Download Apoptosis : physiology and pathology by Douglas R. Green, John C. Reed PDF

By Douglas R. Green, John C. Reed

"Apoptosis, or cellphone dying, will be pathological, an indication of illness and harm, or physiological, a strategy crucial for regular healthiness. This pathological dysregulation of mobile dying could be characterised by means of both an excessive amount of lack of crucial cells within the center, mind, and different tissues with little regenerative means or through too little telephone turnover in self-renewing tissues, giving upward push to melanoma and different maladies. Read more...

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Apoptosis : physiology and pathology

"Apoptosis, or mobile demise, may be pathological, an indication of affliction and harm, or physiological, a procedure crucial for regular well-being. This pathological dysregulation of telephone demise might be characterised through both an excessive amount of lack of crucial cells within the middle, mind, and different tissues with little regenerative potential or by way of too little cellphone turnover in self-renewing tissues, giving upward push to melanoma and different maladies.

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Cell 104:769–80. Conte D, Liston P, Wong JW, Wright KE, Korneluk RG. (2001) Oleksijew A, Oltersdorf T, Rosenberg SH, Shoemaker AR, Tomaselli KJ, Zou H, Fesik SW. (2004) Discovery of potent antagonists of the antiapoptotic protein XIAP for the treat- Thymocyte-targeted overexpression of XIAP transgene disrupts T lymphoid apoptosis and maturation. Proc Natl Acad ment of cancer. J Med Chem 26:4417–26. Perrelet D, Ferri A, Liston P, Muzzin P, Korneluk RG, Kato AC. Sci U S A 98:5049–54. Conze DB, Albert L, Ferrick DA, Goeddel DV, Yeh WC, Mak T, Ashwell JD.

3. 1. 1. Biochemistry of TNF signal transduction The founding member of the TNFSF is a homotrimer of TNF molecules, each 157 amino acids in length. The trimer adopts a characteristic conformation, which is now commonly referred to as the TNF fold. TNF is mainly produced by activated macrophages. Depending on the physiologic or pathological context, it is, however, also expressed by a number of other cell types. The binding of TNF to its receptors triggers a series of intracellular events that primarily induces the activation of NF-κB and the mitogen-activated protein (MAP) kinases c-Jun N-terminal kinase (JNK) and p38.

Whereas cytochrome c release triggers the formation of the apoptosome resulting in activation of caspase9, release of SMAC induces the neutralization of the Xlinked inhibitor of apoptosis protein (XIAP). Once XIAP is inhibited by SMAC, caspase-3, -7, and -9, which are all inhibited by XIAP, are released from inhibition, and cell death can finally ensue (Figure 3-2). Thus, in cells that express high levels of XIAP, the direct activation of caspase-3 by caspase-8 is blocked so that these cells require the pro-mitochondrial changes brought about by the cleavage of BID and its proapoptotic activity on mitochondria to succumb when CD95 is activated.

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