http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Chao, Zhe,Zheng, Xin-Li,Sun, Rui-Ping,Liu, Hai-Long,Huang, Li-Li,Cao, Zong-Xi,Deng, Chang-Yan,Wang, Feng Asian Australasian Association of Animal Productio 2016 Animal Bioscience Vol.29 No.7
Epigenetic processes in the development of skeletal muscle have been appreciated for over a decade. DNA methylation is a major epigenetic modification important for regulating gene expression and suppressing spurious transcription. Up to now, the importance of epigenetic marks in the regulation of Pax7 and myogenic regulatory factors (MRFs) expression is far less explored. In the present study, semi-quantitative the real-time polymerase chain reaction (RT-PCR) analyses showed MyoD and Myf5 were expressed in activated and quiescent C2C12 cells. MyoG was expressed in a later stage of myogenesis. Pax7 was weakly expressed in differentiated C2C12 cells. To further understand the regulation of expression of these genes, the DNA methylation status of Pax7, MyoD, and Myf5 was determined by bisulfite sequencing PCR. During the C2C12 myoblasts fusion process, the changes of promoter and exon 1 methylation of Pax7, MyoD, and Myf5 genes were observed. In addition, an inverse relationship of low methylation and high expression was found. These results suggest that DNA methylation may be an important mechanism regulating Pax7 and MRFs transcription in cell myogenic differentiation.
Fibulin2: a negative regulator of BMSC osteogenic differentiation in infected bone fracture healing
Li Shi-Dan,Xing Wei,Wang Shao-Chuan,Li You-Bin,Jiang Hao,Zheng Han-Xuan,Li Xiao-Ming,Yang Jing,Guo De-Bin,Xie Xiao-Yu,Jiang Ren-Qing,Fan Chao,Li Lei,Xu Xiang,Fei Jun 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-
Bone fracture remains a common occurrence, with a population-weighted incidence of approximately 3.21 per 1000. In addition, approximately 2% to 50% of patients with skeletal fractures will develop an infection, one of the causes of disordered bone healing. Dysfunction of bone marrow mesenchymal stem cells (BMSCs) plays a key role in disordered bone repair. However, the specific mechanisms underlying BMSC dysfunction caused by bone infection are largely unknown. In this study, we discovered that Fibulin2 expression was upregulated in infected bone tissues and that BMSCs were the source of infection-induced Fibulin2. Importantly, Fibulin2 knockout accelerated mineralized bone formation during skeletal development and inhibited inflammatory bone resorption. We demonstrated that Fibulin2 suppressed BMSC osteogenic differentiation by binding to Notch2 and inactivating the Notch2 signaling pathway. Moreover, Fibulin2 knockdown restored Notch2 pathway activation and promoted BMSC osteogenesis; these outcomes were abolished by DAPT, a Notch inhibitor. Furthermore, transplanted Fibulin2 knockdown BMSCs displayed better bone repair potential in vivo. Altogether, Fibulin2 is a negative regulator of BMSC osteogenic differentiation that inhibits osteogenesis by inactivating the Notch2 signaling pathway in infected bone.
Gu, Chao-Jiang,Zheng, Cong-Yi,Zhang, Qian,Shi, Li-Li,Li, Yong,Qu, San-Fu Korean Society for Biochemistry and Molecular Biol 2006 Journal of biochemistry and molecular biology Vol.39 No.1
To prove whether error catastrophe /lethal mutagenesis is the primary antiviral mechanism of action of ribavirin against foot-and-mouth disease virus (FMDV). Ribavirin passage experiments were performed and supernatants of $Rp_1$ to $Rp_5$ were harvested. Morphological alterations as well as the levels of viral RNAs, proteins, and infectious particles in the BHK-21 cells infected using the supernatants of $Rp_1$ to $Rp_5$ and control were measured by microscope, real-time RT-PCR, western-blotting and plaque assays, respectively. The mutation frequency was measured by sequencing the complete P1- and 3D-encoding region of FMDV after a single round of virus infection from ribavirin-treated or untreated FMDV-infected cells. Ribavirin treatment for FMDV caused dramatically inhibition of multiplication in cell cultures. The levels of viral RNAs, proteins, and infectious particles in the BHK-21 cells infected were more greatly reduced along with the passage from $Rp_1$ to $Rp_5$, moreover, nucleocapsid protein could not be detected and no recovery of infectious virus in the supernatant or detection of intracellular viral RNA was observed at the $Rp_5$-infected cells. A high mutation rate, giving rise to an 8-and 11-fold increase in mutagenesis and resulting in some amino acid substitutions, was found in viral RNA synthesized at a single round of virus infection in the presence of ribavirin of $1000\;{\mu}M$ and caused a 99.7% loss in viral infectivity in contrast with parallel untreated control virus. These results suggest that the antiviral molecular mechanism of ribavirin is based on the lethal mutagenesis/error catastrophe, that is, the ribavirin is not merely an antiviral reagent but also an effective mutagen.
