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Abstract Annual Review of Physiology Vol. 60: 601-617 (Volume publication date March 1998) (doi:10.1146/annurev.physiol.60.1.601) CELL CYCLE REGULATION AND APOPTOSIS1 K. L. King* and ­J. A. Cidlowski#­ *Department of Molecular and Cellular Physiology, University of Cincinnati Medical Center, P. O. Box 670576, Cincinnati, Ohio 45267-0576; #National Institutes of Health, National Institute of Environmental Health Sciences, P.O. Box 12233 MD E2-02, Research Triangle Park, North Carolina 27709; e-mail: cidlowski@niehs.nih.gov Tissue homeostasis requires a balance between cell proliferation and death. Apoptosis and proliferation are linked by cell cycle regulators, and apoptotic stimuli affect both cell proliferation and death. Glucocorticoids induce G1 arrest and apoptosis in transformed lymphoid cells. Decreased expression of the cell cycle components c-myc and cyclin D3 is essential for glucocorticoid-induced growth arrest and death in dividing cells. Other G1 regulators, such as p53, pRb, and E2F, have also been implicated in apoptosis. Mice lacking either p53 or E2F display aberrant cell proliferation and tumor formation, suggesting that these proteins are involved in the elimination of abnormal cells through apoptosis. In contrast, pRb induces G1 arrest and suppresses apoptosis in cultured cells. Mice that lack pRb are nonviable and show ectopic mitosis and massive cell death, suggesting that pRb is an apoptotic suppressor. Further analysis of common components of apoptotic and cell cycle machinery may provide insight into the coordinated regulation of these antagonistic processes. 以上內容來自 Journal of Bioenergetics and Biomembranes (Historical Archive) Publisher: Springer Science+Business Media B.V., Formerly Kluwer Academic Publishers B.V. ISSN: 0145-479X (Paper) 1573-6881 (Online) DOI: 10.1007/BF00770028 Issue:  Volume 19, Number 5 Date:  October 1987 Pages: 427 - 442 Mini-Review Proton conductance through phospholipid bilayers: Water wires or weak acids? John Gutknecht1 (1)  Department of Physiology, Duke University, and Duke Marine Laboratory, 28516 Beaufort, North Carolina Received: 2 February 1987  Revised: 15 May 1987   Abstract  The proton/hydroxide (H+/OH–) permeability of phospholipid bilayer membranes at neutral pH is at least five orders of magnitude higher than the alkali or halide ion permeability, but the mechanism(s) of H+/OH– transport are unknown. This review describes the characteristics of H+/OH– permeability and conductance through several types of planar phospholipid bilayer membranes. At pH7, the H+/OH– conductances (G H/OH) range from 2–6 nS cm–2, corresponding to net H+/OH– permeabilities of (0.4–1.7)×10–5 cm sec–1. Inhibitors ofG H/OH include serum albumin, phloretin, glycerol, and low pH. Enhancers ofG H/OH include chlorodecane, fatty acids, gramicidin, and voltages >80 mV. Water permeability andG H/OH are not correlated. The characteristics ofG H/OH in fatty acid (weak acid) containing membranes are qualitatively similar to the controls in at least eight different respects. The characteristics ofG H/OH in gramicidin (water wire) containing membranes are qualitatively different from the controls in at least four different respects. Thus, the simplest explanation for the data is thatG H/OH in unmodified bilayers is due primarily to weakly acidic contaminants which act as proton carriers at physiological pH. However, at low pH or in the presence of inhibitors, a residualG H/OH remains which may be due to water wires, hydrated defects, or other mechanisms. Key Words  Proton conductance - proton permeability - phospholipid bilayer membrane - weak acid - water wire - fatty acid - gramicidin The references of this article are secured to subscribers. 以上內容來自