Wei Zhao

University of Jinan (Jinan, China), Chi-nan-shih, Shandong Sheng, China

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Publications (55)116.33 Total impact

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    ABSTRACT: A novel hydrophobic bifunctionalized hexagonal mesoporous silica (Ph-Am-HMS) material was synthesized with the simultaneous immobilization of phenyl and amino groups on the surface. The composition and structure of Ph-Am-HMS were studied by FT-IR, XRD, N2 adsorption-desorption, and sessile water droplet contact angle measurements, etc., which revealed that this novel bifunctionalized material showed hydrophobicity and good porous properties. Being applied in the adsorption of azo dye Orange IV in aqueous solutions, Ph-Am-HMS exhibited a high adsorption capacity and a rapid adsorption rate. The theoretical maximum adsorption capacity could reach 246.3 mg/g in 60 min at 293 K. Kinetic study indicated that the adsorption of Orange IV on Ph-Am-HMS fitted perfectly to Freundlich adsorption model and followed the pseudo-second-order kinetics. The changes in Gibbs free energy (-10.55 kJ/mol), enthalpy (-7.06 kJ/mol), and entropy (11.83 J/mol) at 293 K showed that the adsorption process was spontaneous and exothermic.
    RSC Advances 09/2014; · 3.71 Impact Factor
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    ABSTRACT: TANK-binding kinase 1 (TBK1) is essential for IFN regulatory factor 3 activation and IFN-β production downstream of various innate receptors. However, how TBK1 activation is terminated is not well defined. In this study, we identified ubiquitin-specific protease (USP) 2b as a new negative regulator for TBK1 activation. Overexpression of USP2b inhibited retinoic acid-inducible gene-I-mediated IFN-β signaling; in contrast, knockdown of USP2b expression by small interfering RNA enhanced retinoic acid-inducible gene-I-mediated IFN-β signaling. Coimmunoprecipitation experiments demonstrated that USP2b interacted with TBK1. As a deubiquitinating enzyme, USP2b was demonstrated to cleave K63-linked polyubiquitin chains from TBK1 to inhibit TBK1 kinase activity. Consistent with the inhibitory roles of USP2b on TBK1 activation, knockdown of USP2b significantly inhibited the replication of vesicular stomatitis virus, whereas overexpression of USP2b resulted in enhanced replication of vesicular stomatitis virus. Therefore, our findings demonstrated that USP2b deubiquitinates K63-linked polyubiquitin chains from TBK1 to terminate TBK1 activation and negatively regulate IFN-β signaling and antiviral immune response.
    Journal of immunology (Baltimore, Md. : 1950). 07/2014;
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    ABSTRACT: NLRP3 inflammasome is a multi-protein complex, which plays crucial roles in host defense against pathogens. The NLRP3 protein level is considered rate limiting for the activation of the inflammasome, thus its expression must be tightly controlled to maintain immune homeostasis. However, the molecular mechanisms that modulate NLRP3 expression, especially at the transcriptional level, remain largely unknown. In the present study, we show that aryl hydrocarbon receptor (AhR) activation inhibits NLRP3 expression, caspase-1 activation and subsequent IL-1β secretion in peritoneal macrophages, whereas siRNA knockdown of AhR has opposite effects. AhR could bind to the xenobiotic response element (XRE) in the NLRP3 promoter and inhibit NLRP3 transcription. Furthermore, AhR activation suppresses Alum-induced peritonitis in vivo. Therefore, we identified AhR as a negative regulator of NLRP3 inflammasome activity by inhibiting the transcription of NLRP3 and suggested AhR as a potential target for the intervention of diseases with uncontrolled inflammasome activation.
    Nature Communications 01/2014; 5:4738. · 10.74 Impact Factor
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    ABSTRACT: Resistance to anoikis and Epithelial-mesenchymal transition (EMT) are two processes critically involved in cancer metastasis. In this study, we demonstrated that after anchorage deprival, hepatocellular carcinoma (HCC) cells not only resisted anoikis, but also exhibited EMT process. Microarray expression profiling revealed that expression of miR-424-5p was significantly decreased in anoikis-resistant HCC cells. Ectopic overexpression of miR-424-5p was sufficient to reverse resistance to anoikis, block EMT process and inhibit malignant behaviors of HCC cells. Target analysis showed that a potent β-catenin inhibitor, ICAT/CTNNBIP1 was a direct target of miR-424-5p. Further study demonstrated that miR-424-5p reversed resistance to anoikis and EMT of HCCs by directly targeting ICAT and further maintaining the E-cadherin/β-catanin complex on the cellular membrance. In vivo study further demonstrated that miR-424-5p significantly inhibited the tumorigenicity of HCC cells in nude mice. Clinical investigation demonstrated that miR-424-5p was significantly downregulated in HCC tissues compared with that of the non-cancerous liver tissues, and this decreased expression of miR-424-5p was significantly correlated with higher pathological grades and more advanced TNM stages. Therefore, aberrant expression of miR-424-5p is critically involved in resistance to anoikis and EMT during the metastatic process of HCC, and its downregulation significantly contributes to liver cancer progression.
