Zobrazeno 1 - 10
of 11
pro vyhledávání: '"Allan F. Mock"'
Publikováno v:
Disease Models & Mechanisms, Vol 5, Iss 6, Pp 921-929 (2012)
SUMMARY Spinocerebellar ataxia type 13 (SCA13) is an autosomal dominant disease caused by mutations in the Kv3.3 voltage-gated potassium (K+) channel. SCA13 exists in two forms: infant onset is characterized by severe cerebellar atrophy, persistent m
Externí odkaz:
https://doaj.org/article/c69954009fee4873b0c6763005ee4637
Publikováno v:
The Journal of General Physiology
During voltage-dependent activation in Shaker channels, four arginine residues in the S4 segment (R1-R4) cross the transmembrane electric field. It has been proposed that R1-R4 movement is facilitated by a "gating charge transfer center" comprising a
Publikováno v:
The Journal of Neuroscience. 31:6831-6841
Whether changes in neuronal excitability can cause neurodegenerative disease in the absence of other factors such as protein aggregation is unknown. Mutations in the Kv3.3 voltage-gated K+channel cause spinocerebellar ataxia type 13 (SCA13), a human
Autor:
Muriel Laine, Benoît Roux, Meng-chin A. Lin, Diane M. Papazian, Allan F. Mock, John P. Bannister, William R. Silverman
Publikováno v:
Neuron. 39(3):467-481
A recently proposed model for voltage-dependent activation in K+ channels, largely influenced by the KvAP X-ray structure, suggests that S4 is located at the periphery of the channel and moves through the lipid bilayer upon depolarization. To investi
Publikováno v:
Zhao, Y; Lin, MCA; Mock, A; Yang, M; & Wayne, NL. (2014). Kisspeptins modulate the biology of multiple populations of gonadotropin-releasing hormone neurons during embryogenesis and adulthood in zebrafish (Danio rerio). PLoS ONE, 9(8). doi: 10.1371/journal.pone.0104330. UCLA: Retrieved from: http://www.escholarship.org/uc/item/65b49223
PloS one, vol 9, iss 8
PLoS ONE, Vol 9, Iss 8, p e104330 (2014)
PLoS ONE
PloS one, vol 9, iss 8
PLoS ONE, Vol 9, Iss 8, p e104330 (2014)
PLoS ONE
Kisspeptin1 (product of the Kiss1 gene) is the key neuropeptide that gates puberty and maintains fertility by regulating the gonadotropin-releasing hormone (GnRH) neuronal system in mammals. Inactivating mutations in Kiss1 and the kisspeptin receptor
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ba114897fb3c5f08cebe7f58472cbd4e
http://www.escholarship.org/uc/item/65b49223
http://www.escholarship.org/uc/item/65b49223
Publikováno v:
Biophysical Journal. 72(4):1489-1500
In voltage-dependent Shaker K+ channels, charged residues E293 in transmembrane segment S2 and R365, R368, and R371 in S4 contribute significantly to the gating charge movement that accompanies activation. Using an intragenic suppression strategy, we
Publikováno v:
Disease Models & Mechanisms, Vol 5, Iss 6, Pp 921-929 (2012)
Disease Models & Mechanisms
Disease Models & Mechanisms
Summary Spinocerebellar ataxia type 13 (SCA13) is an autosomal dominant disease caused by mutations in the Kv3.3 voltage-gated potassium (K+) channel. SCA13 exists in two forms: infant onset is characterized by severe cerebellar atrophy, persistent m
Autor:
Diane M. Papazian, Ngatali A. Minassian, Alexandra Durr, Stefan M. Pulst, Virgilio Gerald H. Evidente, Allan F. Mock, Michael F. Waters, John P. Bannister, Giovanni Stevanin, Dominic B. Fee, Alexis Brice, Karla P. Figueroa, Dagmar Nolte, Ulrich Müller
Publikováno v:
Nature genetics. 38(4)
Potassium channel mutations have been described in episodic neurological diseases. We report that K+ channel mutations cause disease phenotypes with neurodevelopmental and neurodegenerative features. In a Filipino adult-onset ataxia pedigree, the cau
Publikováno v:
The Journal of General Physiology
Extracellular Mg(2+) directly modulates voltage-dependent activation in ether-à-go-go (eag) potassium channels, slowing the kinetics of ionic and gating currents (Tang, C.-Y., F. Bezanilla, and D.M. Papazian. 2000. J. Gen. Physiol. 115:319-337). To
Publikováno v:
Neuron. 14(6)
The S4 segment comprises part of the voltage sensor in Shaker K + channels. We have used a strategy similar to intragenic suppression, but without a genetic selection, to identify electrostatic interactions of the S4 segment that may be important in