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41.
Jin Wei Mia Madel Alfajaro Peter C. DeWeirdt Ruth E. Hanna William J. Lu-Culligan Wesley L. Cai Madison S. Strine Shang-Min Zhang Vincent R. Graziano Cameron O. Schmitz Jennifer S. Chen Madeleine C. Mankowski Renata B. Filler Neal G. Ravindra Victor Gasque Fernando J. de Miguel Ajinkya Patil Huacui Chen Craig B. Wilen 《Cell》2021,184(1):76-91.e13
42.
Ryan A. Flynn Julia A. Belk Yanyan Qi Yuki Yasumoto Jin Wei Mia Madel Alfajaro Quanming Shi Maxwell R. Mumbach Aditi Limaye Peter C. DeWeirdt Cameron O. Schmitz Kevin R. Parker Elizabeth Woo Howard Y. Chang Tamas L. Horvath Jan E. Carette Carolyn R. Bertozzi Craig B. Wilen Ansuman T. Satpathy 《Cell》2021,184(9):2394-2411.e16
43.
Tao Tan Jun Wu Chenyang Si Shaoxing Dai Youyue Zhang Nianqin Sun E Zhang Honglian Shao Wei Si Pengpeng Yang Hong Wang Zhenzhen Chen Ran Zhu Yu Kang Reyna Hernandez-Benitez Llanos Martinez Martinez Estrella Nuñez Delicado W. Travis Berggren Juan Carlos Izpisua Belmonte 《Cell》2021,184(8):2020-2032.e14
44.
James K. Nuñez Jin Chen Greg C. Pommier J. Zachery Cogan Joseph M. Replogle Carmen Adriaens Gokul N. Ramadoss Quanming Shi King L. Hung Avi J. Samelson Angela N. Pogson James Y.S. Kim Amanda Chung Manuel D. Leonetti Howard Y. Chang Martin Kampmann Bradley E. Bernstein Volker Hovestadt Jonathan S. Weissman 《Cell》2021,184(9):2503-2519.e17
45.
Bethany M. Henrick Lucie Rodriguez Tadepally Lakshmikanth Christian Pou Ewa Henckel Aron Arzoomand Axel Olin Jun Wang Jaromir Mikes Ziyang Tan Yang Chen Amy M. Ehrlich Anna Karin Bernhardsson Constantin Habimana Mugabo Ylva Ambrosiani Anna Gustafsson Stephanie Chew Heather K. Brown Petter Brodin 《Cell》2021,184(15):3884-3898.e11
46.
Jun Seong Jeong Min Jee Kim Jeong Sun Park Keon Hee Lee Yong Hun Jo Jun-ichi Takahashi Yong Soo Choi Iksoo Kim 《Journal of Asia》2021,24(2):135-147
The yellow-legged hornet, Vespa velutina nigrithorax (Hymenoptera: Vespidae), invaded South Korea in 2003 through Busan metropolitan city, which is located in the southeast region of the country. Previous studies aiming to trace the origin of V. velutina in Korea used a portion of mitochondrial (mt) COI and detected a single haplotype common to the site of origin. However, no subsequent study on invasive dynamics such as additional entry and/or another site of entry has been performed. In this study, segments of mt COI, CytB, and lrRNA were sequenced from 238 individuals collected in 11 Korean and two Japanese localities, but no variation in each gene was observed. Thus, we developed two intergenic spacer (IGS) sequences from the publicly available mt genome of V. velutina, which provided substantially increased variability (i.e., 19 haplotypes with 1.74% maximum sequence divergence in 1,129–1,146-bp-long concatenated sequences). Population genetic analyses using the concatenated sequences unexpectedly provided higher genetic diversity estimates in the northwest and southwest regions, both of which also harbor international cargo ports, than in the southeast region, in which Busan is located. Furthermore, this genetic result was roughly concordant with our questionnaire survey demonstrating that V. velutina was observed in apiaries located in the northwest and southwest regions up to 2012, when there was no reported prevalent distribution of the hornet beyond the southeast region. These results collectively suggest that the northwest and southwest regions of Korea are additional sites of V. velutina entry to the country, independent from the southeast region origin. 相似文献
47.