    Scientific reports. 01/2014; 4:6248.
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    ABSTRACT: NOD-like receptor family, pyrin domain containing 3 and 1 (NLRP3 and NLRP1) inflammasomes are molecular platforms that sense the damage or danger signals of cells. We investigated whether NLRP3/NLRP1 inflammasomes are involved in the pathogenesis and progression of systemic lupus erythematosus (SLE). Expressions of inflammasome components at the mRNA and protein levels in the peripheral blood mononuclear cells (PBMC) from patients with SLE and healthy controls were investigated by quantitative real-time transcription PCR and Western blot, respectively. Correlations between NLRP3/NLRP1 inflammasome components' expression and clinical disease progression were investigated. Expressions of NLRP3/NLRP1 inflammasomes before and after treatment in the patients with SLE were also analyzed and compared. Our data showed that expressions of NLRP3/NLRP1 inflammasomes were significantly downregulated in PBMC from patients with SLE compared with PBMC from healthy controls. Further, expressions of NLRP3/NLRP1 inflammasomes were negatively correlated with the SLE Disease Activity Index, and regular glucocorticoid treatment significantly corrected this deregulation of these inflammasomes. Further analysis showed that type I interferon (IFN) level was significantly negatively correlated with expression of NLRP3/NLRP1 inflammasomes, which indicated that enhanced IFN-I level in patients with SLE was responsible, at least to a great degree, for the deregulation of inflammasomes. These results indicated deregulation of NLRP3/NLRP1 inflammasomes in patients with SLE, and suggested an important role for inflammasomes in the pathogenesis and progression of SLE.
    The Journal of Rheumatology 12/2013; · 3.26 Impact Factor
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    ABSTRACT: Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors worldwide, and it is always the consequence of chronic hepatitis and liver cirrhosis. The nucleotide-binding domain, leucine-rich family (NLR), pyrin-containing 3 (NLRP3) inflammasome has been shown to orchestrate multiple innate and adaptive immune responses. However, little is known about its role in cancer. This study was performed to investigate the role of the NLRP3 inflammasome in the development and progression of HCC. The expression of NLRP3 inflammasome components was analyzed in HCC tissues and corresponding non-cancerous liver tissues at both the mRNA and protein levels. Our data demonstrate that the expression of all of the NLRP3 inflammasome components was either completely lost or significantly downregulated in human HCC, and that the deficiency correlated significantly with advanced stages and poor pathological differentiation. In addition, our data provide an overview of the expression of NLRP3 inflammasome components in the multi-stage development of HCC and indicate a surprising link between deregulation of the NLRP3 inflammasome molecular platform and HCC progression. In conclusion, this study presents a dynamic expression pattern of NLRP3 inflammasome components in multi-stage hepatocarcinogenesis and demonstrates that deregulated expression of the inflammasome is involved in HCC progression.Laboratory Investigation advance online publication, 28 October 2013; doi:10.1038/labinvest.2013.126.
    Laboratory Investigation 10/2013; · 3.96 Impact Factor
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    ABSTRACT: Lithium salt is a widely used glycogen synthase kinase-3β inhibitor and effective drug for the treatment of psychiatric diseases. However, the effects of lithium in innate immune responses, especially in cellular antiviral responses, are unknown. In this study, we show that lithium chloride attenuates LPS-, polyinosinic-polycytidylic acid-, and Sendai virus-induced IFN-β production and IFN regulatory factor 3 activation in macrophages in a glycogen synthase kinase-3β-independent manner. The ability of the lithium to inhibit IFN-β production was confirmed in vivo, as mice treated with lithium chloride exhibited decreased levels of IFN-β upon Sendai virus infection. In vitro kinase assay demonstrates that lithium suppresses TANK-binding kinase 1 kinase activity. Consistently, lithium significantly enhanced the replication of vesicular stomatitis virus in vitro and in vivo. Severe infiltration of monocytes and tissue damage were observed in the lungs of control mice, compared with lithium-treated mice after virus infection. Our findings suggest lithium as an inhibitor of TANK-binding kinase 1 and potential target for the intervention of diseases with uncontrolled IFN-β production. Furthermore, lithium attenuates host defense to virus infection and may cause severely adverse effects in clinical applications.
