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作者:Saag, Lehti; Metspalu, Mait
作者单位:University of Tartu; Estonian Biocentre
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作者:Williams, Michael J.
作者单位:University of Portsmouth
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作者:Amelio, Ivano
作者单位:University of Konstanz
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作者:Bourzac, Katherine
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作者:Marris, Emma
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作者:Zhou, Hao; Hu, Jiashun; Dal Zilio, Luca; Tang, Ming; Li, Keqing; Hu, Xiumian
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作者:Vazquez Torres, Susana; Benard Valle, Melisa; Mackessy, Stephen P.; Menzies, Stefanie K.; Casewell, Nicholas R.; Ahmadi, Shirin; Burlet, Nick J.; Muratspahic, Edin; Sappington, Isaac; Overath, Max D.; Rivera-de-Torre, Esperanza; Ledergerber, Jann; Laustsen, Andreas H.; Boddum, Kim; Bera, Asim K.; Kang, Alex; Brackenbrough, Evans; Cardoso, Iara A.; Crittenden, Edouard P.; Edge, Rebecca J.; Decarreau, Justin; Ragotte, Robert J.; Pillai, Arvind S.; Abedi, Mohamad; Han, Hannah L.; Gerben, Stacey R.; Murray, Analisa; Skotheim, Rebecca; Stuart, Lynda; Stewart, Lance; Fryer, Thomas J. A.; Jenkins, Timothy P.; Baker, David
作者单位:University of Washington; University of Washington Seattle; University of Washington; University of Washington Seattle; University of Washington; University of Washington Seattle; Technical University of Denmark; University of Northern Colorado; University of Liverpool; Liverpool School of Tropical Medicine; Liverpool School of Tropical Medicine; University of Liverpool; Lancaster University; University of Liverpool; Massachusetts Institute of Technology (MIT); University of Washington; University of Washington Seattle; Howard Hughes Medical Institute
摘要:Snakebite envenoming remains a devastating and neglected tropical disease, claiming over 100,000 lives annually and causing severe complications and long-lasting disabilities for many more1,2. Three-finger toxins (3FTx) are highly toxic components of elapid snake venoms that can cause diverse pathologies, including severe tissue damage3 and inhibition of nicotinic acetylcholine receptors, resulting in life-threatening neurotoxicity4. At present, the only available treatments for snakebites con...
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作者:Pinto, Daniel F. Cardozo; Pomrenze, Matthew B.; Guo, Michaela Y.; Touponse, Gavin C.; Chen, Allen P. F.; Bentzley, Brandon S.; Eshel, Neir; Malenka, Robert C.
作者单位:Stanford University
摘要:The neuromodulators dopamine (DA) and serotonin (5-hydroxytryptamine; 5HT) powerfully regulate associative learning1, 2, 3, 4, 5, 6, 7-8. Similarities in the activity and connectivity of these neuromodulatory systems have inspired competing models of how DA and 5HT interact to drive the formation of new associations9, 10, 11, 12, 13-14. However, these hypotheses have not been tested directly because it has not been possible to interrogate and manipulate multiple neuromodulatory systems in a si...
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作者:Worth, Tammy
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作者:Xie, Xiaowen; Zhang, Olivia; Yeo, Megan J. R.; Lee, Ceejay; Tao, Ran; Harry, Stefan A.; Payne, N. Connor; Nam, Eunju; Paul, Leena; Li, Yiran; Kwok, Hui Si; Jiang, Hanjie; Mao, Haibin; Hadley, Jennifer L.; Lin, Hong; Batts, Melissa; Gosavi, Pallavi M.; D'Angiolella, Vincenzo; Cole, Philip A.; Mazitschek, Ralph; Northcott, Paul A.; Zheng, Ning; Liau, Brian B.
作者单位:University of Washington; University of Washington Seattle; Howard Hughes Medical Institute; University of Washington; University of Washington Seattle; Harvard University; Harvard University; Massachusetts Institute of Technology (MIT); Broad Institute; St Jude Children's Research Hospital; St Jude Children's Research Hospital; Harvard University; Harvard University Medical Affiliates; Massachusetts General Hospital; Harvard University; Harvard T.H. Chan School of Public Health; Harvard University; Harvard Medical School; Harvard University Medical Affiliates; Brigham & Women's Hospital; University of Edinburgh
摘要:Cancer mutations can create neomorphic protein-protein interactions to drive aberrant function1,2. As a substrate receptor of the CULLIN3-RING E3 ubiquitin ligase complex, KBTBD4 is recurrently mutated in medulloblastoma3, the most common embryonal brain tumour in children4. These mutations impart gain-of-function to KBTBD4 to induce aberrant degradation of the transcriptional corepressor CoREST5. However, their mechanism remains unresolved. Here we establish that KBTBD4 mutations promote CoRE...