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排序方式: 共有10000条查询结果,搜索用时 15 毫秒
961.
Maria Carolina Florian Hanna Leins Michael Gobs Yang Han Gina Marka Karin Soller Angelika Vollmer Vadim Sakk Kalpana J. Nattamai Ahmad Rayes Xueheng Zhao Kenneth Setchell Medhanie Mulaw Wolfgang Wagner Yi Zheng Hartmut Geiger 《Aging cell》2020,19(9)
Cdc42 is a small RhoGTPase regulating multiple functions in eukaryotic cells. The activity of Cdc42 is significantly elevated in several tissues of aged mice, while the Cdc42 gain‐of‐activity mouse model presents with a premature aging‐like phenotype and with decreased lifespan. These data suggest a causal connection between elevated activity of Cdc42, aging, and reduced lifespan. Here, we demonstrate that systemic treatment of aged (75‐week‐old) female C57BL/6 mice with a Cdc42 activity‐specific inhibitor (CASIN) for 4 consecutive days significantly extends average and maximum lifespan. Moreover, aged CASIN‐treated animals displayed a youthful level of the aging‐associated cytokines IL‐1β, IL‐1α, and INFγ in serum and a significantly younger epigenetic clock as based on DNA methylation levels in blood cells. Overall, our data show that systemic administration of CASIN to reduce Cdc42 activity in aged mice extends murine lifespan. 相似文献
962.
Acetylation changes tau interactome to degrade tau in Alzheimer’s disease animal and organoid models
Heesun Choi Haeng Jun Kim Jinhee Yang Sehyun Chae Wonik Lee Sunwoo Chung Jisoo Kim Hyunjung Choi Hyeseung Song Chang Kon Lee Jae Hyun Jun Yong Jae Lee Kyunghyeon Lee Semi Kim Hye‐ri Sim Young Il Choi Keun Ho Ryu Jong‐Chan Park Dongjoon Lee Sun‐Ho Han Daehee Hwang Jangbeen Kyung Inhee Mook‐Jung 《Aging cell》2020,19(1)
Alzheimer's disease (AD) is an age‐related neurodegenerative disease. The most common pathological hallmarks are amyloid plaques and neurofibrillary tangles in the brain. In the brains of patients with AD, pathological tau is abnormally accumulated causing neuronal loss, synaptic dysfunction, and cognitive decline. We found a histone deacetylase 6 (HDAC6) inhibitor, CKD‐504, changed the tau interactome dramatically to degrade pathological tau not only in AD animal model (ADLPAPT) brains containing both amyloid plaques and neurofibrillary tangles but also in AD patient‐derived brain organoids. Acetylated tau recruited chaperone proteins such as Hsp40, Hsp70, and Hsp110, and this complex bound to novel tau E3 ligases including UBE2O and RNF14. This complex degraded pathological tau through proteasomal pathway. We also identified the responsible acetylation sites on tau. These dramatic tau‐interactome changes may result in tau degradation, leading to the recovery of synaptic pathology and cognitive decline in the ADLPAPT mice. 相似文献
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964.
Yu‐Guo Yang Xu‐Ping Wang Bing Liu Yuan‐Yuan Zhang Xian‐Shun Lv Jing Li Lei Wei Hua‐Jian Yu Yanyan Hu Hua‐Di Zhang 《Luminescence》2020,35(4):580-585
Dy3+‐doped Y3Al5O12 phosphors were prepared at a relatively low temperature using molten salt synthesis. The phase of the prepared Dy3+‐doped Y3Al5O12 phosphors was confirmed using X‐ray powder diffraction. Results indicated that Dy3+ doping did not change the Y3Al5O12 phase. Following excitation at 352 nm, emission spectra of the Dy3+‐doped Y3Al5O12 phosphors consisted of blue, yellow, and red emission bands. The influence of Dy3+ concentration and excitation wavelength on emission was investigated. The ratio of yellow light to blue light varied with change in Dy3+ doping concentration, due to changes in the structure around Dy3+. Emission intensities also changed when the excitation wavelength was changed. This variation is luminescence generated a system for tunable white light for Dy3+‐doped Y3Al5O12 phosphors. 相似文献
965.
Plasmonics - The effects of surface plasmon (SP) coupling with the excitation radiating dipole on the behaviors of the whispering-gallery resonance (WGR) modes in a hexagonal GaN nanowire cavity... 相似文献
966.
967.
Yumei Li Xinghe Chen Xixi Zeng Shaokun Chen Xi Yang Li Zhang 《Journal of biochemical and molecular toxicology》2020,34(5)
Galectin‐3 (Gal‐3) has been implicated in various biological functions, yet little is known about its role in regulating the dynamics of pulmonary vascular endothelial cells. Gal‐3 was shown to be increased in hypoxic model rats by sequencing analysis. We exposed pulmonary vessel endothelial cells (PVECs) to hypoxia or Gal‐3 stimulation, following which cell apoptosis and autophagy were measured with the relevant methods. The results demonstrated that hypoxia elevated nuclear factor‐κB (NF‐κB) activity and Gal‐3 expression. Gla‐3 decreased the expression of Bcl‐2, Alix, Beclin‐1, Atg5, and LC3A/B. The messenger RNA and protein levels of transient receptor potential channel 1/4 (TRPC1/4) and calpain were reduced after Gal‐3 treatment. Gal‐3 also activated protein kinase B/glycogen synthase kinase‐3 β/mammalian target of rapamycin signaling pathways in PVECs. These results suggest that a hypoxia‐mediated increase in Gal‐3 promotes apoptosis and inhibits autophagy by inhibiting the TRPC1/4 pathway and activating the protein kinase B/glycogen synthase kinase‐3 β/mammalian target of rapamycin signaling pathway in PVECs. Furthermore, these results may provide us with a new direction to explore the pathogenesis of pulmonary artery hypertension. 相似文献
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