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991.
992.
Xinxin Wang Xin Ma Gaobo Wei Weirui Ma Zhen Zhang Xuepeng Chen Lei Gao Zhenbo Liu Yue Yuan Lizhi Yi Jun Wang Toshinobu Tokumoto Junjiu Huang Dahua Chen Jian Zhang Jiang Liu 《基因组蛋白质组与生物信息学报(英文版)》2021,19(1):48-63
DNA methylation is a prevalent epigenetic modification in vertebrates, and it has been shown to be involved the regulation of gene expression and embryo development. However, it remains unclear how DNA methylation regulates sexual development, especially in species without sex chromosomes. To determine this, we utilized zebrafish to investigate DNA methylation reprogramming during juvenile germ cell development and adult female-to-male sex transition.We reveal that primordial germ cells(PGCs) undergo significant DNA methylation reprogramming during germ cell development, and the methylome of PGCs is reset to an oocyte/ovary-like pattern at 9 days post fertilization(9 dpf). When DNA methyltransferase(DNMT) activity in juveniles was blocked after 9 dpf, the zebrafish developed into females. We also show that Tet3 is involved in PGC development. Notably, we find that DNA methylome reprogramming during adult zebrafish sex transition is similar to the reprogramming during the sex differentiation from 9 dpf PGCs to sperm. Furthermore, inhibiting DNMT activity can prevent the female-to-male sex transition, suggesting that methylation reprogramming is required for zebrafish sex transition. In summary, DNA methylation plays important roles in zebrafish germ cell development and sexual plasticity. 相似文献
993.
Jingwen Ai Haocheng Zhang Qiran Zhang Yi Zhang Ke Lin Zhangfan Fu Jieyu Song Yuanhan Zhao Mingxiang Fan Hongyu Wang Chao Qiu Yang Zhou Wenhong Zhang 《Cell research》2022,32(1):103-106
Dear Editor,
As of October,2021,SARS-CoV-2 has infected more than 230 million people;promoting roll-out vaccinations could help build herd immunity for the pand... 相似文献
994.
995.
Michael S. Dahabieh Fan Huang Christophe Goncalves Raúl Ernesto Flores Gonzlez Sathyen Prabhu Alicia Bolt Erminia Di Pietro Elie Khoury John Heath Zi Yi Xu Joelle Rmy-Sarrazin Koren K. Mann Alexandre Orthwein Franois-Michel Boisvert Nancy Braverman Wilson H. Miller Sonia V. del Rincn 《Autophagy》2022,18(3):540
996.
Cailian Fan Sui Liang Mengnan Ye Wanjun Cai Miao Chen Yunlong Hou Jun Guo Yi Dai 《Journal of cellular and molecular medicine》2022,26(9):2607
Pathological cardiac hypertrophy is the most important risk factor for developing chronic heart failure. Therefore, the discovery of novel agents for treating pathological cardiac hypertrophy remains urgent. In the present study, we examined the therapeutic effect and mechanism of periplocymarin (PM)‐mediated protection against pathological cardiac hypertrophy using angiotensinII (AngII)‐stimulated cardiac hypertrophy in H9c2 cells and transverse aortic constriction (TAC)‐induced cardiac hypertrophy in mice. In vitro, PM treatment significantly reduced the surface area of H9c2 cells and expressions of hypertrophy‐related proteins. Meanwhile, PM markedly down‐regulated AngII‐induced translocation of p‐STAT3 into the nuclei and enhanced the phosphorylation levels of JAK2 and STAT3 proteins. The STAT3 specific inhibitor S3I‐201 or siRNA‐mediated depleted expression could alleviate AngII‐induced cardiac hypertrophy in H9c2 cells following PM treatment; however, PM failed to reduce the expressions of hypertrophy‐related proteins and phosphorylated STAT3 in STAT3‐overexpressing cells, indicating that PM protected against AngII‐induced cardiac hypertrophy by modulating STAT3 signalling. In vivo, PM reversed TAC‐induced cardiac hypertrophy, as determined by down‐regulating ratios of heart weight to body weight (HW/BW), heart weight to tibial length (HW/TL) and expressions of hypertrophy‐related proteins accompanied by the inhibition of the JAK2/STAT3 pathway. These results revealed that PM could effectively protect the cardiac structure and function in experimental models of pathological cardiac hypertrophy by inhibiting the JAK2/STAT3 signalling pathway. PM is expected to be a potential lead compound of the novel agents for treating pathological cardiac hypertrophy. 相似文献
997.
998.
Markus Albert Anna K. Jehle Martin Lipschis Katharina Mueller Yi Zeng Georg Felix 《European journal of cell biology》2010,89(2-3):200-207
In this review we focus on pattern recognition receptors in plants that detect extracellular signals indicative for pathogen attack and injury. We start out with a discussion on FLS2, which binds and responds to bacterial flagellin, and then concentrate on ligand–receptor interactions as initial steps in the molecular receptor activation process. Comparison with other receptor kinases, whether involved in plant immunity or regulation of other cellular programs, might indicate common principles of receptor activation. 相似文献
999.
Walters RW Yi SM Keshavjee S Brown KE Welsh MJ Chiorini JA Zabner J 《The Journal of biological chemistry》2001,276(23):20610-20616
Recombinant adeno-associated viruses (AAV) are promising gene therapy vectors. Whereas AAV serotype 2-mediated gene transfer to muscle has partially replaced factor IX deficiency in hemophilia patients, its ability to mediate gene transfer to the lungs for cystic fibrosis is hindered by lack of apical receptors. However, AAV serotype 5 infects human airway epithelia from the lumenal surface. We found that in contrast to AAV2, the apical membrane of airway epithelia contains abundant high affinity receptors for AAV5. Binding and gene transfer with AAV5 was abolished by genetic or enzymatic removal of sialic acid from the cell surface. Furthermore, binding and gene transfer to airway epithelia was competed by lectins that specifically bind 2,3-linked sialic acid. These observations suggest that 2,3-linked sialic acid is either a receptor for AAV5 or it is a necessary component of a receptor complex. Further elucidation of the receptor for this virus should enhance understanding of parvovirus biology and expand the therapeutic targets for AAV vectors. 相似文献
1000.
Southall MD Isenberg JS Nakshatri H Yi Q Pei Y Spandau DF Travers JB 《The Journal of biological chemistry》2001,276(49):45548-45554