( Fei-meng Zheng ),( Wang-bing Chen ),( Tao Qin ),( Li-na Lv ),( Bi Feng ),( Yan-ling Lu ),( Zuo-quan Li ),( Xiao-chao Wang ),( Li-ju Tao ),( Hong-wen Li ),( Shu-you Li ) 생화학분자생물학회(구 한국생화학분자생물학회) 2019 BMB Reports Vol.52 No.9
Lymphoma is one of the most curable types of cancer. However, drug resistance is the main challenge faced in lymphoma treatment. Peroxisomal acyl-CoA oxidase 1 (ACOX1) is the rate-limiting enzyme in fatty acid β-oxidation. Deregulation of ACOX1 has been linked to peroxisomal disorders and carcinogenesis in the liver. Currently, there is no information about the function of ACOX1 in lymphoma. In this study, we found that upregulation of ACOX1 promoted proliferation in lymphoma cells, while downregulation of ACOX1 inhibited proliferation and induced apoptosis. Additionally, overexpression of ACOX1 increased resistance to doxorubicin, while suppression of ACOX1 expression markedly potentiated doxorubicin-induced apoptosis. Interestingly, downregulation of ACOX1 promoted mitochondrial location of Bad, reduced mitochondrial membrane potential and provoked apoptosis by activating caspase-9 and caspase-3 related apoptotic pathway. Overexpression of ACOX1 alleviated doxorubicin-induced activation of caspase-9 and caspase-3 and decrease of mitochondrial membrane potential. Importantly, downregulation of ACOX1 increased p73, but not p53, expression. p73 expression was critical for apoptosis induction induced by ACOX1 downregulation. Also, overexpression of ACOX1 significantly reduced stability of p73 protein thereby reducing p73 expression. Thus, our study indicated that suppression of ACOX1 could be a novel and effective approach for treatment of lymphoma. [BMB Reports 2019; 52(9): 566-571]
Qing-Qing Li,JIN SHENG,Pengcheng Li,Dapeng Li,Cheng-Chao Zheng,Dequan Li,Huairui Shu 한국식물학회 2012 Journal of Plant Biology Vol.55 No.4
Alcohol acyltransferase (AAT) plays an important role in ester biogenesis in ripening fruit. In apple, MdAAT2 is up-regulated in response to treatment with defense-related hormones. We cloned a novel MdAAT2 promoter via thermal asymmetric interlaced PCR (TAIL-PCR). Sequence analysis indicated the presence of salicylic acid (SA)- and methyl jasmonate (MeJA)-responsive elements in the promoter region. To examine further the operational mechanism for transcription factors (TFs) in regulating expression of the MdAAT2 promoter, we isolated and investigated six potential stress-induced TFs -- MdMYB1, MdMYB2, MdMYB6,MdERF1, MdERF2, and WRKY. These were monitored during various stages of fruit development as well as under several hormonal treatments. Reverse transcription-polymerase chain reaction (RT-PCR) analysis showed that all of these TF genes, as well as MdAAT2, were detectable in the stigmas. Levels of expression by MdMYB1, MdMYB2, and MdERF1were significantly correlated with that by MdAAT2 during fruit ontogeny. Moreover, transcription of three TFs (MdMYB1,MdMYB6, and MdERF1) was significantly correlated with that of MdAAT2 upon exposure to ethephon, SA, or MeJA. Sequence analysis demonstrated that CAAT, CCAAT elements,and several MYB transcription factor binding sites (CNGTTmotif,AACCA, and CTAACCA elements) existed in the MdAAT2 promoter region. Using that analysis, we performed modeling of MdMYB1 and MdMYB6 based on PROTEINDNA complex1 and complex3 (PDB Accession Numbers 1H88 and 1H8A). There, similarities were found with the protein complex of CAAT or CCAAT consensus sequences. Thus, we propose that two TFs -- MdMYB1 and MdMYB6-- are directly or indirectly involved in the activation of MdAAT2 expression in apple fruit.
