|1.||Yu, Chao-Lan: 3 articles (01/2012 - 01/2006)|
|2.||Chueh, Fu-Yu: 2 articles (01/2012 - 05/2010)|
|3.||Venkitachalam, Srividya: 2 articles (01/2012 - 05/2010)|
|4.||Frey, Alan B: 2 articles (01/2012 - 12/2007)|
|5.||Cooper, John C: 2 articles (05/2010 - 01/2006)|
|6.||Shi, Mingjian: 2 articles (05/2010 - 01/2006)|
|7.||Liu, Peter P: 2 articles (10/2005 - 06/2002)|
|8.||Miyagi, Y: 2 articles (10/2001 - 02/2001)|
|9.||Harashima, N: 2 articles (10/2001 - 02/2001)|
|10.||Yamada, A: 2 articles (10/2001 - 02/2001)|
11/01/1997 - "In addition, PLCgamma1 and p56(lck) protein levels were dramatically reduced in T cells obtained from patients harboring a glioma. "
11/26/2010 - "These results indicate that the non-receptor tyrosine kinase LCK is critically involved in fractionated radiation-induced expansion of the glioma-initiating cell population and decreased cellular sensitivity to anticancer treatments. "
05/01/2010 - "All together, our data highlight the importance of silencing multiple SOCS genes in tumorigenesis and support the roles of SOCS1 and SOCS3 as tumor suppressors toward oncogenic Lck kinase."
12/01/2007 - "Collectively, our data support the notion that contact of nonlytic TIL with tumor cells, and not with tumor-infiltrating myeloid-derived suppressor cells, causes activation of Shp-1 that rapidly dephosphorylates the p56(lck) activation motif (Y394), thus inhibiting effector phase functions."
12/01/2007 - "Shp-1 is robustly active in nonlytic TIL compared with lytic TIL, colocalizes with p56(lck) in nonlytic TIL, and inhibition of Shp-1 activity in lytic TIL in vitro blocks tumor-induced defective TIL cytolysis. "
12/01/2007 - "In contrast, tumor-induced activation of p56(lck) in lytic TIL is sustained coincident with downstream TCR signaling and lytic function. "
12/01/2007 - "Biochemical analysis of purified nonlytic TIL shows that contact with tumor cells causes transient activation of p56(lck) ( approximately 10 s) which is rapidly inactivated. "
07/01/1998 - "Using human cervical carcinoma HeLa cells stably expressing CD4, p56(lck), or both molecules, we provide direct evidence that expression of CD4 and p56(lck) is required for HIV-1-induced NF-kappaB translocation. "
05/01/1999 - "In the present study, we investigated the expression of the zeta-chain molecule and the p56(lck) and p59(fyn) protein tyrosine kinase (PTK) levels in peripheral blood T lymphocytes (T-PBL) from patients with advanced gastric carcinomas; for this, flow cytometric analysis and immunoblotting, respectively, were used. "
11/04/1996 - "We have reported that tumor-associated T or natural killer (NK) lymphocytes purified from ascites of women with ovarian carcinoma show defective expression and function of signaling proteins, including reduced expression of TcR-zeta chains and p56(lck). "
|4.||HIV Infections (HIV Infection)
|1.||Protein-Tyrosine Kinases (Tyrosine Kinase)
|2.||Proteins (Proteins, Gene)
|3.||Proto-Oncogene Proteins c-fyn
|4.||NF-kappa B (NF-kB)
|6.||zeta chain antigen T cell receptor (TCR zeta chain)
|9.||DNA (Deoxyribonucleic Acid)
|10.||tyrosine receptor (receptor, tyrosine)