T cell-induced normalization of transformed malignant fibroblasts: A lymphokine with normalization factor activity

1989 ◽  
Vol 108 (4) ◽  
pp. 1473-1476
Author(s):  
I. Ya. Stonans ◽  
N. K. Gorlina ◽  
A. N. Cheredeev ◽  
M. E. Bogdanov ◽  
O. A. Khoperskaya ◽  
...  
Keyword(s):  
T Cell ◽  
Factor Activity ◽  
Normalization Factor

scholarly journals Protein Kinase D1 attenuates tumorigenesis in colon cancer by modulating β-catenin/T cell factor activity

Oncotarget ◽  
2014 ◽  
Vol 5 (16) ◽  
pp. 6867-6884 ◽  
Author(s):  
Vasudha Sundram ◽  
Aditya Ganju ◽  
Joshua E. Hughes ◽  
Sheema Khan ◽  
Subhash C. Chauhan ◽  
...  
Keyword(s):  
Colon Cancer ◽  
T Cell ◽  
Protein Kinase ◽  
Factor Activity ◽  
Protein Kinase D1 ◽  
T Cell Factor

Murine T-cell hybridomas that produce lymphokine with macrophage-activating factor activity as a constitutive product

1982 ◽  
Vol 72 (1) ◽  
pp. 195-201 ◽  
Author(s):  
Kent L. Erickson ◽  
Lucienne Cicurel ◽  
Eilene Gruys ◽  
Isaiah J. Fidler
Keyword(s):  
T Cell ◽  
Factor Activity

scholarly journals Notch1 promotes survival of E2A-deficient T cell lymphomas through pre–T cell receptor–dependent and –independent mechanisms

Blood ◽  
2006 ◽  
Vol 107 (10) ◽  
pp. 4115-4121 ◽  
Author(s):  
Erica J. Reschly ◽  
Christina Spaulding ◽  
Tomas Vilimas ◽  
W. Vallen Graham ◽  
Rachel L. Brumbaugh ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Ectopic Expression ◽  
Cell Receptor ◽  
Transcription Factor Activity ◽  
Factor Activity ◽  
Second Hit ◽  
Intracellular Form ◽  
T Cell Lymphomas ◽  
Dependent Mechanism

Loss of E2A transcription factor activity or activation of the intracellular form of Notch1 (ICN) leads to the development of leukemia or lymphoma in humans or mice, respectively. Current models propose that ICN functions by suppressing E2A through a pre–T cell receptor (TCR)–dependent mechanism. Here we show that lymphomas arising in E2A–/– mice require the activation of Notch1 for their survival and have accumulated mutations in, or near, the Notch1 PEST domain, resulting in increased stability and signaling. In contrast, lymphomas arising in p53–/– mice show the activation of Notch1, but no mutations were identified in ICN. The requirement for Notch1 signaling in E2A–/– lymphomas cannot be overcome by ectopic expression of pTα; however, pTα is required for optimal survival and expansion of these cells. Our findings indicate that the activation of Notch1 is an important “second hit” for the transformation of E2A–/– T cell lymphomas and that Notch1 promotes survival through pre–TCR-dependent and -independent mechanisms.

scholarly journals Interaction of FOXO with β-Catenin Inhibits β-Catenin/T Cell Factor Activity

2008 ◽  
Vol 283 (14) ◽  
pp. 9224-9230 ◽  
Author(s):  
Diana Hoogeboom ◽  
Marieke A. G. Essers ◽  
Paulien E. Polderman ◽  
Erik Voets ◽  
Lydia M. M. Smits ◽  
...  
Keyword(s):  
T Cell ◽  
Factor Activity ◽  
T Cell Factor
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