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Articles by Jing Chen
Total Records ( 12 ) for Jing Chen
  Jing Chen and James Galbraith
  We present the implications of a simple analytical theory in which economic crisis emerges from rising real resource costs in systems with high fixed costs relative to variable costs. We show the integral role played by financial fraud in this process, and explain the effects of austerity and stimulus policies in the face of crisis under differing combinations of fixed and variable costs.
  Xueli Zheng , Jingqi Fu , Yan Wu and Jing Chen
  In this study, the GMR sensor and triaxial attitude sensor were used to constitute a geomagnetic azimuth measurement system. Based on the error analysis of the triaxial GMR sensor and carrier interfering field, the study proposed an error compensation model which includes the non-orthogonal compensation, sensitivity compensation, zero compensation, hard and soft magnetic interference compensation. Meanwhile, the inversion algorithm based on model identification is studied and the parameter of error characteristics is calculated by it. After compensation, the azimuth error of the measurement system is reduced to 0.34% from 3.83% and the expected objective is realized.
  Jing Chen , XiaLiu and Deqiang Dou
  To find the bidirectional effective components of Atractylodis Macrocephalae Rhizoma (AMR) on gastrointestinal peristalsis (GIP). Multi-mode separation methods (solvent partition method and macroporous adsorptive resins) were used to split AMR component; HPLC and GC-MS were used to analyze the main compounds of fractions; the indexes included gastric residual rate and intestinal propulsive rate were used to observe the effects of AMR and its fractions on GIP; ELISA was used to examine the level of Vasoactive Intestinal Peptide (VIP) and P substance (SP) in antrum and ileum. The Water Decoction (WD) of AMR was separated into five fractions, namely, Volatile Oil Fraction (VOF), Petroleum Ether Fraction (PEF), Alcohol Eluate Fraction (AEF), Water Eluate Fraction (WEF) and polysaccharides (CPF); the GIP was promoted in mice with dose of 1.0 g kg–1 WD, VOF, CPF and WEF. However, GIP was inhibited in mice with dose of WD (10.0 g kg–1), PEF and AEF. The AMR had bidirectional regulation effects on gastrointestinal function; the VOF (contained monoterpenes and sesquiterpenes components), WEF (contained 5-hydroxymethyl furfural and small molecular sugar) and CPF (contained inulin-type oligosaccharides) are the fractions of AMR for promotion effects on GIP and PEF (contained sesquiterpene lactone) and AEF (contained polyacetylene) of AMR played opposite action; the underlying action mechanism maybe relate to the SP and VIP levels.
  Jing Chen , Wenjie Wang , Shanshan Xu , Saizhen Chen and LinglingZhang
  Background and Objective: Arctigenin, a phenylpropanoid dibenzyl butyrolactone lignan, is one of the major active components in Fructus Arctii, has protective effects in cerebral Ischemia/Reperfusion (I/R) injury. However, the role of arctigenin in cerebral I/R injury has not been fully understood. This study aimed to investigate the possible antioxidant stress effects of arctigenin and its mechanism on cerebral I/R injured rats. Materials and Methods: A rat model of cerebral I/R injury was established and treated with arctigenin. The activity of SOD and the levels of MDA and ROS were determined by chemical analysis. The expressions of NQO1, HO-1, Nrf2 and Keap1 were detected in Cortex and hippocampus using Western blot. The binding affinity of the Keap1 to the arctigenin was assessed by molecular docking. Results: Current results indicated that arctigenin could remarkably restrict the brain infarction area and ameliorate neuronal functional deficit. After treatment, the activities of SOD were significantly up-regulated and the levels of MDA and ROS were significantly down-regulated in cortex tissue and hippocampus tissue. Meanwhile, increased Keap1, Nrf2, HO-1 and NQO1 expression levels were detected in cerebral I/R injury rats treated with arctigenin. Additionally, molecular docking revealed that potential interaction of arctigenin with the Nrf2-binding site in the Keap1 protein through hydrogen and hydrophobic interactions. Conclusion: This study suggested that arctigenin exerted a protective effect on cerebral ischemia/reperfusion injury in rats, which is probably related to activate Keap1-Nrf2 signaling pathway to alleviate oxidative stress damage.
