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RISS 인기검색어
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- 저자 : Chunmei Xie (검색결과 3 건)
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Metabolic Regulation of Gene Expression by Histone Lysine β-Hydroxybutyrylation
Xie, Zhongyu,Zhang, Di,Chung, Dongjun,Tang, Zhanyun,Huang, He,Dai, Lunzhi,Qi, Shankang,Li, Jingya,Colak, Gozde,Chen, Yue,Xia, Chunmei,Peng, Chao,Ruan, Haibin,Kirkey, Matt,Wang, Danli,Jensen, Lindy M. Elsevier 2016 Molecular cell Vol.62 No.2
<P><B>Summary</B></P> <P>Here we report the identification and verification of a β-hydroxybutyrate-derived protein modification, lysine β-hydroxybutyrylation (Kbhb), as a new type of histone mark. Histone Kbhb marks are dramatically induced in response to elevated β-hydroxybutyrate levels in cultured cells and in livers from mice subjected to prolonged fasting or streptozotocin-induced diabetic ketoacidosis. In total, we identified 44 histone Kbhb sites, a figure comparable to the known number of histone acetylation sites. By ChIP-seq and RNA-seq analysis, we demonstrate that histone Kbhb is a mark enriched in active gene promoters and that the increased H3K9bhb levels that occur during starvation are associated with genes upregulated in starvation-responsive metabolic pathways. Histone β-hydroxybutyrylation thus represents a new epigenetic regulatory mark that couples metabolism to gene expression, offering a new avenue to study chromatin regulation and diverse functions of β-hydroxybutyrate in the context of important human pathophysiological states, including diabetes, epilepsy, and neoplasia.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Lysine β-hydroxybutyrylation (Kbhb) is a new type of histone mark </LI> <LI> 44 non-redundant histone Kbhb sites are identified in human and mouse cells </LI> <LI> Histone Kbhb increases under starvation and STZ-induced ketoacidosis </LI> <LI> Starvation-induced H3K9bhb is associated with active gene expression </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>
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Lan Li,Peng Wang,Jing Jin,Chunmei Xie,Bin Xue,Jiancheng Lai,Liya Zhu,Qing Jiang 한국생체재료학회 2022 생체재료학회지 Vol.26 No.4
Background: The meniscus injury is a common disease in the area of sports medicine. The main treatment for this disease is the pain relief, rather than the meniscal function recovery. It may lead to a poor prognosis and accelerate the progression of osteoarthritis. In this study, we designed a meniscal scaffold to achieve the purposes of meniscal function recovery and cartilage protection. Methods: The meniscal scaffold was designed using the triply periodic minimal surface (TPMS) method. The scaffold was simulated as a three-dimensional (3D) intact knee model using a finite element analysis software to obtain the results of different mechanical tests. The mechanical properties were gained through the universal machine. Finally, an in vivo model was established to evaluate the effects of the TPMS-based meniscal scaffold on the cartilage protection. The radiography and histological examinations were performed to assess the cartilage and bony structures. Different regions of the regenerated meniscus were tested using the universal machine to assess the biomechanical functions. Results: The TPMS-based meniscal scaffold with a larger volume fraction and a longer functional periodicity demonstrated a better mechanical performance, and the load transmission and stress distribution were closer to the native biomechanical environment. The radiographic images and histological results of the TPMS group exhibited a better performance in terms of cartilage protection than the grid group. The regenerated meniscus in the TPMS group also had similar mechanical properties to the native meniscus. Conclusion: The TPMS method can affect the mechanical properties by adjusting the volume fraction and functional periodicity. The TPMS-based meniscal scaffold showed appropriate features for meniscal regeneration and cartilage protection.
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Li Dandan,Jiang Hua,Jin Faguang,Pan Lei,Xie Yonghong,Zhang Liang,Li Chunmei 한국유전학회 2023 Genes & Genomics Vol.45 No.1
Background There is high mortality rate and poor prognosis in lung cancer, especially non-small-cell lung cancer (NSCLC). Recent study showed that concurrent classic driver oncogene mutation with ROS1 rearrangement was found in NSCLC patients. However, whether this would affect the development and prognosis of NSCLC is still unclear. Objective To explore the clinical characteristics and prognosis of NSCLC patients harboring concurrent classic driver oncogene mutation with ROS1 rearrangement. Methods A retrospective study was conducted on 220 patients diagnosed with NSCLC. All samples were screened for EGFR and KRAS using amplification-refractory mutation system assay, and for ALK, ROS1 using RT-PCR. The clinical characteristics and clinical outcomes of concurrent gene alterations with ROS1 rearrangement were analyzed. Results In 220 patients, 12 (5.45%) were ROS1 rearrangement, who tend to be younger, non-smokers. The mutation rates of EGFR, KRAS, ALK and ROS1 in NSCLC were 28.64%, 1.82%, 3.64% and 5.45%, respectively. ROS1 rearrangement was identified to co-occur in 5 (2.27%) NSCLC patients. ROS1/EGFR co-alterations were found in 3.17% of NSCLC patients, 16.67% of ROS1-positive NSCLC patients. Concomitant ROS1/ALK rearrangement constituted 37.50% in ALK-positive patients, and 25.00% in ROS1-positive patients. SDC4-ROS1 was the most common fusion partner in concurrent ROS1 rearrangement patients. The median overall survival of NSCLC with concurrent ROS1 rearrangement group and single ROS1 rearrangement group were 25 months and 14 months. Conclusion Concurrent driver oncogenes mutation with ROS1 rearrangement defines a unique subgroup of NSCLC. Patients with concomitant ROS1 rearrangement might have a better prognosis.
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