( Liang Lei ),( Xin-fei Xu ),( Jiong-jie Yu ),( Ju-dong Li ),( Zhen-li Li ),( Jun Han ),( Han Zhang ),( Hao Xing ),( Han Wu ),( Ming-da Wang ),( Chao Li ),( Zheng Wang ),( Feng Shen ),( Meng-chao Wu ) 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
Aims: The prognosis of hepatocellular carcinoma (HCC) with portal vein tumor thrombus (PVTT) is very poor. According to the BCLC treatment recommendations, sorafenib or other palliative treatment (PT) is recommended as the first-line therapy when it happens. In real world, however, a significant number of selected patients with HCC and PVTT suffered from surgical resection (SR). Methods: PubMed, Embase, Medline and Cochrane library were searched for studies comparing SR with PT (including TACE, sorafenib, etc.) for HCC with PVTT, which were published before September 2017. Results: 4,810 patients from 7 studies were enrolled in this meta-analysis, which divided into the SR group (n = 2,344) and the PT group (n = 2476). When compared with the PT group, the pooled hazard ratio (HR) for the 1, 3 and 5-year OS rates of the SR group were 0.56 (95% CI 0.52-0.60, P=0.03), 0.56 (95% CI 0.53-0.59, P<0.001) and 0.55 (95% CI 0.54-0.57, P<0.001). For subgroup analysis, when compared with the mere TACE group, the pooled HR for the 1, 3 and 5-year OS rates of the SR group were 0.54 (95% CI 0.43-0.67, P=0.81), 0.75 (95% CI 0.65-0.87, P=0.25) and 0.76 (95% CI 0.67-0.88, P=0.25). Conclusions: This meta-analysis demonstrated SR had better OS than TACE or other palliative therapy for HCC with PVTT. SR may be suitable as the first-line treatment for selected patients with resectable HCC and removable PVTT.
Li, Qiong,Yin, Jun,Wang, Xu,Wang, Li-Ming,Shi, Yi-Jun,Zheng, Liang,Tang, Wei-Feng,Ding, Guo-Wen,Liu, Chao,Liu, Rui-Ping,Gu, Hai-Yong,Sun, Jia-Ming,Chen, Suo-Cheng Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.7
Aim: Apoptosis has been considered as a fundamental component in cancer pathogenesis, and related genetic factors might play an important role in gastric cardiac adenocarcinoma (GCA) genesis. Methods: We conducted a hospital based case.control study to evaluate the genetic effects of functional single nucleotide polymorphisms (SNPs): BCL2 rs17757541 C>G, BCL2 rs12454712 T>C, FAS rs2234767 G>A, FASL/FASLG rs763110 C>T, ERBB2 rs1136201 A>G and VEGFR2/KDR rs11941492 C>T on the development of GCA. A total of 243 GCA cases and 476 controls were recruited for the study and genotypes were determined using a custom-by-design 48-Plex SNPscan$^{TM}$ Kit. Results: The BCL2 rs17757541 C>G polymorphism was associated with increased risk of GCA. However, there was no significant associations with the other five SNPs. Stratified analyses indicated a significantly increased risk of GCA associated with the BCL2 rs17757541 C>G polymorphism among males, older patients and those with a history of smoking or drinking. Conclusion: These findings indicated that the functional polymorphism BCL2 rs17757541 C>G might contribute to GCA susceptibility. However, our results were limited by small sample size. Future larger studies are required to confirm our current findings.