Nan Cheng Chang Jin Ping Jin Dan Zhu Zuoxu Hou 《Journal of cellular and molecular medicine》2021,25(13):6137-6147
High glucose promoted expression of AKT3, a direct target gene of miR-29b, by regulating circHIPK3 that functioned as ceRNA to sponge and down-regulate miR-29b. As a potential target gene of miR-29b, AKT3 plays a crucial role in the pathogenesis of myocardial ischaemia/reperfusion (I/R) injury, and this study aimed to investigate the potential role of high glucose in the outcome of I/R injury. qPCR and luciferase assay were carried out to investigate the relationship between the expression of circHIPK3, miR-29b and ATK3 mRNA. Immunohistochemistry and TUNEL were performed to analyse the relationship between AKT3 expression and apoptosis of myocardiocytes in vivo. No obvious difference in myocardial functions was observed between I/R and control rats under hyperglycaemia (HG) and normal glucose (NG) conditions, except that the infarct size/area at risk (IS/AR) ratio and the amount of h-FABP expression were different under HG and NG conditions. The expression of circHIPK3 and ATK3 was significantly elevated in the rats preconditioned by NG, whereas the expression of miR-29a was remarkably decreased. Meanwhile, the apoptosis of myocardial tissue was reduced in the rats preconditioned by NG. Luciferase assay confirmed that miR-29a played a repressive role in the expression of circHIPK3 and ATK3. And subsequent study indicated that the over-expressed AKT3 could rescue the increased cell apoptosis rate induced by the knockdown of circHIPK3. In this study, we demonstrated that high glucose protects cardiomyocytes against I/R associated injury by suppressing apoptosis and high glucose promoted the expression of AKT3 by regulating the expression of circHIPK3/miR-29b. 相似文献
48.
49.
Derlin-1 plays a critical role in endoplasmic reticulum-associated protein degradation (ERAD) of a particular subset of proteins. Although it is generally accepted that Derlin-1 mediates the export of ERAD substrates from the ER to the cytosol, little is known about how Derlin-1 interacts with these substrates. Human cytomegalovirus (HCMV) US11 exploits Derlin-1-dependent ERAD to degrade major histocompatibility complex class I (MHC-I) molecules and evade immune surveillance. US11 requires the cytosolic tail of the MHC-I heavy chain to divert MHC-I molecules into the ERAD pathway for degradation; however, the underlying mechanisms remain unknown. Here, we show that the cytosolic tail of the MHC-I heavy chain, although not required for interaction with US11, is required for tight binding to Derlin-1 and thus for US11-induced dislocation of the MHC-I heavy chain to the cytosol for proteasomal degradation. Surprisingly, deletion of a single C-terminal amino acid from the cytosolic tail disrupted the interaction between MHC-I molecules and Derlin-1, rendering mutant MHC-I molecules resistant to US11-induced degradation. Consistently, deleting the C-terminal cytosolic region of Derlin-1 prevented it from binding to MHC-I molecules. Taken together, these results suggest that the cytosolic region of Derlin-1 is involved in ERAD substrate binding and that this interaction is critical for the Derlin-1-mediated dislocation of the MHC-I heavy chain to the cytosol during US11-induced MHC-I degradation. 相似文献
50.
Yan Sun Chong-Chong Xu Jin Li Xi-Yin Guan Lu Gao Li-Xiang Ma Rui-Xi Li Yu-Wen Peng Guo-Pei Zhu 《PloS one》2013,8(2)
Demyelination contributes to the functional impairment of irradiation injured spinal cord. One potential therapeutic strategy involves replacing the myelin-forming cells. Here, we asked whether transplantation of Olig2+-GFP+-oligodendrocyte precursor cells (OPCs), which are derived from Olig2-GFP-mouse embryonic stem cells (mESCs), could enhance remyelination and functional recovery after spinal cord irradiation injury. We differentiated Olig2-GFP-mESCs into purified Olig2+-GFP+-OPCs and transplanted them into the rats’ cervical 4–5 dorsal spinal cord level at 4 months after irradiation injury. Eight weeks after transplantation, the Olig2+-GFP+-OPCs survived and integrated into the injured spinal cord. Immunofluorescence analysis showed that the grafted Olig2+-GFP+-OPCs primarily differentiated into adenomatous polyposis coli (APC+) oligodendrocytes (54.6±10.5%). The staining with luxol fast blue, hematoxylin & eosin (LFB/H&E) and electron microscopy demonstrated that the engrafted Olig2+-GFP+-OPCs attenuated the demyelination resulted from the irradiation. More importantly, the recovery of forelimb locomotor function was enhanced in animals receiving grafts of Olig2+-GFP+-OPCs. We concluded that OPC transplantation is a feasible therapy to repair the irradiated lesions in the central nervous system (CNS). 相似文献