T
Tullia Lindsten
Researcher at Memorial Sloan Kettering Cancer Center
Publications - 93
Citations - 28566
Tullia Lindsten is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: T cell & Bcl-2 Homologous Antagonist-Killer Protein. The author has an hindex of 55, co-authored 93 publications receiving 27273 citations. Previous affiliations of Tullia Lindsten include Children's Hospital of Philadelphia & University of Michigan.
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Journal ArticleDOI
Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death
Michael C. Wei,Michael C. Wei,Wei-Xing Zong,Emily H. Cheng,Tullia Lindsten,Vily Panoutsakopoulou,Andrea J. Ross,Kevin A. Roth,Grant R. MacGregor,Craig B. Thompson,Stanley J. Korsmeyer +10 more
TL;DR: In this article, the authors found that doubly deficient cells are resistant to multiple apoptotic stimuli that act through disruption of mitochondrial function: staurosporine, ultraviolet radiation, growth factor deprivation, etoposide, and the endoplasmic reticulum stress stimuli thapsigargin and tunicamycin.
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bcl-x, a bcl-2-related gene that functions as a dominant regulator of apoptotic cell death
Lawrence H. Boise,Maribel González-García,Christina E. Postema,Liyun Ding,Tullia Lindsten,Laurence A. Turka,Xiaohong Mao,Gabriel Núñez,Craig B. Thompson +8 more
TL;DR: Data suggest that bcl-x plays an important role in both positive and negative regulation of programmed cell death, as well as in tissues containing long-lived postmitotic cells, such as adult brain.
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BCL-2, BCL-XL Sequester BH3 Domain-Only Molecules Preventing BAX- and BAK-Mediated Mitochondrial Apoptosis
Emily H. Cheng,Michael C. Wei,Solly Weiler,Richard A. Flavell,Tak W. Mak,Tullia Lindsten,Stanley J. Korsmeyer +6 more
TL;DR: In mammals, BH3 domain-only molecules activate multidomain proapoptotic members to trigger a mitochondrial pathway, which both releases cytochrome c to activate caspases and initiates caspase-independent mitochondrial dysfunction.
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Growth factor regulation of autophagy and cell survival in the absence of apoptosis
Julian J. Lum,Daniel E. Bauer,Mei Kong,Marian H. Harris,Chi Li,Tullia Lindsten,Craig B. Thompson +6 more
TL;DR: Using growth factor-dependent cells from Bax/Bak-deficient mice, it is demonstrated that apoptosis is not essential to limit cell autonomous survival and growth factor signal transduction is required to direct the utilization of sufficient exogenous nutrients to maintain cell viability.
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The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues.
Tullia Lindsten,Andrea J. Ross,Ayala King,Wei-Xing Zong,Jeffrey C. Rathmell,Helena Shiels,Eugen Ulrich,Katrina G. Waymire,Patryce L. Mahar,Kenneth A. Frauwirth,Yifeng Chen,Michael C. Wei,Vicki M. Eng,David M. Adelman,M. Celeste Simon,Averil Ma,Jeffrey A. Golden,Gerard I. Evan,Stanley J. Korsmeyer,Grant R. MacGregor,Craig B. Thompson +20 more
TL;DR: Bax and Bak have overlapping roles in the regulation of apoptosis during mammalian development and tissue homeostasis and are found to be developmentally normal and reproductively fit.