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Cell Cycle-Related Protein Kinases and T Cell Death

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Glycoimmunology

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 376))

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Abstract

Programmed cell death (PCD), or apoptosis, involves the activation of a specific suicide program within a cell. PCD is responsible for such diverse activities as the elimination of cells during normal embryological development and determination of the immune receptor repertoire (1–9). Even though PCD was first experimentally defined over twenty years ago, very little is known about the molecular events involved in this process. Emerging data indicate that there are multiple ways by which apoptosis can be triggered in various cell types. It is not yet known whether these triggers share a common pathway, or multiple pathways that share one or more components. Several genes have been cloned from C. elegans that are clearly involved in PCD during development (ced genes), but many of their functions have been inferred by analysis of the predicted protein structure and by genetic disruptions (8). Recent work has revealed the function of at least two ced genes. The ced-3 gene is the C. elegans homologue of the mammalian interleukin-1β-converting enzyme (ICE), and encodes a cysteine protease (10). ced-9 encodes the C. elegans homologue of the bcl-2 gene product (11). From these studies it is apparent that certain aspects of PCD have been well conserved evolutionarily.

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Authors and Affiliations

  1. Department of Tumor Cell Biology, St. Jude Children’s Research Hospital, Memphis, Tennessee, 38105, USA

    Jill M. Lahti, Jialing **ang & Vincent J. Kidd

  2. Department of Cell Biology, University of Alabama at Birmingham, Birmingham, Alabama, 35294, USA

    Jialing **ang

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  1. St. George’s Hospital Medical School, University of London, London, England

    Azita Alavi  & John S. Axford  & 

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Lahti, J.M., **ang, J., Kidd, V.J. (1995). Cell Cycle-Related Protein Kinases and T Cell Death. In: Alavi, A., Axford, J.S. (eds) Glycoimmunology. Advances in Experimental Medicine and Biology, vol 376. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1885-3_27

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