Peng Deng

Nanfang Hospital, Shengcheng, Guangdong, China

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Publications (44)40.9 Total impact

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    ABSTRACT: Gut-derived endotoxin and pathogenic bacteria may be important causative factors of morbidity and death during heat stroke. However, as the key component of intestinal mucosal barrier, the molecular mechanism of how intestinal epithelial cells are injured by heat shock is remains unclear. After rat intestinal epithelial cells (IEC-6) had been exposed to heat shock, their viability was measured. Propofol, which plays an important role in anti-inflammation and organ protection, was investigated to see how it affected viability under this stress. Changes of high mobility group box 1 (HMGB1) in IEC-6 cells were measured with RT-PCR and Western blot assay at transcription and translational levels, respectively. Ethyl pyruvate (EP), a specific inhibitor of HMGB1 that can inhibit the release of HMGB1 without affecting its intracellular synthesis, was also investigated. Heat shock significantly reduced the intracellular level of HMGB1, and propofol inhibit its reduction. Propofol protected the heat shock-injured cells, at least partly through inhibiting the release of intracellular HMGB1 to reduce the direct or indirect cell damage caused by HMGB1. Pretreatment with high concentrations of EP also attenuated heat-shock injury.
    Cell Biology International 01/2013; · 1.64 Impact Factor
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    ABSTRACT: Microsatellite instability (MSI) is present in about 15% of colorectal cancers and plays critical roles in the development and progression of these cancers. The goal of this study is to determine the global effect of microsatellite instability on the signaling pathways and network in colon cancer cells. We profiled the expression and phosphorylation of 110 proteins in six colon cancer cell lines by using Protein Pathway Array. The pathways and network constituted by these proteins were identified by using Ingenuity Pathway Analysis. Our results showed that 25 proteins and phosphoproteins change more than 1.5-fold between MSI and microsatellite stable (MSS) cells. Sixteen major pathways were affected in MSI cells, including p53 and 14-3-3ß pathways, with p53 and HGF being the most important pathways. Finally, although the EGFR/K-RAS/MEK pathway was not affected in MSI cells, collateral pathways such as the p70S6K and p90RSK pathways were activated in MSI cells. Thus, suppression of the p53 pathway and activation of the HGF pathway in MSI cells may be critical in the tumorigenesis of MSI colorectal cancer.
    Frontiers in bioscience (Elite edition) 01/2013; E5:574-582.
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    ABSTRACT: To establish a new method for studying the mechanism of nuclear localization signal (NLS)-mediated nuclear translocation in living cells. The cells were treated with 67 mg/L 3-[(3-Cholamidopropyl)dimethylammonio]propanesulfonate (CHAPS), followed by incubation with 1 g/L wheat germ agglutinin (WGA), and their effects on interferon- γ (IFN-γ)-induced nuclear translocation of signal transducer and activator of transcription 1 (STAT1) were observed. Treatment with CHAPS alone had no effect on IFN-γ-induced nuclear translocation of STAT1, while this process was blocked by further WGA incubation. We established a new, simple but effective method for studying the mechanism of NLS-mediated nuclear translocation in living cells by perforating the cell membrane with CHAPS treatment.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 08/2012; 32(8):1148-50.
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    ABSTRACT: p38 MAPK, one of the four MAPK subfamilies in mammalian cells, is activated by environmental stresses and pro-inflammatory cytokines, playing fundamental roles in many biological processes. Despite all that is known on the structure and functions of p38, many questions still exist. The coupling of activation and nuclear translocation represents an important aspect of p38 signaling. In our effort in exploring the potential chaperone for p38 translocation, we performed an endogenous pull-down assay and identified HSP70 as a potential interacting protein of p38. We confirmed the interaction between p38 and HSP70 in vitro and in vivo, and identified their interaction domains. We also showed stress-induced nuclear co-localization of these two proteins. Our preliminary result indicated that HSP70 was related to the phosphorylation of MK2, a specific nuclear downstream target of p38, suggesting HSP70 is a potential chaperone for the nuclear translocation of p38.
