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Articles by F Li
Total Records ( 16 ) for F Li
  G Hong , S Jiang , M Yu , Y Yang , F Li , F Xue and Z. Wei

The complete mitochondrial genome (mitogenome) of Artogeia melete was determined as being composed of 15,140 bp, including 13 protein-coding genes (PCGs), 2 rRNA genes, 22 tRNA genes, and one control region. The gene order of A. melete mitogenome is typical of Lepidoptera and differs from the insect ancestral type in the location of trnM. The A. melete mitogenome has a total of 119 bp of intergenic spacer sequences spread over 10 regions, ranging in sizes between 1 and 48 bp. The nucleotide composition of the A. melete mitogenome is also biased toward A + T nucleotides (79.77%), which is higher than that of Ochrogaster lunifer (77.84%), but lower than nine other lepidopterans sequenced. The PCGs have typical mitochondrial start codons, except for cox1, which contains the unusual CGA. The cox1, cox2, nad2, and nad5 genes of the A. melete mitogenome have incomplete stop codons (T). The A. melete A + T-rich region contains some conserved structures that are similar to those found in other lepidopteran mitogenomes, including a structure combining the motif ‘ATAGA’, a 19-bp poly(T) stretch, a microsatellite (AT)n element, and a 9-bp poly(A) upstream trnM. The A. melete mitogenome contains a duplicated 36-bp repeat element, which consists of a 26-bp core sequence flanked by 10-bp perfectly inverted repeats.

  B Hou , F Li , X Yang and G. Hong

In Rhizobium leguminosarum bv. viciae, NodD, as a member of the LysR-type transcriptional regulators (LTTRs), exerts auto-regulation and activates transcription of other nod genes in the presence of naringenin. LTTRs were typically composed of N-terminal DNA-binding domain and C-terminal regulatory domain. In this study, by systematic insertion mutation, a region of 12 amino acids in length of NodD was identified as functional domain. Insertion mutants in this region appeared to acquire the ability of constitutively activating nodA gene and retained their auto-regulation properties. This identified region was shown to be a hinge of NodD as revealed through the model built using Swiss-PDB Viewer software. It is the first time to report that as a member of LysR family, NodD has been shown to contain a short intramolecular domain that influences its performance.

  B Hou , F Li , X Yang and G. Hong

In Rhizobium leguminosarum bv. viciae, NodD, a member of the LysR-type transcriptional regulators, while auto-regulating, activates transcription of other nod genes in the presence of naringenin. A hinge region of NodD was previously identified in our laboratory as a functional region independent of its N-terminal DNA-binding and C-terminal regulatory domain. Further study was carried out to see the possible effect of the length variation in the hinge region on NodD's properties. To our surprise, as many as seven classes of phenotypes were observed. Class I is deficient of activating nodA transcription and abolishes auto-regulation; class II is able to activate nodA transcription independently of naringenin and abolishes auto-regulation; class III retains auto-regulating but partial activating ability; class IV is able to activate transcription independently of naringenin and retains auto-regulation; in class V, nodA is transcribed constitutively but the transcription level is drastically down-regulated in the presence of naringenin; in class VI, nodA is transcribed constitutively with higher induction ratio; in class VII, nodA is transcribed constitutively with lower induction ratio. To learn more about the possible mechanism, circular permutation assays were done, which showed that the length variation of the hinge of NodD caused by mutation led to the change in bend angles of nod promoter. This finding should help to get an insight into how transcriptional regulation is mediated by NodD at the molecular level as well as to understand the regulatory system of this important family.

