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Ion channels in neurodevelopment:lessons from the Integrin-KCNB1 channel complex

Neural Regeneration Research 2023年第11期18卷 2365-2369页

作者： Alessandro Bortolami federico sesti Department of Neuroscience and Cell Biology Robert Wood Johnson Medical SchoolRutgers UniversityWest PiscatawayNJUSA

Ion channels modulate cellular excitability by regulating ionic fluxes across biological *** mutations in ion channel genes give rise to epileptic disorders that are among the most frequent neurological diseases affecting millions of individuals *** are trigge red by an imbalance between excitatory and inhibitory ***,pathogenic mutations in the same allele can give rise to loss-of-function and/or gain-of-function va riants,all able to trigger ***,certain alleles are associated with brain malformations even in the absence of a clear electrical *** body of evidence argues that the underlying epileptogenic mechanisms of ion channels are more diverse than originally *** focusing on ion channels in prenatal cortical development have shed light on this apparent *** picture that emerges is that ion channels play crucial roles in landmark neurodevelopmental processes,including neuronal migration,neurite outgrowth,and synapse ***,pathogenic channel mutants can not only cause epileptic disorders by alte ring excitability,but further,by inducing morphological and synaptic abnormalities that are initiated during neocortex formation and may persist into the adult brain.

关键词： developmental and epileptic encephalopathies epilepsy K+channel KCNB1 Kv2.1 neurodevelopment potassium channel

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Oxidation of KCNB1 K^+ channels in central nervous system and beyond

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World Journal of Biological Chemistry 2014年第2期5卷 85-92页

作者： federico sesti Xilong Wu Shuang Liu Department of Neuroscience and Cell Biology Obert Wood Johnson Medical School Rutgers University Piscataway NJ 08854 United States Department of Neurology Jinan Central Hospital

KCNB1, a voltage-gated potassium(K+) channel that conducts a major delayed rectifier current in the brain, pancreas and cardiovascular system is a key player in apoptotic programs associated with oxidative stress. As a result, this protein represents a bona fide drug target for limiting the toxic effects of oxygen radicals. Until recently the consensus view was that reactive oxygen species trigger a pro-apoptotic surge in KCNB1 current via phosphorylation and SNARE-dependent incorpora-tion of KCNB1 channels into the plasma membrane. However, new evidence shows that KCNB1 can be modified by oxidants and that oxidized KCNB1 channels can directly activate pro-apoptotic signaling pathways. Hence, a more articulated picture of the pro-apoptotic role of KCNB1 is emerging in which the protein induces cell's death through distinct molecular mechanisms and activation of multiple pathways. In this review article we discuss the diverse functional, toxic and protective roles that KCNB1 channels play in the major organs where they are expressed.

关键词： Apoptosis Kv2.1 Aging Reactive oxygen species Alzheimer’ s disease

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The nlitogenic role of K+ currents in rat UMR 106-01 osteoblastic cells

The nlitogenic role of K+ currents in rat UMR 106-01 osteobl...

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第十五届国际药理学大会

作者： Hernandez Leonardo Park Ki Ho sesti federico University of Wisconsin. UMDNJ. UMDNJ.

＜正＞ We investigated the role of K+ currents in the mechanisms regulating the proliferation of UMR 106-01 osteoblastic osteosarcoma cells. Specific inhibitors of K+ channels, tetraethylammonium （TEA） and the class Ⅲ antiarrhythmic methane-sulfonanilide E-4031, affected cell proliferation in opposite ways: TEA inhibited proliferation by 65 % whereas E-4031 enhanced it by 83 % . Electrophysiological analysis showed that UMR 106- 01 cells produce robust K+ currents that are selectively inhibited by the two drugs. Application of TEA or E-4031 in the bath solution did not induce instantaneous changes in the level of cytosolic calcium, however, the calcium content was increased upon prolonged incubation with E-4031. Taken together these data indicate that distinct K+ currents can exert opposite effects on the proliferation rate of bone osteoblast cells through distinct mechanisms

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