By Hermann Steller
Apoptosis and Development, the most recent quantity of Current themes in Developmental Biology maintains the legacy of this finest serial with caliber chapters authored by way of leaders within the box.
This quantity covers study tools in apoptosis and improvement, and contains sections on such subject matters because the non-lethal function of apoptotic proteins and germ line telephone loss of life in Drosophila.
- Continues the legacy of this optimal serial with caliber chapters authored through leaders within the field
- Includes descriptions of the newest advances within the field
- Covers learn tools in apoptosis and improvement, and comprises sections on such issues because the non-lethal function of apoptotic proteins and germ line telephone dying in Drosophila
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R. (2011). SPK-1, an SR protein kinase, inhibits programmed cell death in Caenorhabditis elegans. Proceedings of the National Academy of Sciences of the United States of America, 108, 1998–2003. , & Hengartner, M. O. (2000). A conserved checkpoint pathway mediates DNA damage-induced apoptosis and cell cycle arrest in C. elegans. Molecular Cell, 5, 435–443. , & Ben-Sasson, S. A. (1992). Identification of programmed cell death in situ via specific labeling of nuclear DNA fragmentation. The Journal of Cell Biology, 119, 493–501.
Egl-1(lf ) and ced-9(gf ) mutations block germ cell death in response to ionizing radiation (Gartner, Milstein, Ahmed, Hodgkin, & Hengartner, 2000); however, as in the tail-spike cell, neither mutation affects normal physiological cell death in the germ line. Other regulators appear to take charge here (Fig. 2). Mutants in pax-2 and egl-38, encoding Pax2/5/8 family transcriptional regulators, have increased rates of germ cell death. Overexpression of these genes reduces germline apoptosis (Park, Jia, Rajakumar, & Chamberlin, 2006).
Diva, a Bcl-2 homologue that binds directly to Apaf-1 and induces BH3-independent cell death. The Journal of Biological Chemistry, 273, 32479–32486. , & Tschopp, J. (1997). Direct physical interaction between the Caenorhabditis elegans ‘death proteins’ CED-3 and CED-4. FEBS Letters, 406, 189–190. , Hartman, P. , et al. (1998). A mutation in succinate dehydrogenase cytochrome b causes oxidative stress and ageing in nematodes. Nature, 394, 694–697. , & Conradt, B. (2005). DRP-1-mediated mitochondrial fragmentation during EGL-1-induced cell death in C.