    The Journal of Immunology 09/2013; · 5.52 Impact Factor
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    ABSTRACT: Circulating endothelial progenitor cells (EPCs) play a critical role in maintaining endothelial integrity and keeping vascular homeostasis. Previously, we reported that EPCs were involved in repair and remodeling of aneurismal wall. In the present study, we verified this hypothesis by investigating the proliferative ability and count of EPCs in peripheral blood of patients with unruptured intracranial aneurysms (UIAs). Twenty-four patients with UIAs (UIA group) and 24 negative controls (control group) were included in this study. Peripheral blood monocytes (PBMCs) were harvested and selectively cultured. The colony-forming ability of cultured cells was analyzed and the biological functions were examined by testing the adsorption of ulex europaeus agglutinin-1 labeled by fluorescein isothiocyanate and acetylated low-density lipoprotein internalization. The migratory and adhesive ability of cultured EPCs were assessed. In vitro cultured PBMCs were identified as EPCs by examining surface markers CD34, CD133 and vascular endothelial growth factor receptor 2 using flow cytometry. EPCs from UIA group possessed significantly decreased proliferative, migratory and adhesive capacities compared with EPCs from control group. Furthermore, EPCs count in UIA group was significantly decreased. Collectively, these results indicated that the circulating EPCs of UIA patients may be involved in intracranial aneurysm repair and remodeling.
    Neurological Sciences 05/2013; · 1.41 Impact Factor
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    ABSTRACT: Silver nanoparticles were added into anaerobic batch reactors to enhance acidogenesis and fermentative hydrogen production simultaneously. The effects of silver nanoparticles concentration (0-200nmolL(-1)) and inorganic nitrogen concentration (0-4.125gL(-1)) on cell growth and hydrogen production were investigated using glucose-fed mixed bacteria dominated by Clostridium butyricum. The tests with silver nanoparticles exhibited much higher H2 yields than the blank, and the maximum hydrogen yield (2.48mol/molglucose) was obtained at the silver concentration of 20nmolL(-1). Presence of silver nanoparticles reduced the yield of ethanol, but increased the yield of acetic acid. The high silver nanoparticles had higher cell biomass production rate. Further study using the alkaline pretreated culture as inoculum was carried out to verify the positive effect of silver nanoparticles on H2 production. Results demonstrated that silver nanoparticles could not only increase the hydrogen yield, but reduce the lag phase for hydrogen production simultaneously.
    Bioresource Technology 05/2013; 142C:240-245. · 5.04 Impact Factor
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    ABSTRACT: Protein ubiquitination plays an essential role in the regulation of RIG-I activation and antiviral immune response. However, the function of the opposite process of deubiquitination in RIG-I activation remains elusive. In this study, we have identified the deubiquitinating enzyme Ubiquitin-specific protease 4 (USP4) as a new regulator for RIG-I activation through deubiquitination and stabilization of RIG-I. USP4 expression was attenuated after virus-induced RIG-I activation. Overexpression of USP4 significantly enhanced RIG-I protein expression and RIG-I-triggered IFN-β signaling, at the same time, inhibited VSV replication. siRNA knockdown of USP4 expression has an opposite effect. Furthermore, USP4 was found to interact with RIG-I and remove K48-linked polyubiquitinattion chains from RIG-I. Therefore, our study identified USP4 as a new positive regulator for RIG-I through deubiquitinating K48-linked ubiquitin chains and stabilizing RIG-I.
    Journal of Virology 02/2013; · 5.08 Impact Factor
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    Wei Zhao
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    ABSTRACT: TANK-binding kinase 1 (TBK1) plays pivotal roles in antiviral innate immunity. TBK1 mediates the activation of interferon regulatory factor (IRF) 3, leading to the induction of type I IFNs (IFN-α/β) following viral infections. TBK1 must be tightly regulated to effectively control viral infections and maintain immune homeostasis. TBK1 activity can be regulated in a variety of ways, such as phosphorylation, ubiquitination, kinase activity modulation and prevention of functional TBK1-containing complexes formation. Furthermore, multiple viruses have evolved elaborate strategies to circumvent IFN responses by targeting TBK1. Here we provide an overview of TBK1 in antiviral immunity and recent developments on the regulation of TBK1 activity.
    FEBS letters 02/2013; · 3.54 Impact Factor
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    ABSTRACT: Head and neck squamous cell carcinoma (HNSCC) is a common type of cancer. Better understanding of molecular aberrations associated with HNSCC might identify new diagnostic and therapeutic strategies for this disease. In this study, we found ubiquitin-specific protease 4 (USP4) was significantly upregulated in HNSCC. USP4 negatively regulates RIP1-mediated NF-κB activation and promotes TNF-α-induced apoptosis in FaDu cells. USP4 directly interacts with receptor-interacting protein 1 (RIP1) and deubiquitinates K63-linked ubiquitination from RIP1. Therefore, our results indicate that USP4 has tumor suppressor roles in HNSCC and suggest USP4 as a potential therapeutic target for HNSCC. STRUCTURED SUMMARY OF PROTEIN INTERACTIONS: RIP1physically interacts with USP4 by anti tag coimmunoprecipitation (View Interaction: 1, 2, 3) RIP1physically interacts with USP4 by anti bait coimmunoprecipitation (View interaction).
