Franklin

a| 9781615045396 (electronic bk.)

z| 9781615045389 (pbk.)

a| 10.4199/C00080ED1V01Y201303BBC003 2| doi

a| (CaBNVSL)CDLLS201303BBC003

a| (CaBNVSL)201303BBC003

a| (PU)6198057-penndb-Voyager

a| CaBNVSL c| CaBNVSL d| CaBNVSL

a| QH671 b| .Y252 2013

a| QU 375 b| Y252a 2013

a| 571.936 2| 23

a| Yang, Ning.

a| Apoptosis h| [electronic resource] / c| Ning Yang and Ing Swie Goping.

a| San Rafael, Calif. (1537 Fourth Street, San Rafael, CA 94901 USA) : b| Morgan & Claypool, c| c2013.

a| 1 online resource (viii, 101 p.) : b| ill

a| Colloquium series on building blocks of the cell, x| 2328-305X ; v| # 3

a| Restricted for use by site license.

a| Also available in print.

a| Mode of access: World Wide Web.

a| Part of: Colloquium digital library of life sciences.

a| Title from PDF t.p. (viewed on May 22, 2013).

a| Series from website.

a| Includes bibliographical references (p. 77-100).

a| 1. Historical perspective of apoptosis -- 1.1 Natural cell death in the 19th century -- 1.2 Explosion of interest in cell death in the 20th century -- 1.3 Definitions of cell death -- 1.4 Roles of apoptosis -- 1.4.1 Apoptosis in developing tissue -- 1.4.2 Apoptosis maintains adult tissue homeostasis -- 1.4.3 Apoptosis eliminates damaged cells --

a| 2. C. elegans and discovery of the caspases -- 2.1 Caenorhabditis elegans as a model system -- 2.2 Identification of C. elegans cell death genes -- 2.3 Definition and function of caspases in apoptosis -- 2.4 The caspase family -- 2.5 Mechanism of caspase activation --

a| 3. Engulfment of apoptotic cells: "find me" and "eat me" signals -- 3.1 "Find-me" signals -- 3.2 "Eat me" signals -- 3.3 Impaired engulfment of apoptotic corpses leads to autoimmune disease --

a| 4. Extrinsic and intrinsic apoptotic signals -- 4.1 Extrinsic signals -- 4.2 Intrinsic signals -- 4.2.1 Cytochrome c induces a caspase cascade -- 4.2.2 Other proteins released from mitochondria that contribute to caspase cascade -- 4.2.3 Caspase-independent apoptotic pathway -- 4.2.4 Inhibitor of apoptosis proteins (IAPs) --

a| 5. The Bcl-2 family -- 5.1 The discovery of Bcl-2 -- 5.2 Family members -- 5.3 Mouse knock-out studies demonstrate specialization of function and overlapping function -- 5.4 Protein-protein interactions between Bcl-2 family members dictate function -- 5.5 The bax, bak pore -- 5.6 BH3-only proteins transmit death signals --

a| 6. Apoptosis and cancer -- 6.1 Diminished apoptosis in cancer -- 6.2 Bcl-2 family antagonists -- 6.3 IAP antagonists --

a| 7. Summary -- References -- Author biographies.

a| Multi-cellular organisms eliminate individual cells through a self-destruct process known as apoptosis. Apoptosis is critical for proper development and maintenance of tissue homeostasis. The importance of this process is highlighted by the fact that too much or too little apoptosis is the underlying cause of pathologies such as cancer, autoimmune diseases (e.g., lupus, arthritis), and neurodegenerative disorders (e.g., Parkinson's, Alzheimer's). In the early days, apoptotic cells were identified strictly by cell morphology. Now we know that biochemical signatures define a number of death programs, of which apoptosis is the most widely understood. In this review, we discuss genetic insights gained from C. elegans, the importance of caspases, engulfment of apoptotic cells, apoptotic signals, the role of mitochondria, the Bcl-2 family, and the link between dysfunctional apoptosis and disease. Within each topic, we highlight landmark studies that contributed to our current understanding of apoptosis. All together, this research exemplifies tremendous scientific synergy between the disciplines of genetics, biochemistry, developmental cell biology, and structural biology. Continued exploration into mechanisms that regulate apoptosis will undoubtedly lead to insights into disease processes with potential therapeutic strategies.

a| Apoptosis.

a| Apoptosis.

a| Goping, Ing Swie.

i| Print version: z| 9781615045389

a| Colloquium digital library of life sciences

a| Colloquium series on building blocks of the cell ; v| # 3. x| 2328-305X

u| http://hdl.library.upenn.edu/1017.12/1322819 z| Connect to full text