    Biochemical and Biophysical Research Communications 07/2012; 425(2):357-62. · 2.41 Impact Factor
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    ABSTRACT: To construct eukaryotic expression vectors for different domains (V and VC1) of the extracellular region of the receptor of advanced glycation end products (RAGE) and investigate the roles of these domains in prostate cancer. The coding sequence of V and VC1 domains was amplified from the plasmid pcDNA3-HA-RAGE by PCR and cloned into the pcDNA3-HA vector following routine procedures. After identification by PCR and sequencing, the vectors including V and VC1 domains were transfected into PC-3 cells. Western blotting and immunofluorescence were used to detect the expression and distribution of the expressed products in transfected PC-3 cells. The expression vectors containing V and VC1 domains of RAGE were successfully constructed as confirmed by PCR and DNA sequence analysis. The V and VC1 domains of RAGE were highly expressed and showed a cytoplasmic distribution in transfected PC-3 cells. The constructed eukaryotic expression vectors for V and VC1 domains of RAGE can be efficiently expressed in prostate cancer cells.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 04/2012; 32(4):507-10.
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    ABSTRACT: Hydrogen peroxide (H(2)O(2)) is a potent reactive oxygen species that causes cardiomyocytes injury. As an important cytokine, interleukin 6 (IL-6) has cardioprotective effects as it plays an essential role in the late phase of preconditioning. Our work is to investigate if IL-6 preconditioning has protective effects on neonatal rat ventricular cardiomyocytes in response to H(2)O(2) and its underlying mechanism. Gel-based comparative proteomic approach along with small interfering RNA (siRNA) and Western blot analysis was used to analyse mechanisms of IL-6 preconditioning on H(2)O(2)-induced neonatal rat ventricular cardiomyocytes injury. IL-6 preconditioning protected cardiomyocytes against H(2)O(2)-induced cell death. Proteomic analysis showed that IL-6 pretreatment further increased the expression of prohibitin and improved the viability of cardiomyocytes exposed to H(2)O(2). Knocking down of prohibitin with siRNA abrogated this protection by increasing apoptosis rate. Tyrosine kinase inhibitor AG490 decreased signal transducers and activators of transcription 3 (STAT3) phosphorylation and down-regulated prohibitin expression in cardiomyocytes pretreated with IL-6 and exposed to H(2)O(2), which further dampened the protective effects of IL-6 preconditioning. Our results provide direct evidence that prohibitin is a protective factor of IL-6 preconditioning in H(2)O(2)-induced neonatal rat ventricular cardiomyocytes death. The upregulation of prohibitin by IL-6 is, at least, partially regulated through STAT3 phosphorylation.
    Cell Biochemistry and Function 03/2012; 30(5):426-31. · 1.85 Impact Factor
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    ABSTRACT: Objective: Hydrogen peroxide (H2O2) is a potent reactive oxygen species that causes cardiomyocytes injury. As an important cytokine, interleukin 6 (IL‐6) has cardioprotective effects as it plays an essential role in the late phase of preconditioning. Our work is to investigate if IL‐6 preconditioning has protective effects on neonatal rat ventricular cardiomyocytes in response to H2O2 and its underlying mechanism. Methods: Gel‐based comparative proteomic approach along with small interfering RNA (siRNA) and Western blot analysis was used to analyse mechanisms of IL‐6 preconditioning on H2O2‐induced neonatal rat ventricular cardiomyocytes injury. Results: IL‐6 preconditioning protected cardiomyocytes against H2O2‐induced cell death. Proteomic analysis showed that IL‐6 pretreatment further increased the expression of prohibitin and improved the viability of cardiomyocytes exposed to H2O2. Knocking down of prohibitin with siRNA abrogated this protection by increasing apoptosis rate. Tyrosine kinase inhibitor AG490 decreased signal transducers and activators of transcription 3 (STAT3) phosphorylation and down‐regulated prohibitin expression in cardiomyocytes pretreated with IL‐6 and exposed to H2O2, which further dampened the protective effects of IL‐6 preconditioning. Conclusion: Our results provide direct evidence that prohibitin is a protective factor of IL‐6 preconditioning in H2O2‐induced neonatal rat ventricular cardiomyocytes death. The upregulation of prohibitin by IL‐6 is, at least, partially regulated through STAT3 phosphorylation. Copyright © 2012 John Wiley & Sons, Ltd.
