By Joachim R. Kalden, Martin Herrmann
This can be the 1st accomplished e-book in regards to the courting among apoptosis and autoimmune ailments. It deals a special up to date evaluate on learn effects at the faulty execution of apoptosis and the unfinished clearance of apoptotic cells. The molecular and mobile mechanisms concerned are defined intimately. As a potential final result of apoptotic disorder, the improvement of serious autoimmune illnesses (e.g., rheumatoid arthritis, systemic lupus erythematosus) is mentioned. An outlook on destiny examine issues comprises the review of novel healing techniques.
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Extra resources for Apoptosis and Autoimmunity: From Mechanisms to Treatments
And Wallach, D. A novel protein that interacts with the death domain of Fas/APO1 contains a sequence motif related to the death domain. J Biol Chem 1995, 270, 7795–8. Medema, J. , Kischkel, F. , Krammer, P. H. and Peter, M. E. FLICE is activated by association with the CD95 death-inducing signaling complex (DISC). EMBO J 1997, 16, 2794–804. Kischkel, F. , Krammer, P. H. and Peter, M. E. Cytotoxicity-dependent APO-1 (Fas/CD95)-associated proteins form a death-inducing signaling complex (DISC) with the receptor.
A related illustration of this caveat is the potential for variation between mice strains. The caspase-3 knockout, for example, is embryonic lethal in 100% of offspring on one pure background strain . On a different background, however, survival of knockout mice reaches approximately two-thirds of expected Mendelian inheritance levels. Thus, there are likely to be strain-specific caspase activity-modifying factors which may affect interpretation of results. These data reinforce the fact that it is difficult to exclude a particular caspase as significant for a cell death paradigm if its function can be assumed by another caspase.
Antisense oligonucleotides to caspase-2 inhibit b-amyloid-induced apoptosis in PC-12 cells, and sympathetic neurons from caspase-2 knockout mice are resistant to b-amyloid-induced apoptosis, even after extended exposure . Evaluation of lymphocyte apoptosis in caspase-2 knockout mice centered on a paradigm for cytotoxic T lymphocytes (CTL), which can induce apoptosis in target cells through the release of the serine protease granzyme B and perforin. Consistent with the ability of granzyme B to cleave caspase-2 in vitro, B lymphoblasts from caspase-2 knockout mice were resistant to apoptosis induced by granzyme B/perforin, but not to anti-Fas, doxorubicin, etoposide, c-irradiation or staurosporine .
Apoptosis and Autoimmunity: From Mechanisms to Treatments by Joachim R. Kalden, Martin Herrmann