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排序方式: 共有206条查询结果,搜索用时 15 毫秒
81.
David Danko Daniela Bezdan Evan E. Afshin Sofia Ahsanuddin Chandrima Bhattacharya Daniel J. Butler Kern Rei Chng Daisy Donnellan Jochen Hecht Katelyn Jackson Katerina Kuchin Mikhail Karasikov Abigail Lyons Lauren Mak Dmitry Meleshko Harun Mustafa Beth Mutai Russell Y. Neches Stas Zubenko 《Cell》2021,184(13):3376-3393.e17
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82.
Leandro H Gallo April N Meyer Khatereh Motamedchaboki Katelyn N Nelson Martin Haas 《Cell cycle (Georgetown, Tex.)》2014,13(24):3964-3976
NFκB signaling plays a significant role in human disease, including breast and ovarian carcinoma, insulin resistance, embryonic lethality and liver degeneration, rheumatoid arthritis, aging and Multiple Myeloma (MM). Inhibitor of κB (IκB) kinase β (IKKβ) regulates canonical Nuclear Factor κB (NFκB) signaling in response to inflammation and cellular stresses. NFκB activation requires Lys63-linked (K63-linked) ubiquitination of upstream proteins such as NEMO or TAK1, forming molecular complexes with membrane-bound receptors. We demonstrate that IKKβ itself undergoes K63-linked ubiquitination. Mutations in IKKβ at Lys171, identified in Multiple Myeloma and other cancers, lead to a dramatic increase in kinase activation and K63-linked ubiquitination. These mutations also result in persistent activation of STAT3 signaling. Liquid chromatography (LC)-high mass accuracy tandem mass spectrometry (MS/MS) analysis identified Lys147, Lys418, Lys555 and Lys703 as predominant ubiquitination sites in IKKβ. Specific inhibition of the UBC13-UEV1A complex responsible for K63-linked ubiquitination establishes Lys147 as the predominant site of K63-ubiquitin conjugation and responsible for STAT3 activation. Thus, IKKβ activation leads to ubiquitination within the kinase domain and assemblage of a K63-ubiquitin conjugated signaling platform. These results are discussed with respect to the importance of upregulated NFκB signaling known to occur frequently in MM and other cancers. 相似文献
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Hsin‐Chieh Yeh John P. Bantle Maria Cassidy‐Begay George Blackburn George A. Bray Tim Byers Jeanne M. Clark Mace Coday Caitlin Egan Mark A. Espeland John P. Foreyt Katelyn Garcia Valerie Goldman Edward W. Gregg Helen P. Hazuda Louise Hesson James O. Hill Edward S. Horton John M. Jakicic Robert W. Jeffery Karen C. Johnson Steven E. Kahn William C. Knowler Mary Korytkowski Anne Kure Cora E. Lewis Christos Mantzoros Maria Meacham Maria G. Montez David M. Nathan Nicholas Pajewski Jennifer Patricio Anne Peters F. Xavier Pi‐Sunyer Henry Pownall Donna H. Ryan Monika Safford Rebecca L. Sedjo Helmut Steinburg Mara Vitolins Thomas A. Wadden Lynne E. Wagenknecht Rena R. Wing Antonio C. Wolff Holly Wyatt Susan Z. Yanovski 《Obesity (Silver Spring, Md.)》2020,28(9):1678-1686
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Sophia A. Pacheco Katelyn M. Powers Flora Engelmann Ilhem Messaoudi Georgiana E. Purdy 《PloS one》2013,8(6)
Non-human primates, notably rhesus macaques (Macaca mulatta, RM), provide a robust experimental model to investigate the immune response to and effective control of Mycobacterium tuberculosis infections. Changes in the function of immune cells and immunosenescence may contribute to the increased susceptibility of the elderly to tuberculosis. The goal of this study was to examine the impact of age on M. tuberculosis host-pathogen interactions following infection of primary alveolar macrophages derived from young and aged rhesus macaques. Of specific interest to us was whether the mycobactericidal capacity of autophagic macrophages was reduced in older animals since decreased autophagosome formation and autophagolysosomal fusion has been observed in other cells types of aged animals. Our data demonstrate that alveolar macrophages from old RM are as competent as those from young animals for autophagic clearance of M. tuberculosis infection and controlling mycobacterial replication. While our data do not reveal significant differences between alveolar macrophage responses to M. tuberculosis by young and old animals, these studies are the first to functionally characterize autophagic clearance of M. tuberculosis by alveolar macrophages from RM. 相似文献
88.
Laura J. Claxton Jeffrey M. Haddad Katelyn Ponto Joong Hyun Ryu Sean C. Newcomer 《PloS one》2013,8(8)
Independent stance is one of the most difficult motor milestones to achieve. Newly standing infants exhibit exaggerated body movements and can only stand for a brief amount of time. Given the difficult nature of bipedal stance, these unstable characteristics are slow to improve. However, we demonstrate that infants can increase their stability when engaged in a standing goal-directed task. Infants'' balance was measured while standing and while standing and holding a visually attractive toy. When holding the toy, infants stood for a longer period of time, exhibited less body sway, and more mature postural dynamics. These results demonstrate that even with limited standing experience, infants can stabilize posture to facilitate performance of a concurrent task. 相似文献
89.
Christine M. Shortt Anne Fredsted Aidan Bradford Ken D. O’Halloran 《The journal of histochemistry and cytochemistry》2013,61(7):487-499
Respiratory muscle remodeling occurs in human sleep apnea—a common respiratory disorder characterized by chronic intermittent hypoxia (CIH) due to recurrent apnea during sleep. We sought to determine if CIH causes remodeling in rat sternohyoid (upper airway dilator) and diaphragm muscles. Adult male Wistar rats were exposed to CIH (n=8), consisting of 90 sec of hypoxia (5% at the nadir; SaO2 ~80%)/90 sec of normoxia, 8 hr per day, for 7 consecutive days. Sham animals (n=8) were exposed to alternating air/air cycles in parallel. The effect of CIH on myosin heavy-chain (MHC) isoform (1, 2a, 2x, 2b) distribution, sarcoplasmic reticulum calcium ATPase (SERCA) isoform distribution, succinate dehydrogenase activity, glycerol phosphate dehydrogenase activity, and Na+/K+ ATPase pump content was determined. Sternohyoid muscle structure was unaffected by CIH treatment. CIH did not alter oxidative/glycolytic capacity or the Na+/K+-ATPase pump content of the diaphragm. CIH significantly increased the areal density of MHC 2b fibers in the rat diaphragm, and this was associated with a shift in SERCA proteins from SERCA2 to SERCA1. We conclude that CIH causes a slow-to-fast fiber transition in the rat diaphragm after just 7 days of treatment. Respiratory muscle functional remodeling may drive aberrant functional plasticity such as decreased muscle endurance, which is a feature of human sleep apnea. 相似文献
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