    Cell Biochemistry and Function 01/2012; 30(5). · 1.85 Impact Factor
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    ABSTRACT: p53 plays a fundamental role in the maintenance of genome integrity after DNA damage, deciding whether cells repair and live, or die. However, the rules that govern its choice are largely undiscovered. Here we show that the functional relationship between p38 and p53 is crucial in defining the cell fate after DNA damage. Upon low dose ultraviolet (UV) radiation, p38 and p53 protect the cells from apoptosis separately. Conversely, they function together to favor apoptosis upon high dose UV exposure. Taken together, a UV-induced, dose-dependent interaction between p38 and p53 acts as a switch to determine cell fate.
    FEBS letters 11/2010; 584(23):4711-6. · 3.54 Impact Factor
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    ABSTRACT: To construct pNTAP-MK2 eukaryotic expression plasmid and establish a HEK293 cell line stably expressing tandam affinity purification (TAP)-tagged MK2. The MK2-encoding region was subcloned into the vector pNTAP to construct the recombinant plasmid pNTAP-MK2, which was subsequently transformed into DH5 alpha.E.coli. After identification by PCR, digestion with restriction endonuclease and sequencing, the recombinant expression plasmid was transfected into HEK293 cells via liposome, and the cell line with stable expression of exogenous TAP tag-MK2 gene was selected by antibiotic G418. The expression and localization of the fusion protein TAP tag-MK2 were detected by Western blotting and immunofluorescence assay. The results of PCR, restriction endonuclease digestion and sequencing all confirmed the correct construction of the recombinant eukaryotic expression plasmid pNTAP-MK2. Western blotting showed that the recombinant plasmid was expressed stably in HEK293 cells after transfection with G418 selection. Immunofluorescence assay identified the expression product TAP tag-MK2 mainly in the cell nuclei. The eukaryotic expression vector pNTAP-MK2 has been successfully constructed, and in the established cell line with stable expression of TAP tag-MK2, TAP tag does not influence the localization of exogenous MK2.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 10/2010; 30(10):2310-3.
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    ABSTRACT: p38 mitogen-activated protein kinase (MAPK) is of fundamental importance in a cell's response to environmental stresses, cytokines and DNA damage. p38 resides in the cytoplasm of resting cells, and translocates into the nucleus upon activation, yet the exact mechanisms remain largely unclear. We show here that the phosphorylation-dependent nuclear translocation of p38 is a common phenomenon when cells are stimulated with various stresses. On the other hand, the nuclear export of p38 requires its dephosphorylation, and it is exported both in a MK2-dependent and a nuclear export signal (NES)-independent manner. Although different p38-regulated/activated protein kinase (PRAK) mutants all dictate the intracellular localization of p38, results from a PRAK-deficient cell line indicate that it plays no role in this process. Microtubule depolymerizing reagent nocodazole and dynein inhibitor EHNA both block the nuclear translocation of p38, demonstrating roles for microtubules and dynein in p38 transport. Taken together, stress-induced nuclear accumulation of p38 is a phosphorylation-dependent, microtubule- and dynein-associated process.