  H Cheng , N Sun , X Sun , B Chen , F Li , J Feng , L Cheng and Y. Cao

Platinum-based chemotherapeutics are the most common regimens for advanced non-small-cell lung cancer (NSCLC) patients. However, it is difficult to identify platinum resistance in clinical treatment. Genetic factors are thought to represent important determinants of drug efficacy. In this study, we investigated whether single-nucleotide polymorphisms (SNPs) in human mutS homolog 2 (hMSH2) and the human mutL homolog 1 (hMLH1) were associated with the tumor response in advanced NSCLC patients received platinum-based chemotherapy in Chinese population. Totally, 96 patients with advanced NSCLC were routinely treated with cisplatin- or carboplatin-based chemotherapy. The three-dimensional (3D), polyacrylamide gel-based DNA microarray method was used to evaluate the genotypes of hMSH2 gIVS12-6T/C and hMLH1-1151T/A with peripheral lymphocytes. We found that there was a significantly increased chance of treatment response to platinum-based chemotherapy with the hMSH2 gIVS12-6T/C polymorphism. The 3D polyacrylamide gel-based DNA microarray method is accurate, high-throughput, and inexpensive, especially suitable for a large scale of SNP genotyping in population.

  L He , H Zeng , F Li , J Feng , S Liu , J Liu , J Yu , J Mao , T Hong , A. F Chen , X Wang and G. Wang

Hyperhomocysteinemia (HHcy) has been associated with impaired vascular endothelial function. Our previous study demonstrated significantly higher secretion of the chemokine monocyte chemoattractant protein-1 from monocytes in response to lipopolysaccharide in patients with HHcy. In the present study, we investigated whether coronary endothelial function was damaged in patients with chronic HHcy (plasma level of homocysteine >15 µmol/l) and, if so, whether this impaired endothelial function is induced by the uncoupling of endothelial nitric oxide synthase (eNOS). When tetrahydrobiopterin levels are inadequate, eNOS is no longer coupled to l-arginine oxidation, which results in reactive oxygen species rather than nitric oxide production, thereby inducing vascular endothelial dysfunction. The 71 participants were divided into two groups, control (n = 50) and HHcy (n = 21). Quantification of coronary flow velocity reserve (CFVR) was after rest and after adenosine administration done by noninvasive Doppler echocardiography. Plasma levels of nitric oxide and tetrahydrobiopterin were significantly lower in patients with HHcy than in controls (99.54 ± 32.23 vs. 119.50 ± 37.68 µmol/l and 1.43 ± 0.46 vs. 1.73 ± 0.56 pmol/ml, all P < 0.05). Furthermore, CFVR was significantly lower in the HHcy than the control group (2.76 ± 0.49 vs. 3.09 ± 0.52, P < 0.05). In addition, plasma level of homocysteine was negatively correlated with CFVR. Chronic HHcy may contribute to coronary artery disease by inducing dysfunction of the coronary artery endothelium. The uncoupling of eNOS induced by HHcy in patients with chronic HHcy may explain this adverse effect in part.

  F Li , P Yang , X Liu , C Wang , S Hou and A. Kijlstra

Objectives  To analyze the expression and potential role of interleukin (IL) 21 in the pathogenesis of Vogt-Koyanagi-Harada (VKH) disease.

Methods  Blood samples were obtained from patients with VKH disease and from healthy control subjects. Serum IL-21 level and IL-21 messenger RNA (mRNA) expression by peripheral blood mononuclear cells (PBMCs) were determined by enzyme-linked immunosorbent assay and by reverse transcriptase–polymerase chain reaction, respectively. Interleukin 17 and interferon levels in the supernatants of PBMCs and CD4+ T cells cultured with anti-CD3 and anti-CD28 antibodies in the presence or absence of recombinant IL-21 were detected by enzyme-linked immunosorbent assay.

Results  The results showed a significantly increased serum IL-21 level, as well as higher IL-21 mRNA expression by PBMCs, in patients having chronic or recurrent active VKH disease compared with patients having inactive VKH disease and with controls. In vitro experiments showed that recombinant IL-21 significantly increased IL-17 production by PBMCs and by CD4+ T cells from patients and from controls. However, recombinant IL-21 did not affect interferon expression by PBMCs or by CD4+ T cells.

Conclusion  Interleukin 21 may be involved in the pathogenesis of chronic or recurrent VKH disease, possibly by promoting IL-17 secretion.

