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        A R2R3-type MYB transcription factor gene from soybean, GmMYB12, is involved in flavonoids accumulation and abiotic stress tolerance in transgenic Arabidopsis

        Feibing Wang,Xuqin Ren,Fan Zhang,Mingyang Qi,Huiyun Zhao,Xinhong Chen,Yuxiu Ye,Jiayin Yang,Shuguang Li,Yi Zhang,Yuan Niu,Qing Zhou 한국식물생명공학회 2019 Plant biotechnology reports Vol.13 No.3

        The R2R3-type MYB transcription factors have been shown to increase flavonoids accumulation by regulating the expression of key enzyme genes related to flavonoid biosynthesis pathway. However, the roles and underlying mechanisms of the soybean GmMYB12 gene in regulation of flavonoids accumulation and tolerance to abiotic stresses are rarely known. In the present study, the GmMYB12 gene was isolated and its function was characterized. Sequence and yeast one-hybrid analyses showed that GmMYB12 contained two MYB domains and belonged to R2R3-MYB protein with transactivation activity. Subcellular localization analysis in onion epidermal cells indicated that GmMYB12 was localized to the nucleus. Overexpression of GmMYB12 increased the production of downstream flavonoids and the expression of related genes in the flavonoid biosynthesis pathway. It also improved resistance to salt and drought stresses during seed germination, root development, and growing stage. Further component and enzymatic analyses showed significant increases of proline content, pyrroline-5-carboxylate synthase (P5CS), superoxide dismutase (SOD), and peroxidase (POD) activities, as well as significant reduction of H2O2 and malonaldehyde (MDA) content under salt and drought stresses in transgenic plants. Meanwhile, the expression level of AtP5CS, AtSOD and AtPOD genes was up-regulated against salt and drought stresses. Together, our finding indicated that changing the expression level of GmMYB12 in plants alters the accumulation of flavonoids and regulates plantlet tolerance to abiotic stress by regulating osmotic balance, protecting membrane integrity and maintaining ROS homeostasis. The GmMYB12 gene has the potential to be used to increase the content of valuable flavonoids and improve the tolerance to abiotic stresses in plants

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        The upregulation of keratocan promotes the progression of human pancreatic cancer

        Gao Huijie,Qian Ruikun,Ren Qiang,Zhang Litao,Qin Wei,Zhou Caiju,Wang Huiyun,Liu Chao,Zhang Yuntao 대한독성 유전단백체 학회 2024 Molecular & cellular toxicology Vol.20 No.2

        Background The role of the extracellular matrix (ECM) in oncogenic contexts has been studied previously, but the expression patterns and functional role of keratocan, a classical small leucine-rich proteoglycan found in the ECM, in tumors remain poorly understood. As pancreatic cancer (PC) is characterized by desmoplasia in the ECM, this study sought to assess the significance of keratocan in PC. Objective In this study, Gene Expression Profiling Interactive Analysis (GEPIA) was first used to analyze the expression pattern of keratocan in PC. Keratocan, P53, and P21 levels were evaluated in PDAC patient tissues and the role of keratocan was additionally directly assessed via transfecting PDAC cell lines with a pENTER-human keratocan construct. Results Patients with PC showing high levels of keratocan had low survival rates. A significantly upregulated expression of keratocan was observed in the PC tumor tissues in comparison to healthy paracancerous tissues. Keratocan upregulation in BxPC-3 and PANC-1 cells markedly enhanced their proliferation and migration, but reduced cellular apoptosis. Furthermore, the P53 and P21 expression levels were significantly reduced in pancreatic ductal adenocarcinoma cells overexpressing keratocan. P53 and P21 were downregulated in PC tumor tissues. Conclusions All results showed that keratocan played important roles in the promoting of PC. Background The role of the extracellular matrix (ECM) in oncogenic contexts has been studied previously, but the expression patterns and functional role of keratocan, a classical small leucine-rich proteoglycan found in the ECM, in tumors remain poorly understood. As pancreatic cancer (PC) is characterized by desmoplasia in the ECM, this study sought to assess the significance of keratocan in PC. Objective In this study, Gene Expression Profiling Interactive Analysis (GEPIA) was first used to analyze the expression pattern of keratocan in PC. Keratocan, P53, and P21 levels were evaluated in PDAC patient tissues and the role of keratocan was additionally directly assessed via transfecting PDAC cell lines with a pENTER-human keratocan construct. Results Patients with PC showing high levels of keratocan had low survival rates. A significantly upregulated expression of keratocan was observed in the PC tumor tissues in comparison to healthy paracancerous tissues. Keratocan upregulation in BxPC-3 and PANC-1 cells markedly enhanced their proliferation and migration, but reduced cellular apoptosis. Furthermore, the P53 and P21 expression levels were significantly reduced in pancreatic ductal adenocarcinoma cells overexpressing keratocan. P53 and P21 were downregulated in PC tumor tissues. Conclusions All results showed that keratocan played important roles in the promoting of PC.

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        Altered Expression of Substance P and NK1R in CCR3+ and CD123+HLA-DR− Basophils Under Airway Allergic Conditions

        Geng Shiyang,Xie Hua,Chen Liping,Chen Dong,Lu Sijing,Zhao Nan,Yang Ruiming,Wang Zhao,He Shaoheng,Zhang Huiyun 대한천식알레르기학회 2022 Allergy, Asthma & Immunology Research Vol.14 No.6

        Purpose: To explore expression of SP and NK1R in basophils of allergic asthma (AA), allergic rhinitis (AR) and AR combined with AA (ARA), and influence of allergens and immunoglobulin E (IgE) mediated mechanisms on SP and NK1R expression. Methods: Expression of SP and NK1R was detected by flow cytometry, NK1R mRNA expression was detected by real time quantitative polymerase chain reaction (qPCR), and mouse AR and AA models were employed for in vivo study. Results: SP+ and NK1R+ cells increased in CCR3+ and CD123+HLA-DR− granulocytes of AA. PPE elevated proportions of SP+ cells in CCR3+ and CD123+HLA-DR− granulocytes, whereas ASWE and HDME augmented SP+ cells in CD123+HLA-DR− granulocytes of AR and ARA patients. ASWE, HDME and PPE increased proportions of NK1R+ cells in CCR3+ PBMC and CD123+HLA-DR− granulocytes of AR patients. OVA, Der p1, IL-33, IL-37, IgE and SP enhanced NK1R expression on KU812 cells. NK1R expressing basophils were increased in blood of OVA sensitized and challenged AR and AA mice. FcεRI-KO AA mice seemed to have less NK1R+ basophils than WT AA mice in their blood. Conclusion: CCR3+ and CD123+HLA-DR− cells are likely involved in AA and AR via SP and NK1R. IgE-related mechanism may participate in upregulation of NK1R expression.

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