    Journal of Cellular Biochemistry 08/2010; 110(6):1420-9. · 3.06 Impact Factor
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    ABSTRACT: It has been well documented that both endogenous inflammatory mediator advanced glycation end products (AGEs) and exogenous inflammatory inducer lipopolysaccharide play key roles in the initiation and development of inflammatory diseases. However, the combined inflammation-stimulatory effect of AGEs and lipopolysaccharide on endothelial cells, and, furthermore, the underlying signal transduction pathways involved, have not been fully elucidated. We found that in vitro co-stimulation with AGE-human serum albumin (HSA) and lipopolysaccharide exhibits a synergistic effect on proinflammatory cytokine/chemokine interleukin-6, interleukin-8 and monochemoattractant protein-1 production in human umbilical vein endothelial cells. Similar to lipopolysaccharide, AGE-HSA stimulation induced mitogen-activated protein kinase phosphorylation and nuclear factor-kappaB nuclear translocation in human umbilical vein endothelial cells, which was further enhanced by a combination of the two stimulants. Pharmacological inhibitions of each individual signaling pathway, including p38, extracellular signal-regulated kinase 1/2, Jun N-terminal kinase and nuclear factor-kappaB, revealed that activation of all of these four pathways is necessary for the effective induction of interleukin-6, interleukin-8 and monochemoattractant protein-1 by both AGE-HSA and lipopolysaccharide. These results suggest that AGEs and lipopolysaccharide cooperatively induce proinflammatory cytokine/chemokine production by activating mitogen-activated protein kinases and nuclear factor-kappaB in endothelial cells, thus amplifying the inflammatory response and resulting in tissue damage.
    FEBS Journal 08/2009; 276(16):4598-606. · 4.25 Impact Factor
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    ABSTRACT: To construct a eukaryotic expression vector for alpha-1-antitrypsin (AAT) and detect its expression and localization in NIH 3T3 cells. The total RNA was extracted from the liver tissue of BALB/c mice, and the corresponding coding sequences for mouse AAT (GenBank accession No. NM_009243) were amplified by RT-PCR and cloned into hemagglutinin (HA)-tagged vector pcDNA3-HA. The construct was then transfected into NIH 3T3 cells, which were observed under fluorescence microscope. The recombinant plasmid was verified by PCR, enzyme digestion and sequence analysis, and the fusion protein was highly expressed in NIH 3T3 cells. Under fluorescence microscope, the fusion protein was found to distribute mainly in the cytoplasm. The expression vector for AAT-HA fusion protein has been successfully constructed and effectively expressed in mammalian cells to allow future functional study of AAT in mammalian cells.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 04/2009; 29(3):408-11.
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    ABSTRACT: To construct the expression plasmid of S2 extracellular domain (S2ED) of SARS-coronavirus (SARS- Cov) spike protein (S protein) and enhanced green fluorescent protein (EGFP) to obtain the fusion protein expressed in prokaryotic cells. S2ED based on bioinformatics prediction and EGFP sequence were amplified by PCR and inserted into pET-14b plasmid. The recombinant protein His-S2ED-EGFP was expressed in E. coli by IPTG induction. After purification by Ni-NTA agarose beads, the soluble fractions of the fusion protein were collected and identified by SDS-PAGE and Western blotting. The fusion of S2ED with Hela cell membranes was observed with fluorescent microscope. The pET-14b-S2ED-EGFP plasmid was correctly constructed and highly expressed in BL21 (DE3). When incubated with Hela cells, the purified protein could not internalize through membrane fusion. The expression plasmid containing S2ED of SARS-Cov S protein and EGFP sequence is constructed successfully. Although the recombinant protein obtained has not shown the expected fusion effect with Hela cell membrane, this work may enrich the understanding of the process of membrane fusion mediated by S2 protein and lay the foundation for future study of targeting cell transport system based on cell-specific binding peptide.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 04/2009; 29(3):381-6.
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    ABSTRACT: p38 regulated/activated protein kinase (PRAK) plays a key role in cell senescence and tumor suppression. The aim of this study was to investigate if PRAK had effect on cell proliferation. The growth of PRAK +/+ and PRAK −/− mouse embryonic fibroblast (MEF) cells was measured by methylthiazoletetrazolium (MTT) colorimetric assay, and the proportion of the cell number in different phases of the cell cycle was analyzed by flow cytometry. The growth curves showed that the growth rate was notably decreased, and cell double time was elongated in PRAK −/− cells; moreover, the number of PRAK −/− cells was decreased by 44.5% compared with that of PRAK +/+ cells cultured for 96 h, suggesting that G2/M transition is inhibited in PRAK −/− cells. Meanwhile, G1/S transition was also inhibited in PRAK −/− cells, observed with flow cytometry analysis. The ratios of G0/G1, G2/M, and S phases of PRAK +/+ cells were 44.9%, 12.2%, and 42.9%, respectively, while those of PRAK −/− cells were 55.3%, 7.3%, and 37.4%, respectively. There were 23.1% increase and 12.7% decrease of the number of PRAK −/− cells in G1 and S phases in comparison with that of PRAK +/+ cells, respectively. Taken together, PRAK gene knockout in MEF cells leads to cell cycle arrest and proliferation inhibition.
