By William B. Guggino (Eds.)
The volume of recent info at the molecular biology of chloride channels has grown vastly in recent times. this huge volume of data offers a few detailed and, in a few circumstances, awesome insights into the functionality and constitution of chloride channels that are found in each telephone. This quantity encompasses a sequence of in-depth studies of chloride channel body structure, biophysics, and molecular biology. The stories disguise chloride channels present in the plasma membrane in addition to in organelles of either plant and animal cells. Key gains* Discusses CFTR, the cystic fibrosis transmembrane regulator, that is chargeable for CF and the CIC-family of chloride channels liable for myotonia congenita* In-depth reports of chloride channel body structure, biophysics, and molecular biology* stories chloride channels present in the plasma membrane and in organelles of either plant and animal cells
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Additional info for Chloride Channels
And Sigworth, F. J. Improved patch-clamp techniques for high-resolution current recording from cells and cell-free membrane patches. PJuegers Arch. 391, 85-100. + 1 . Voltage-Dependent Chloride Channels 31 Hedrich, R.. and Jeromin, A. (1992). A new scheme of symbiosis: Ligand- and voltagegated anion channels in plants and animals. Proc. R . Soc. London. Ser. B 338, 31-38. , and Neher, E. (1987). Cytoplasmic calcium regulates voltage-dependent ion channels in plant vacuoles. Nature (London) 329, 833-836.
1990). As illustrated in the Hodgkin-Huxley cycle of GCACl (Fig. 13) initial depolarization to slightly negative potentials to -100 rnV activates a few anion channels which in turn further depolarize the plasma membrane toward &-. Due to the voltage- and time-dependent inactivation of GCACl (see Fig. 6), the membrane repolarizes again. Calcium and K + channels may also contribute to the shape of this transient change in membrane potential. Wilting hormone (absicisic acid)-induced or CRAC-like calcium conducIs Please note.
G. MS chloride channels have a smaller conductance and different voltage dependence than GCACI). Rainer Hedrich 26 A Depolarization pGcf \ Initial Inactivation Depolarization of GCAC 1 Repolarization Resting potential B Voltage gate shifts Inactivation (pK*I PH*) FIGURE 13 Hodgkin-Huxley cycle of transient conductance changes in the plasma membrane of guard cells. during excitation, when the initial "input" was a depolarization (A. uoltage change) caused by a Ca'+ permeability (upper cycle) and signal transduction, when (B)ligands modify GCACl directly (lower cycle).
Chloride Channels by William B. Guggino (Eds.)