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您的检索式：作者名="Pingjun Zhu"
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| 1 | Anisotropic thermoelectric properties of layered compound SnSe2显示文摘Similar to high performance SnSe thermoelectrics, SnSe2 is also a layered structured semiconductor.However, its anisotropic thermoelectric properties are less experimentally investigated. In this work,Cl-doped SnSe2 bulk materials are successfully prepared, and their thermal stability and anisotropic transport properties are systematically studied. Unexpectedly, different from the theoretical prediction and other typical layered thermoelectric compounds like Bi_2Te_3, the out-of-plane zT_c value is higher than in-plane zT_a for the same composition. The zT value is significantly enhanced by Cl doping. A maximum zT_c of ~0.4 at 673 K is achieved in SnSe_(1.88)Cl_(0.12), twice higher than previously reported Cl-doped SnSe_2 synthesized by the solvothermal method. | Peipei Xu Tiezheng Fu Jiazhan Xin Yintu Liu Pingjun Ying Xinbing Zhao Hongge Pan Tiejun Zhu | 2017 | Science Bulletin2017，62，24： | 4 |
| 2 | DNA-PKcs promotes alcohol-related liver disease by activating Drp1-related mitochondrial fission and repressing FUNDC1-required mitophagy显示文摘DNA-dependent protein kinase catalytic subunit(DNA-PKcs)is a novel housekeeper of hepatic mitochondrial homeostasis outside the DNA repair process.In this study,DNA-PKcs was upregulated in the livers of mice that were exposed to alcohol;the expression of DNA-PKcs positively correlated with hepatic steatosis,fibrosis,apoptosis,and mitochondrial damage.Functional studies revealed that liver-specific DNA-PKcs knockout(DNA-PKcsLKO)mice were protected from chronic ethanol-induced liver injury and mitochondrial damage.Mechanistic investigations established that DNA-PKcs promoted p53 activation,which elevated dynamin-related protein 1(Drp1)-related mitochondrial fission but repressed FUN14 domain containing 1(FUNDC1)-required mitophagy.Excessive fission and defective mitophagy triggered mtDNA damage,mitochondrial respiratory inhibition,mROS overproduction,cardiolipin oxidation,redox imbalance,calcium overload,and hepatic mitochondrial apoptosis.In contrast,the deletion of DNA-PKcs rescued these phenotypic alterations,which alleviated the susceptibility of hepatocytes to alcohol-induced cytotoxicity.Additionally,we also showed that orphan nuclear receptor subfamily 4 group A member 1(NR4A1)was the upstream signal for DNA-PKcs activation and that the genetic ablation of NR4A1 ameliorated the progression of alcohol-related liver disease(ARLD);these results were similar to those obtained in DNA-PKcs knockout mice.Collectively,our results identified the NR4A1/DNA-PKcs/p53 axis as a novel signaling pathway responsible for ARLD pathogenesis that acts by activating Drp1-related mitochondrial fission and restricting FUNDC1-required mitophagy.The findings have potential implications for new approaches for ARLD therapy. | Hao Zhou Pingjun Zhu Jin Wang Sam Toan Jun Ren | 2019 | Signal Transduction and Targeted Therapy2019，4，1： | 1 |
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