    Frontiers of Medicine in China 01/2009; 3(4):379-383.
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    ABSTRACT: Severe burn shock remains an unsolved clinical problem with urgent needs to explore novel therapeutic approaches. In this study, the in vivo bioactivity of a series of synthetic lactosyl derivatives (oligosaccharides) was assessed on rats with burn shock to elucidate the underlying mechanisms. Administration of An-2 and Gu-4, two lactosyl derivatives with di- and tetravalent beta-D: -galactopyranosyl-(1-4)-beta-D: -glucopyranosyl ligands, significantly prolonged the survival time (P < 0.05 vs. saline), stabilized blood pressure and ameliorated the injuries to vital organs after burn. Flow chamber assay displayed that An-2 and Gu-4 markedly decreased the adhesion of leukocytes to microvessel endothelial cells. Competitive binding assay showed that a CD11b antibody significantly interrupted the interaction of An-2 and Gu-4 with leukocytes from rats with burn shock. With fluorescent microscopy, we further found that the oligosaccharides were selectively bound to leukocytes and with a colocalization of CD11b on the cell membrane. Interestingly, the lectin domain-deficient form of CD11b failed to bind with An-2 and Gu-4. The results suggest that both An-2 and Gu-4 significantly inhibit the adhesion of leukocytes to endothelial cells by binding to CD11b and thereby exert protective effects on severe burn shock.
    Glycoconjugate Journal 12/2008; 26(2):173-88. · 1.88 Impact Factor
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    ABSTRACT: To construct eukaryotic expression vectors for HA-tagged receptor for advanced glycation end products (RAGE) mutants. Site-directed mutagenesis was applied to wild-type RAGE gene cloned in the pcDNA3 vector with HA tag to obtain the mutants pcDNA3-HA-RAGE(S391A), pcDNA3-HA-RAGE(S399A), pcDNA3-HA-RAGE(S400A), and pcDNA3-HA-RAGE(T401A). After identification by sequencing, the mutants were transfected into HEK293 cells, and the expression of these mutants were detected by Western blotting using anti-HA antibody. The HA-tagged RAGE mutants constructed were verified successfully by sequencing, and highly expressed in HEK293 cells. The success in constructing HA-tagged RAGE mutants, which are highly expressed in eukaryotic cells, may facilitate the functional study of RAGE in cell signal transduction.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 11/2008; 28(10):1779-81.
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    ABSTRACT: To investigate the effect of p38 mitogen-activated protein kinase (MAPK) gene knockout on the proliferation of embryonic fibroblasts in mice (MEFs). The expression of p38 in MEFs p38+/+ and p38(-/-) cells were detected by Western blotting. The growth curves of p38+/+ and p38(-/-) cells were plotted with the results of methylthiazoletetrazolium (MTT) colorimetric assay, and the ratios of different cell phases of p38+/+ and p38(-/-) cells were analyzed by flow cytometry. The growth curves showed that the growth rate was notably retarded and cell double time elongated in p38(-/-) cells, and there was 15.5% decrease of the number of p38(-/-) cells in comparison with that of p38+/+ cells in 96-hour culture. G2/M transition was inhibited in p38(-/-) cells. Meanwhile, G1/S transition was also inhibited in p38(-/-) cells, as shown by the results of flow cytometry. The ratios of G0/G1, G2/M, and S phases of p38+/+ cells were 34.47%, 10.81%, and 54.72%, respectively; while those of p38(-/-) cells were 48.49%, 4.06%, and 47.44%, respectively. There were 40.7% increase and 13.3% decrease in the cell numbers of G1 and S phases of p38(-/-) cells in comparison with those of p38+/+ cells, respectively. p38 gene knockout in MEFs leads to cell cycle arrest and decreased cell proliferation.
    Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue 10/2008; 20(9):527-9.
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    ABSTRACT: To construct different mutants of human p53 for expression in eukaryotic cells and investigate the effects of these mutants on stress-induced cell apoptosis. Human p53 cDNA was amplified by PCR and cloned into pcDNA3/HA vector following the routine procedures. The Ser15 and Ser46 of p53 were mutated to Ala and identified by enzyme digestion and PCR, and these mutants were expressed in NIH3T3 cells and detected by Western blotting. After transfection with the plasmids of different p53 mutants, the NIH3T3 cells were double-stained with AnnexinV-FITC and propidium iodide for apoptotic analysis using flow cytometry. The recombinant plasmids of HA-tagged wild-type p53, HA-p53(WT), and its mutants, HA-p53(S15A) and HA-p53(S46A), were successfully constructed and expressed efficiently in NIH3T3 cells. The apoptotic ratio of p53(WT)-transfected cells induced by arsenite increased and that of p53(S15A)-transfected cells decreased significantly after arsenite stimulation, but no significant changes occurred in the apoptosis of p53(S46A)-transfected cells. The phosphorylation on Ser15 of p53 plays an important role in mediating arsenite-induced cell apoptosis.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 06/2008; 28(5):671-4.
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    ABSTRACT: To establish a new method for the study of DNA-protein interaction. Six SPF BALB/c mice were divided into two groups, the lipopolysaccharide (LPS)-treated group (n=3) and the normal control group (n =3). The LPS-treated mice were subjected to tail vein-injection of LPS (25 mg/kg) to reproduce an endotoxic shock model. The biotin-labeled DNA probe for the LPS inducible gene (LIG) promoter was amplified by polymerase chain reaction (PCR). The cell nuclear extracts from liver of mice were prepared and mixed together. DNA pull-down assays were performed by using magnetic beads conjugated with streptavidin. Proteins binding on the beads were eluted by salts with different concentrations. The samples were resolved by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and displayed by silver-stain to compare differential bands between two groups. Fifteen proteins in the nuclear extracts were found to be different between the mice of two groups. Analysis of the differential bands of SDS-PAGE displayed that, compared with normal control group, there were four proteins increased and one protein declined in the mice treated with LPS when eluted with low salt. While under the condition of high affinity elution, there were nine proteins increased and one disappeared after LPS treatment. In this study, a novel method was set up by combining the biotin-streptavidin system and magnetic beads isolation technique, providing a new way to study DNA-protein interaction. This strategy is helpful for further understanding the regulation of gene expression with a view of "omics".
    Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue 02/2008; 20(1):14-7.
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    ABSTRACT: To investigate the role of p53 gene in serum-induced cell migration. The effects of p53 knockout on serum-induced formation of lamellipodia and cell migration were observed using Transwell cell migration system. p53(+/+) cells developed lamellipodia upon serum stimulation and showed enhanced activity of cell migration, but these effects were not observed in p53 knockout cells after serum stimulation. p53 plays a role in serum-induced cell migration.
    Nan fang yi ke da xue xue bao = Journal of Southern Medical University 09/2007; 27(8):1132-5.

Publication Stats

156 Citations
40.90 Total Impact Points

Institutions

  • 2003–2012
    • Nanfang Hospital
      Shengcheng, Guangdong, China
  • 2002–2010
    • Southern Medical University
      • Department of Pathophysiology
      Guangzhou, Guangdong Sheng, China
  • 2008
    • Nanjing Normal University
      • Jiangsu Key Laboratory for Molecular and Medical Biotechnology
      Nan-ching, Jiangsu Sheng, China
  • 2005
    • Guangzhou Institute of Respiratory Disease
      Shengcheng, Guangdong, China