Clinical Relevance  Findings from the present study suggest that IL-21 may be a potential target in the development of therapy for VKH disease.

  Z Xiao , G Li , Y Chen , M Li , F Peng , C Li , F Li , Y Yu , Y Ouyang and Z. Chen

Formalin-fixed, paraffin-embedded (FFPE) tissue specimens represent a potentially valuable resource for protein biomarker investigations. In this study, proteins were extracted by a heat-induced antigen retrieval technique combined with a retrieval solution containing 2% SDS from FFPE tissues of normal nasopharyngeal epithelial tissues (NNET) and three histological types of nasopharyngeal carcinoma (NPC) with diverse differentiation degrees. Then two-dimensional liquid chromatography-tandem mass spectrometry coupled with isobaric tags for relative and absolute quantification (iTRAQ) labeling was employed to quantitatively identify the differentially expressed proteins among the types of NPC FFPE tissues. Our study resulted in the identification of 730 unique proteins, the distributions of subcellular localizations and molecular functions of which were similar to those of the proteomic database of human NPC and NNET that we had set up based on the frozen tissues. Additionally, the relative expression levels of cathepsin D, keratin8, SFN, and stathmin1 identified and quantified in this report were consistent with the immunohistochemistry results acquired in our previous study. In conclusion, we have developed an effective approach to identifying protein changes in FFPE NPC tissues utilizing iTRAQ technology in conjunction with an economical and easily accessible sample preparation method. (J Histochem Cytochem 58:517–527, 2010)

  B Cubero , Y Nakagawa , X. Y Jiang , K. J Miura , F Li , K. G Raghothama , R. A Bressan , P. M Hasegawa and J. M. Pardo

Insertion mutations that disrupt the function of PHT4;6 (At5g44370) cause NaCl hypersensitivity of Arabidopsis seedlings that is characterized by reduced growth of the primary root, enhanced lateral branching, and swelling of root tips. Mutant phenotypes were exacerbated by sucrose, but not by equiosmolar concentrations of mannitol, and attenuated by low inorganic phosphate in the medium. Protein PHT4;6 belongs to the Major Facilitator Superfamily of permeases that shares significant sequence similarity to mammalian type-I Pi transporters and vesicular glutamate transporters, and is a member of the PHT4 family of putative intracellular phosphate transporters of plants. PHT4;6 localizes to the Golgi membrane and transport studies indicate that PHT4;6 facilitates the selective transport of Pi but not of chloride or inorganic anions. Phenotypic similarities with other mutants displaying root swelling suggest that PHT4;6 likely functions in protein N-glycosylation and cell wall biosynthesis, which are essential for salt tolerance. Together, our results indicate that PHT4;6 transports Pi out of the Golgi lumenal space for the re-cycling of the Pi released from glycosylation processes.

  D Osato , K Rogers , Q Guo , F Li , G Richmond , F Klug and L. Simpson

The RNA ligase-containing or L-complex is the core complex involved in uridine insertion/deletion RNA editing in trypanosome mitochondria. Blue native gels of glycerol gradient-separated fractions of mitochondrial lysate from cells transfected with the TAP-tagged editing protein, LC-8 (TbMP44/KREPB5), show a ~1 MDa L-complex band and, in addition, two minor higher molecular weight REL1-containing complexes: one (L*a) co-sedimenting with the L-complex and running in the gel at around 1.2 MDa; the other (L*b) showing a continuous increase in molecular weight from 1 MDa to particles sedimenting over 70S. The L*b-complexes appear to be mainly composed of L-complex components, since polypeptide profiles of L- and L*b-complex gradient fractions were similar in composition and L*b-complex bands often degraded to L-complex bands after manipulation or freeze–thaw cycles. The L*a-complex may be artifactual since this gel shift can be produced by various experimental manipulations. However, the nature of the change and any cellular role remain to be determined. The L*b-complexes from both lysate and TAP pull-down were sensitive to RNase A digestion, suggesting that RNA is involved with the stability of the L*b-complexes. The MRP1/2 RNA binding complex is localized mainly in the L*b-complexes in substoichiometric amounts and this association is RNase sensitive. We suggest that the L*b-complexes may provide a scaffold for dynamic interaction with other editing factors during the editing process to form the active holoenzyme or "editosome."

