Therapeutic targets in cancer cell metabolism and autophagy

H Cheong, C Lu, T Lindsten, CB Thompson - Nature biotechnology, 2012 - nature.com
The metabolism of cancer cells is reprogrammed both by oncogene signaling and by
dysregulation of metabolic enzymes. The resulting altered metabolism supports cellular …

[PDF][PDF] BCL-2, BCL-XL sequester BH3 domain-only molecules preventing BAX-and BAK-mediated mitochondrial apoptosis

…, MC Wei, S Weiler, RA Flavell, TW Mak, T Lindsten… - Molecular cell, 2001 - cell.com
Critical issues in apoptosis include the importance of caspases versus organelle dysfunction,
dominance of anti- versus proapoptotic BCL-2 members, and whether commitment occurs …

bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell death

…, M González-García, CE Postema, L Ding, T Lindsten… - cell, 1993 - cell.com
… During T cell development in the thymus, each individual T cell precursor generates a
unique T cell antigen receptor by combinatorial rearrangement of T cell antigen receptor gene …

Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death

MC Wei, WX Zong, EHY Cheng, T Lindsten… - Science, 2001 - science.org
Multiple death signals influence mitochondria during apoptosis, yet the critical initiating event
for mitochondrial dysfunction in vivo has been unclear. tBID, the caspase-activated form of …

Anomalous Type 17 Response to Viral Infection by CD8+ T Cells Lacking T-bet and Eomesodermin

…, CS DeJong, H Shin, CA Hunter, EJ Wherry, T Lindsten… - Science, 2008 - science.org
… We show that CD8 + T cells deficient in the transcription factors T-… T cells lacking both T-bet
and Eomes differentiate into an interleukin-17–secreting lineage, reminiscent of the helper T

[PDF][PDF] The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues

T Lindsten, AJ Ross, A King, WX Zong, JC Rathmell… - Molecular cell, 2000 - cell.com
… lation of mature B and T cells led to massive enlargement deficient mice failed to … had similar
frequencies of CD4 and CD8 T cells (Figure 5A). However, the T cells that accumulate in the …

[HTML][HTML] Growth factor regulation of autophagy and cell survival in the absence of apoptosis

JJ Lum, DE Bauer, M Kong, MH Harris, C Li, T Lindsten… - Cell, 2005 - cell.com
In animals, cells are dependent on extracellular signals to prevent apoptosis. However, using
growth factor-dependent cells from Bax/Bak-deficient mice, we demonstrate that apoptosis …

tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c

MC Wei, T Lindsten, VK Mootha, S Weiler… - Genes & …, 2000 - genesdev.cshlp.org
… To assess whether BAK was involved in tBID-induced cytochrome c release, we turned to
Bak-deficient mice generated by gene targeting (T. Lindsten and CB Thompson, in prep.). …

BH3-only proteins that bind pro-survival Bcl-2 family members fail to induce apoptosis in the absence of Bax and Bak

WX Zong, T Lindsten, AJ Ross… - Genes & …, 2001 - genesdev.cshlp.org
The BH3-only proteins Bim and Bad bind to the antiapoptotic Bcl-2 proteins and induce
apoptosis in wild-type cells and cells from eitherbax −/− or bak −/− animals. In contrast, …

Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis

WX Zong, C Li, G Hatzivassiliou, T Lindsten… - The Journal of cell …, 2003 - rupress.org
… Similarly, overexpression of full-length and truncated caspase 12 (t-caspase 12) induced
cell death in both wild-type and bax − / − bak − / − cells, and t-caspase 12 had a higher killing …