  Taira Matsuo , Jing Chen , Yusuke Minato , Wakano Ogawa , Tohru Mizushima , Teruo Kuroda and Tomofusa Tsuchiya
  We cloned genes, designated smdAB, that encode a multidrug efflux pump from the chromosomal DNA of clinically isolated Serratia marcescens NUSM8906. For cells of the drug-hypersensitive strain Escherichia coli KAM32 harboring a recombinant plasmid carrying smdAB, structurally unrelated antimicrobial agents such as norfloxacin, tetracycline, 4`,6-diamidino-2-phenylindole (DAPI), and Hoechst 33342 showed elevated MICs. The deduced amino acid sequences of both SmdA and SmdB exhibited similarities to the sequences of ATP-binding cassette (ABC)-type multidrug efflux pumps. The efflux of DAPI and Hoechst 33342 from E. coli cells expressing SmdAB was observed, and the efflux activities were inhibited by sodium o-vanadate, which is a well-known ATPase inhibitor. The introduction of smdA or smdB alone into E. coli KAM32 did not elevate the MIC of DAPI; thus, both SmdA and SmdB were required for function. These results indicate that SmdAB is probably a heterodimeric multidrug efflux pump of the ABC family in S. marcescens.
  Feng-Mei Nie , Fei Lu , Wen-Yu Shang and Jing Chen
  Two new mononuclear cobalt(II) complexes [Co(ntb)(pic)](ClO4) · (CH3OH)2.35 (1) and [Co(ntb)(nic)](ClO4) · CH3OH (2) were synthesized and structurally characterized, where ntb is tris(2-benzimidazolylmethyl)amine, pic is the anion of picolinic acid, and nic is the anion of nicotinic acid. The X-ray analysis indicates that the Co(II) center is six-coordinate in distorted octahedral and five-coordinate in distorted trigonal bipyramidal geometry for 1 and 2, respectively. In 1, the picolinate anion coordinates to Co(II) in a bidentate μ2-N,O chelating mode. In 2, the nicotinate anion coordinates with Co(II) through a monodentate carboxylate oxygen. 1-D chain structures were formed by intermolecular hydrogen bonds in the two complexes and π-π interactions are important for the stabilization of the structures.
  Feng-Mei Nie , Jing Chen , Zhen Li and Fei Lu
  Two picolinate-containing nickel(II) complexes [Ni(bbma)(pic)(H2O)]ClO4 · CH3OH (1) and [Ni(ntb)(pic)]Cl · CH3OH · 3H2O (2) were synthesized and characterized by infrared, elemental analysis, UV-Vis, and X-ray diffraction analyses, where bbma is bis(benzimidazol-2-yl-methyl)amine, ntb is tris(2-benzimidazolylmethyl)amine, pic is the anion of picolinic acid. X-ray analysis shows that both complexes are mononuclear with picolinate coordinated to Ni(II) in a μ2-N,O chelating mode. Both complexes adopt distorted octahedral geometry. Intermolecular N-H ··· O and O-H ··· O hydrogen bonds and π-π interactions in 1 and 2 are important in stabilization of the crystal structures.
