site. J Biol Chem 274:5454-61
Fu, Y H; Nishinaka, T; Yokoyama, K et al. (1998) A retinoblastoma susceptibility gene product, RB, targeting protease is regulated through the cell cycle. FEBS Lett 421:89-93

Showing the most recent 10 out of 11 publications