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001-es BibID:	BIBFORM113131
035-os BibID:	(cikkazonosító)121 (scopus)85160315499 (wos)000994418900002
Első szerző:	Ashwood, Lauren M.
Cím:	Genomic, functional and structural analyses elucidate evolutionary innovation within the sea anemone 8 toxin family / Ashwood Lauren M., Elnahriry Khaled A., Stewart Zachary K., Shafee Thomas, Naseem Muhammad Umair, Szanto Tibor G., van der Burg Chloé A., Smith Hayden L., Surm Joachim M., Undheim Eivind A. B., Madio Bruno, Hamilton Brett R., Guo Shaodong, Wai Dorothy C. C., Coyne Victoria L., Phillips Matthew J., Dudley Kevin J., Hurwood David A., Panyi Gyorgy, King Glenn F., Pavasovic Ana, Norton Raymond S., Prentis Peter J.
Dátum:	2023
ISSN:	1741-7007
Megjegyzések:	Background The ShK toxin from Stichodactyla helianthus has established the therapeutic potential of sea anemone venom peptides, but many lineage-specific toxin families in Actiniarians remain uncharacterised. One such peptide family, sea anemone 8 (SA8), is present in all five sea anemone superfamilies. We explored the genomic arrangement and evolution of the SA8 gene family in Actinia tenebrosa and Telmatactis stephensoni, characterised the expression patterns of SA8 sequences, and examined the structure and function of SA8 from the venom of T. stephensoni. Results We identified ten SA8-family genes in two clusters and six SA8-family genes in five clusters for T. stephen- soni and A. tenebrosa, respectively. Nine SA8 T. stephensoni genes were found in a single cluster, and an SA8 peptide encoded by an inverted SA8 gene from this cluster was recruited to venom. We show that SA8 genes in both spe- cies are expressed in a tissue-specific manner and the inverted SA8 gene has a unique tissue distribution. While the functional activity of the SA8 putative toxin encoded by the inverted gene was inconclusive, its tissue localisation is similar to toxins used for predator deterrence. We demonstrate that, although mature SA8 putative toxins have similar cysteine spacing to ShK, SA8 peptides are distinct from ShK peptides based on structure and disulfide connectivity. Conclusions Our results provide the first demonstration that SA8 is a unique gene family in Actiniarians, evolving through a variety of structural changes including tandem and proximal gene duplication and an inversion event that together allowed SA8 to be recruited into the venom of T. stephensoni.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk
Megjelenés:	BMC Biology. - 21 : 1 (2023), p. 1-25. -
További szerzők:	Elnahriry, Khaled A. Stewart, Zachary K. Shafee, Thomas Naseem, Muhammad Umair (1993-) (biofizikus, molekuláris biológus) Szántó Gábor Tibor (1980-) (vegyész) van der Burg, Chloé A. Smith, Hayden L. Surm, Joachim M. Undheim, Eivind A. B. Madio, Bruno Hamilton, Brett R. Guo, Shaodong Wai, Dorothy C. C. Coyne, Victoria L. Phillips, Matthew J. Dudley, Kevin J. Hurwood, David A. Panyi György (1966-) (biofizikus) King, Glenn F. Pavasovic, Ana Norton, Raymond S. Prentis, Peter
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM076188
035-os BibID:	(WoS)000442351000026 (Scopus)85051815682
Első szerző:	Richards, Kay L.
Cím:	Selective NaV 1.1 activation rescues Dravet syndrome mice from seizures and premature death / Richards Kay L., Milligan Carol J., Richardson Robert J., Jancovski Nikola, Grunnet Morten, Jacobson Laura H., Undheim Eivind A. B., Mobli Mehdi, Chow Chun Yuen, Herzig Volker, Csoti Agota, Panyi Gyorgy, Reid Christopher A., King Glenn F., Petrou Steven
Dátum:	2018
ISSN:	0027-8424 1091-6490
Megjegyzések:	Dravet syndrome is a catastrophic, pharmacoresistant epileptic encephalopathy. Disease onset occurs in the first year of life, followed by developmental delay with cognitive and behavioral dysfunction and substantially elevated risk of premature death. The majority of affected individuals harbor a loss-of-function mutation in one allele of SCN1A, which encodes the voltage-gated sodium channel Na V 1.1. Brain Na 1.1 is primarily localized to fast-spiking inhibitory interneurons; thus the mechanism of epileptogenesis in Dravet syndrome is hypothesized to be reduced inhibitory neurotransmission leading to brain hyperexcitability. We show that selective activation of Na V V 1.1 by venom peptide Hm1a restores the function of inhibitory interneurons from Dravet syndrome mice without affecting the firing of excitatory neurons. Intracerebroventricular infusion of Hm1a rescues Dravet syndrome mice fromseizures and premature death. This precision medicine approach, which specifically targets the molecular deficit in Dravet syndrome, presents an opportunity for treatment of this intractable epilepsy.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk genetic epilepsy spider venom targeted drug therapy seizures Dravet syndrome
Megjelenés:	Proceedings Of The National Academy Of Sciences Of The United States Of America. - 115 : 34 (2018), p. E8077-E8085. -
További szerzők:	Milligan, Carol J. Richardson, Robert J. Jancovski, Nikola Grunnet, Morten Jacobson, Laura H. Undheim, Eivind A. B. Mobli, Mehdi Chow, Chun Yuen Herzig, Volker Csóti Ágota (1989-) (biológus) Panyi György (1966-) (biofizikus) Reid, Christopher A. King, Glenn F. Petrou, Steven
Pályázati támogatás:	GINOP-2.3.2-15-2016-00044 GINOP Australian National Health and Medical Research Council Program Grant 10915693 Egyéb by Citizen's United for Research in Epilepsy Pediatrics Award 353711 Egyéb Principal Research Fellowships Egyéb
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