  Shuai Chen , Tiancen Hu , Jian Zhang , Jing Chen , Kaixian Chen , Jianping Ding , Hualiang Jiang and Xu Shen
  SARS-CoV 3C-like protease (3CLpro) is an attractive target foranti-severe acute respiratory syndrome (SARS) drug discovery,and its dimerization has been extensively proved to be indispensablefor enzymatic activity. However, the reason why the dissociatedmonomer is inactive still remains unclear due to the absenceof the monomer structure. In this study, we showed that mutationof the dimer-interface residue Gly-11 to alanine entirely abolishedthe activity of SARS-CoV 3CLpro. Subsequently, we determinedthe crystal structure of this mutant and discovered a completecrystallographic dimer dissociation of SARS-CoV 3CLpro. Themutation might shorten the α-helix A` of domain I and cause amis-oriented N-terminal finger that could not correctly squeezeinto the pocket of another monomer during dimerization, thusdestabilizing the dimer structure. Several structural featuresessential for catalysis and substrate recognition are severelyimpaired in the G11A monomer. Moreover, domain III rotates dramaticallyagainst the chymotrypsin fold compared with the dimer, fromwhich we proposed a putative dimerization model for SARS-CoV3CLpro. As the first reported monomer structure for SARS-CoV3CLpro, the crystal structure of G11A mutant might provide insightinto the dimerization mechanism of the protease and supply directstructural evidence for the incompetence of the dissociatedmonomer.
  Sumin Kang , Shaozhong Dong , Ailan Guo , Hong Ruan , Sagar Lonial , Hanna Jean Khoury , Ting-Lei Gu and Jing Chen
  The Ser/Thr kinase ribosomal S6 kinase 2 (RSK2) has been demonstrated to phosphorylate transcription factor CREB (cyclic AMP-responsive-binding protein) and histone H3 in response to mitogenic stimulation by epidermal growth factor (EGF). EGF activates the MEK/ERK pathway to activate RSK2. We recently reported that receptor tyrosine kinase fibroblast growth factor receptor 3 (FGFR3) directly tyrosine phosphorylates RSK2 at Tyr-529, which consequently regulates RSK2 activation by facilitating inactive ERK binding to RSK2 that is required for ERK-dependent phosphorylation and activation of RSK2 (Kang, S., Dong, S., Gu, T. L., Guo, A., Cohen, M. S., Lonial, S., Khoury, H. J., Fabbro, D., Gilliland, D. G., Bergsagel, P. L., Taunton, J., Polakiewicz, R. D., and Chen, J. (2007) Cancer Cell 12, 201–214). Here we report that upon treatment of EGF, RSK2 was tyrosine-phosphorylated at Tyr-529 and activated in 293T and COS7 cells that do not express FGFR3. In contrast to FGFR3, the receptor tyrosine kinase EGF receptor did not directly phosphorylate RSK2 at Tyr-529 in an in vitro kinase assay using recombinant RSK2 and active EGF receptor or FGFR3. By mass spectroscopy-based studies, we identified Src tyrosine kinase family members Src and Fyn as upstream kinases of RSK2 Tyr-529. Treatment of Src inhibitor PP2 effectively attenuated EGF-dependent activation and Tyr-529 phosphorylation of RSK2, suggesting that Src family members are the kinases that phosphorylate RSK2 at Tyr-529 in response to EGF. Src and Fyn were able to directly phosphorylate RSK2 at Tyr-529 in the in vitro kinase assay. In vitro reconstitution of Tyr-529 phosphorylation by Src in glutathione S-transferase-tagged RSK2 enhanced inactive ERK binding to RSK2 wild type, but not the Y529F mutant. Together, our findings suggest that Src-dependent phosphorylation at Tyr-529 facilitates inactive ERK binding to RSK2, which might be a general requirement for RSK2 activation by EGF through the MEK/ERK pathway.