  W Hu , F Li , S Mahavadi and K. S. Murthy

Initial Ca2+-dependent contraction of intestinal smooth muscle is inhibited upon IL-1β treatment. The decrease in contraction reflects the upregulation of regulator of G protein signaling-4 (RGS4) via the canonical inhibitor of NF-B kinase-2 (IKK2)/IB-/NF-B pathway. Here, we show that the activation of various protein kinases, including ERK1/2, p38 MAPK, and phosphoinositide 3-kinase (PI3K), differentially modulates IL-1β-induced upregulation of RGS4 in rabbit colonic muscle cells. IL-1β treatment caused a transient phosphorylation of ERK1/2 and p38 MAPK. It also caused the phosphorylation of Akt and glycogen synthase kinase-3β (GSK3β), sequential downstream effectors of PI3K. Pretreatment with PD-98059 (an ERK inhibitor) and SB-203580 (a p38 MAPK inhibitor) significantly inhibited IL-1β-induced RGS4 expression. In contrast, LY-294002 (a PI3K inhibitor) augmented, whereas GSK3β inhibitors inhibited, IL-1β-induced RGS4 expression. PD-98059 blocked IL-1β-induced phosphorylation of IKK2, degradation of IB-, and phosphorylation and nuclear translocation of NF-B subunit p65, whereas SB-203580 had a marginal effect, implying that the effect of ERK1/2 is exerted on the canonical IKK2/IB-/p65 pathway of NF-B activation but that the effect of p38 MAPK may not predominantly involve NF-B signaling. The increase in RGS4 expression enhanced by LY-294002 was accompanied by an increase in the phosphorylation of IKK2/IB-/p65 and blocked by pretreatment with inhibitors of IKK2 (IKK2-IV) and IB- (MG-132). Inhibition of GSK3β abolished IL-1β-induced phosphorylation of IKK2/p65. These findings suggest that ERK1/2 and p38 MAPK enhance IL-1β-induced upregulation of RGS4; the effect of ERK1/2 reflects its ability to promote IKK2 phosphorylation and increase NF-B activity. GSK3β acts normally to augment the activation of the canonical NF-B signaling. The PI3K/Akt/GSK3β pathway attenuates IL-1β-induced upregulation of RGS4 expression by inhibiting NF-B activation.

  F Li , D. Y Hu , S Liu , S Mahavadi , W Yen , K. S Murthy , K Khalili and W. Hu

Regulator of G protein signaling 4 (RGS4) regulates the strength and duration of G protein signaling and plays an important role in smooth muscle contraction, cardiac development, and psychiatric disorders. Little is known about the posttranscriptional regulation of RGS4 expression. We cloned the full-length cDNA of rabbit RGS4, which contains a long 3'-untranslated region (UTR) with several AU-rich elements (AREs). We determined whether RGS4 mRNA stability is mediated by the RNA-binding protein human antigen R (HuR) and contributes to IL-1β-induced upregulation of RGS4 expression. We show that IL-1β treatment in colonic smooth muscle cells doubled the half-life of RGS4 mRNA. Addition of RGS4 3'-UTR to the downstream of Renilla luciferase reporter induced dramatic reduction in the enzyme activity and mRNA expression of luciferase, which was attenuated by the site-directed mutation of the two 3'-most ARE sites. IL-1β increased luciferase mRNA stability in a UTR-dependent manner. Knockdown of HuR significantly aggravated UTR-mediated instability of luciferase and inhibited IL-1β-induced upregulation of RGS4 mRNA. In addition, IL-1β increased cytosolic translocation and RGS4 mRNA binding of HuR. These findings suggest that 3'-most ARE sites within RGS4 3'-UTR are essential for the instability of RGS4 mRNA and IL-1β promotes the stability of RGS4 mRNA through HuR.

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