New Approaches and Therapeutics Targeting Apoptosis in Disease

Fischer, Ute; Schulze‐Osthoff, Klaus

doi:10.1124/pr.57.2.6

Cited by 231 publications

(190 citation statements)

References 200 publications

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“…Mutations in the Bcl-2 family are also commonly found. The significance of p53 and the Bcl-2 family and other molecules that drive apoptosis have provided the most opportunities for pharmaceutical exploitation [88,89]. Some of these efforts have resulted in novel agents now being tested in the clinic.…”

Section: Targeted Approaches To Activating Cell Deathmentioning

confidence: 99%

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Chemotherapeutic Approaches for Targeting Cell Death Pathways

2006

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Learning Objectives After completing this course, the reader will be able to: List the multiple cell death pathways that are activated in response to chemotherapeutic agents. Identify signaling molecules involved and morphological changes that occur in the different types of cell death pathways. Describe mechanisms targeted by novel chemotherapeutic agents. Access and take the CME test online and receive 1 AMA PRA category 1 credit at http://CME.TheOncologist.com For several decades, apoptosis has taken center stage as the principal mechanism of programmed cell death in mammalian tissues. It also has been increasingly noted that conventional chemotherapeutic agents not only elicit apoptosis but other forms of nonapoptotic death such as necrosis, autophagy, mitotic catastrophe, and senescence. This review presents background on the signaling pathways involved in the different cell death outcomes. A re‐examination of what we know about chemotherapy‐induced death is vitally important in light of new understanding of nonapoptotic cell death signaling pathways. If we can precisely activate or inhibit molecules that mediate the diversity of cell death outcomes, perhaps we can succeed in more effective and less toxic chemotherapeutic regimens.

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Section: Targeted Approaches To Activating Cell Deathmentioning

confidence: 99%

“…[90]. Oblimersen was not approved for treatment of melanoma because results from phase III trials showed it did not extend survival [89]. But oblimersen showed a favorable outcome when combined with docetaxel in patients with hormone-refractory prostate cancer [91].…”

Section: Targeted Approaches To Activating Cell Deathmentioning

confidence: 99%

Chemotherapeutic Approaches for Targeting Cell Death Pathways

2006

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“…In addition, inhibition of apoptosis is emerging as a potential therapeutic tool for various forms of cardiovascular disease. 12 Since reduction of the CaD expression leads to apoptosis of the cardiomyocytes and cleavage of scaromeric proteins in vivo, this molecule may become a player in future therapeutic strategies for the regeneration of cardiac damage suffering from ischemic insult. (C1/C2) A normal heart (C1, circled) with cone pattern was outlined by DAPI staining (C2, circled) in a 2dpf control.…”

Section: © 2 0 0 9 L a N D E S B I O S C I E N C E D O N O T D I S mentioning

confidence: 99%

Reduction of caldesmon expression induces apoptosis and causes disassembly of the sarcomeric protein complex in cardiomyocytes in vivo

Zheng¹,

Severijnen²,

Willemsen³

et al. 2009

Cell Cycle

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“…Downregulation of p85 leads to nuclear exclusion of apoptin and impairs cell death induction, indicating that interaction with the p85 PI3-K subunit essentially contributes to the cytotoxic activity of apoptin. Oncogene (2008) 27, 3060-3065;doi:10.1038/sj.onc.1210958;published online 3 December 2007 Keywords: anticancer drugs; apoptin; apoptosis; PI3-kinase Apoptin, a 14 kDa protein encoded by VP3 gene of chicken anemia virus, represents a novel potential anticancer therapeutic, because it induces apoptotic death specifically in tumor but not normal cells (Fischer and Schulze-Osthoff, 2005;Alvisi et al, 2006). The mechanism by which apoptin is able to distinguish between tumor and normal cells remains to be elucidated.…”

mentioning

confidence: 99%

Interaction with PI3-kinase contributes to the cytotoxic activity of Apoptin

et al. 2007

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Apoptin, a small protein from the chicken anemia virus, has attracted attention because of its specificity in killing tumor cells. Localization of apoptin in the nucleus of tumor cells has been shown to be vital for proapoptotic activity, however, targeted expression of apoptin in the nucleus of normal cells does not harm the cells, indicating that nuclear localization of apoptin is insufficient for its cytotoxicity. Here, we demonstrate for the first time that apoptin interacts with the SH3 domain of p85, the regulatory subunit of phosphoinositide 3-kinase (PI3-K), through its proline-rich region. Apoptin derivatives devoid of this proline-rich region do not interact with p85, are unable to activate PI3-K, and show impaired apoptosis induction. Moreover, apoptin mutants containing the proline-rich domain are sufficient to elevate PI3-K activity and to induce apoptosis in cancer cells. Downregulation of p85 leads to nuclear exclusion of apoptin and impairs cell death induction, indicating that interaction with the p85 PI3-K subunit essentially contributes to the cytotoxic activity of apoptin.

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New Approaches and Therapeutics Targeting Apoptosis in Disease

Cited by 231 publications

References 200 publications

Chemotherapeutic Approaches for Targeting Cell Death Pathways

Chemotherapeutic Approaches for Targeting Cell Death Pathways

Reduction of caldesmon expression induces apoptosis and causes disassembly of the sarcomeric protein complex in cardiomyocytes in vivo

Interaction with PI3-kinase contributes to the cytotoxic activity of Apoptin

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