  Ganchimeg Ishdorj , Bonnie A. Graham , Xiaojie Hu , Jing Chen , James B. Johnston , Xianjun Fang and Spencer B. Gibson
  Histone deacetylases (HDACs) catalyze the removal of acetyl groups from histones and contribute to transcriptional repression. In addition, the HDAC inhibitors induce apoptosis in cancer cells through alterations in histone acetylation and activation of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) apoptotic pathway. Lysophosphatidic acid (LPA) is a growth factor that promotes survival of cancer cells through activation of G protein-coupled receptors. Here we show that HDAC inhibitors can induce apoptosis through activation of the TRAIL apoptotic pathway, and LPA prevented HDAC inhibitor-induced apoptosis and increased TRAIL receptor DR4 (death receptor 4) protein expression. This was associated with increased HDAC1 recruitment to the DR4 promoter following LPA treatment and a reduction in HDAC inhibitor-induced histone acetylation in the DR4 promoter. In addition, LPA induces HDAC enzyme activity in a dose- and time-dependent manner, and this is associated with HDAC1 activation and increased binding of HDAC1 to HDAC2. Reducing the expression of HDAC1 significantly lowered LPA-induced HDAC activity and increased histone acetylation. LPA induction of HDAC activity was blocked by the LPA receptor antagonist, Ki16425, or by inhibiting receptor activation with pertussis toxin. Reducing the expression of the LPA receptor LPA1 also blocked LPA-induced HDAC activation. In addition, LPA reduced histone acetyltransferase enzymatic activity. Finally, LPA attenuated the ability of the HDAC inhibitor to reduce HDAC activity. Thus, LPA enhances survival of cancer cells by increasing HDAC activity and reducing histone acetylation.
  Tiancen Hu , Dalei Wu , Jing Chen , Jianping Ding , Hualiang Jiang and Xu Shen
  The meso-diaminopimelate decarboxylase (DAPDC, EC 4.1.1.2[EC]0) catalyzes the final step of L-lysine biosynthesis in bacteria and is regarded as a target for the discovery of antibiotics. Here we report the 2.3Å crystal structure of DAPDC from Helicobacter pylori (HpDAPDC). The structure, in which the product L-lysine forms a Schiff base with the cofactor pyridoxal 5'-phosphate, provides structural insight into the substrate specificity and catalytic mechanism of the enzyme, and implies that the carboxyl to be cleaved locates at the si face of the cofactor. To our knowledge, this might be the first reported external aldimine of DAPDC. Moreover, the active site loop of HpDAPDC is in a "down" conformation and shields the ligand from solvent. Mutations of Ile148 from the loop greatly impaired the catalytic efficiency. Combining the structural analysis of the I148L mutant, we hypothesize that HpDAPDC adopts an induced-fit catalytic mechanism in which this loop cycles through "down" and "up" conformations to stabilize intermediates and release product, respectively. Our work is expected to provide clues for designing specific inhibitors of DAPDC.
  Shenyuan L. Zhang , J. Ashot Kozak , Weihua Jiang , Andriy V. Yeromin , Jing Chen , Ying Yu , Aubin Penna , Wei Shen , Victor Chi and Michael D. Cahalan
  We evaluated currents induced by expression of human homologs of Orai together with STIM1 in human embryonic kidney cells. When co-expressed with STIM1, Orai1 induced a large inwardly rectifying Ca2+-selective current with Ca2+-induced slow inactivation. A point mutation of Orai1 (E106D) altered the ion selectivity of the induced Ca2+ release-activated Ca2+ (CRAC)-like current while retaining an inwardly rectifying I-V characteristic. Expression of the C-terminal portion of STIM1 with Orai1 was sufficient to generate CRAC current without store depletion. 2-APB activated a large relatively nonselective current in STIM1 and Orai3 co-expressing cells. 2-APB also induced Ca2+ influx in Orai3-expressing cells without store depletion or co-expression of STIM1. The Orai3 current induced by 2-APB exhibited outward rectification and an inward component representing a mixed calcium and monovalent current. A pore mutant of Orai3 inhibited store-operated Ca2+ entry and did not carry significant current in response to either store depletion or addition of 2-APB. Analysis of a series of Orai1-3 chimeras revealed the structural determinant responsible for 2-APB-induced current within the sequence from the second to third transmembrane segment of Orai3. The Orai3 current induced by 2-APB may reflect a store-independent mode of CRAC channel activation that opens a relatively nonselective cation pore.
 
 
 
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