排序方式: 共有16条查询结果,搜索用时 31 毫秒
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Jie Wu Sol Kim Man Sup Kwak Jang Bin Jeong Hyun Jin Min Ho-Geun Yoon Jin-Hyun Ahn Jeon-Soo Shin 《The Journal of biological chemistry》2014,289(29):20000-20011
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Masaoka A Gassman NR Kedar PS Prasad R Hou EW Horton JK Bustin M Wilson SH 《The Journal of biological chemistry》2012,287(33):27648-27658
In mammalian cells, the nucleosome-binding protein HMGN1 (high mobility group N1) affects the structure and function of chromatin and plays a role in repair of damaged DNA. HMGN1 affects the interaction of DNA repair factors with chromatin and their access to damaged DNA; however, not all of the repair factors affected have been identified. Here, we report that HMGN1 affects the self-poly(ADP-ribosyl)ation (i.e., PARylation) of poly(ADP-ribose) polymerase-1 (PARP-1), a multifunctional and abundant nuclear enzyme known to recognize DNA lesions and promote chromatin remodeling, DNA repair, and other nucleic acid transactions. The catalytic activity of PARP-1 is activated by DNA with a strand break, and this results in self-PARylation and PARylation of other chromatin proteins. Using cells obtained from Hmgn1(-/-) and Hmgn1(+/+) littermate mice, we find that in untreated cells, loss of HMGN1 protein reduces PARP-1 self-PARylation. A similar result was obtained after MMS treatment of these cells. In imaging experiments after low energy laser-induced DNA damage, less PARylation at lesion sites was observed in Hmgn1(-/-) than in Hmgn1(+/+) cells. The HMGN1 regulation of PARP-1 activity could be mediated by direct protein-protein interaction as HMGN1 and PARP-1 were found to interact in binding assays. Purified HMGN1 was able to stimulate self-PARylation of purified PARP-1, and in experiments with cell extracts, self-PARylation was greater in Hmgn1(+/+) than in Hmgn1(-/-) extract. The results suggest a regulatory role for HMGN1 in PARP-1 activation. 相似文献
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Toshihiro Kurahashi Takashi Furusawa Tetsuya Ueda Michael Bustin 《Journal of cellular biochemistry》2010,109(1):49-57
Glucose homeostasis requires the coordinated actions of various organs and is critically dependent on the proper functioning of the various cell types present in the pancreatic Langerhans islets. Here we report that chromatin architectural protein HMGN3 is highly expressed in all pancreatic endocrine islet cells, and that Hmgn3?/? mice which have a mild diabetic phenotype, have reduced glucagon levels in their blood. To elucidate the mechanism leading to altered glucagon secretion of Hmgn3?/? mice, we tested whether HMGN3 affect glucagon synthesis and secretion in αTC1‐9 cells, a glucagon secreting cell line that is used to study pancreatic α‐cell function. We find that in these cells deletion of either HMGN3 or other HMGN variants, does not significantly affect glucagon gene expression or glucagon secretion. Our studies demonstrate a link between HMGN3 and glucagon blood levels that is not directly dependent of the function of pancreatic α‐cells. J. Cell. Biochem. 109: 49–57, 2010. Published 2009 Wiley‐Liss, Inc. 相似文献
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人 LAK 细胞免疫效应分子 HMGN2 的鉴定 总被引:3,自引:0,他引:3
为分离纯化人淋巴因子激活的杀伤细胞(LAK)小分子抗菌多肽,应用制备尿素-聚丙烯酰胺凝胶电泳技术和反向高效液相色谱技术分离纯化人LAK细胞酸溶性提取物,纯化出一个具抗菌活性的多肽HLP-3p21.蛋白质N端氨基酸测序、质谱精确分子质量测定、蛋白质印迹分析证明HLP-3p21为HMGN2.最小抑菌浓度(MIC)和最小杀菌浓度(MBC)试验证明HMGN2有抗大肠杆菌ML-35p氨苄青霉素耐药株、铜绿假单胞菌ATCC27853、白色念珠菌ATCC 10231活性,无抗金黄色葡萄球菌ATCC25923活性.制备HMGN2多克隆抗体,应用免疫荧光化学、酶联免疫吸附测定和蛋白质印迹方法对HMGN2进行定位分析,证明单个核细胞经IL-2刺激成为LAK细胞时部分HMGN2由胞核转移至胞浆,进而分泌到胞外.提示HMGN2是LAK细胞一个新的免疫效应分子. 相似文献
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CRISPR‐Cas gene editing holds substantial promise in many biomedical disciplines and basic research. Due to the important functional implications of non‐histone chromosomal protein HMG‐14 (HMGN1) in regulating chromatin structure and tumor immunity, gene knockout of HMGN1 is performed by CRISPR in cancer cells and the following proteomic regulation events are studied. In particular, DIA mass spectrometry (DIA‐MS) is utilized, and more than 6200 proteins (protein‐ FDR 1%) and more than 82 000 peptide precursors are reproducibly measured in the single MS shots of 2 h. HMGN1 protein deletion is confidently verified by DIA‐MS in all of the clone‐ and dish‐ replicates following CRISPR. Statistical analysis reveals 147 proteins change their expressions significantly after HMGN1 knockout. Functional annotation and enrichment analysis indicate the deletion of HMGN1 induces histone inactivation, various stress pathways, remodeling of extracellular proteomes, cell proliferation, as well as immune regulation processes such as complement and coagulation cascade and interferon alpha/ gamma response in cancer cells. These results shed new lights on the cellular functions of HMGN1. It is suggested that DIA‐MS can be reliably used as a rapid, robust, and cost‐effective proteomic‐screening tool to assess the outcome of the CRISPR experiments. 相似文献