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961.
Zhu Kai Guo Song Han Guoyi Qiang Xiancheng Ma Mengmeng Xu Qinglei Tang Wenjie Tan Jun 《Molecular biology reports》2022,49(5):3783-3792
Molecular Biology Reports - Oxidative stress in the intervertebral disc leads to nucleus pulposus (NP) degeneration by inducing cell apoptosis. However, the molecular mechanisms underlying this... 相似文献
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Cheng Zhuru Zhu Xiaonian Zeng Dan Feng Qiao Tian Baodong Zheng Haiqing Tan Shengkui Zhu Chunjiang 《Molecular biology reports》2022,49(7):6199-6205
Molecular Biology Reports - The hematological phenotype and genotype analysis of hemoglobin New York (Hb New York) combined with α or β thalassemia has been rarely reported, and whether... 相似文献
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Luxi Sun Rong Tan Jianquan Xu Justin LaFace Ying Gao Yanchun Xiao Myriam Attar Carola Neumann Guo-Min Li Bing Su Yang Liu Satoshi Nakajima Arthur S. Levine Li Lan 《Nucleic acids research》2015,43(13):6334-6347
Cellular DNA is organized into chromosomes and capped by a unique nucleoprotein structure, the telomere. Both oxidative stress and telomere shortening/dysfunction cause aging-related degenerative pathologies and increase cancer risk. However, a direct connection between oxidative damage to telomeric DNA, comprising <1% of the genome, and telomere dysfunction has not been established. By fusing the KillerRed chromophore with the telomere repeat binding factor 1, TRF1, we developed a novel approach to generate localized damage to telomere DNA and to monitor the real time damage response at the single telomere level. We found that DNA damage at long telomeres in U2OS cells is not repaired efficiently compared to DNA damage in non-telomeric regions of the same length in heterochromatin. Telomeric DNA damage shortens the average length of telomeres and leads to cell senescence in HeLa cells and cell death in HeLa, U2OS and IMR90 cells, when DNA damage at non-telomeric regions is undetectable. Telomere-specific damage induces chromosomal aberrations, including chromatid telomere loss and telomere associations, distinct from the damage induced by ionizing irradiation. Taken together, our results demonstrate that oxidative damage induces telomere dysfunction and underline the importance of maintaining telomere integrity upon oxidative damage. 相似文献
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FERONIA receptor kinase interacts with S‐adenosylmethionine synthetase and suppresses S‐adenosylmethionine production and ethylene biosynthesis in Arabidopsis 下载免费PDF全文
Dandan Mao Feng Yu Jian Li Bram Van de poel Dan Tan Jianglin Li Yanqionq Liu Xiushang Li Mengqiu Dong Liangbi Chen Dongping Li Sheng Luan 《Plant, cell & environment》2015,38(12):2566-2574
Environmental inputs such as stress can modulate plant cell metabolism, but the detailed mechanism remains unclear. We report here that FERONIA (FER), a plasma membrane receptor‐like kinase, may negatively regulate the S‐adenosylmethionine (SAM) synthesis by interacting with two S‐adenosylmethionine synthases (SAM1 and SAM2). SAM participates in ethylene, nicotianamine and polyamine biosynthetic pathways and provides the methyl group for protein and DNA methylation reactions. The Arabidopsis fer mutants contained a higher level of SAM and ethylene in plant tissues and displayed a dwarf phenotype. Such phenotype in the fer mutants was mimicked by over‐expressing the S‐adenosylmethionine synthetase in transgenic plants, whereas sam1/2 double mutant showed an opposite phenotype. We propose that FER receptor kinase, in response to environmental stress and plant hormones such as auxin and BR, interacts with SAM synthases and down‐regulates ethylene biosynthesis. 相似文献