    FEBS letters 01/2013; · 3.54 Impact Factor
  • Journal of Computational and Theoretical Nanoscience, vol. 10, issue 1, pp. 73-77. 01/2013; 10(1):73-77.
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    ABSTRACT: TANK-binding kinase 1 (TBK1) plays an essential role in Toll-like receptor (TLR)- and retinoic acid-inducible gene I (RIG-I)-mediated induction of type I interferon (IFN; IFN-α/β) and host antiviral responses. How TBK1 activity is negatively regulated remains largely unknown. We report that TNF receptor-associated factor (TRAF)-interacting protein (TRIP) promotes proteasomal degradation of TBK1 and inhibits TLR3/4- and RIG-I-induced IFN-β signaling. TRIP knockdown resulted in augmented activation of IFN regulatory factor 3 (IRF3) and enhanced expression of IFN-β in TLR3/4- and RIG-I-activated primary peritoneal macrophages, whereas overexpression of TRIP had opposite effects. Consistently, TRIP impaired Sendai virus (SeV) infection-induced IRF3 activation and IFN-β production and promoted vesicular stomatitis virus (VSV) replication. As an E3 ubiquitin ligase, TRIP negatively regulated the cellular levels of TBK1 by directly binding to and promoting K48-linked polyubiquitination of TBK1. Therefore, we identified TRIP as a negative regulator in TLR3/4- and RIG-I-triggered antiviral responses and suggested TRIP as a potential target for the intervention of diseases with uncontrolled IFN-β production.
    Journal of Experimental Medicine 09/2012; 209(10):1703-11. · 13.21 Impact Factor
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    ABSTRACT: Aerobic granular sludge was successfully cultivated with the effluent of internal circulation (IC) reactor in a pilot-scale sequencing batch reactor (SBR) using activated sludge as seeding sludge. N removal was investigated in the start-up of aerobic granulation process. Initially, the phenomenon of partial nitrification was observed and nitrite accumulation rates (NO(2) (-)-N/NO (x) (-) -N) were between 84.6 and 99.1 %. It was potentially caused by ammonium oxidizing bacteria (AOB) in the seeding activated sludge, high external environmental temperature (~32 °C) and free ammonia (FA) concentration. After 50 days' running, the aerobic granules-based bioreactor demonstrated perfect performance in simultaneous removal of organic matter and ammonia nitrogen, and average removal efficiencies were maintained above 93 and 96 %, respectively. The maximum nitrogen removal efficiency of 83.1 % was achieved after the formation of aerobic granules. The average diameter of mature aerobic granular sludge mostly ranged from 0.5 to 1.0 mm. Furthermore, one typical cyclic test indicated that pH and DO profiles could be used as effective parameters for biological reactions occurring in the aerobic/anoxic process. The obtained results could provide further information on the cultivation of aerobic granular sludge with practical wastewater, especially with regard to nitrogen-rich industrial wastewater.
    Bioprocess and Biosystems Engineering 05/2012; 35(9):1489-96. · 1.87 Impact Factor
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    ABSTRACT: Recognition of RNA virus through TLR and RIG-I-like receptor results in rapid expression of type I IFNs, which play an essential role in host antiviral responses. However, the mechanisms to terminate the production of type I IFNs are not well defined. In the current study, we identified a member of the tripartite motif (TRIM) family, TRIM38, as a negative regulator in TLR3/4- and RIG-I-mediated IFN-β signaling. Knockdown of TRIM38 expression by small interfering RNA resulted in augmented activation of IFN regulatory factor 3 and enhanced expression of IFN-β, whereas overexpression of TRIM38 had opposite effects. Coimmunoprecipitation and colocalization experiments demonstrated that TRIM38 interacted with NF-κB-activating kinase-associated protein 1 (NAP1), which is required for TLR-induced IFN regulatory factor 3 activation and IFN-β production. As an E3 ligase, TRIM38 promoted K48-linked polyubiquitination and proteasomal degradation of NAP1. Thus, knockdown of TRIM38 expression resulted in higher protein level of NAP1 in primary macrophages. Consistent with the inhibitory roles in TLR3/4- and RIG-I-mediated IFN-β signaling, knockdown of TRIM38 significantly inhibited the replication of vesicular stomatitis virus. Overexpression of TRIM38 resulted in enhanced replication of vesicular stomatitis virus. Therefore, our results demonstrate that TRIM38 is a negative regulator for TLR and RIG-I-mediated IFN-β production by targeting NAP1 for ubiquitination and subsequent proteasome-mediated degradation.
    The Journal of Immunology 04/2012; 188(11):5311-8. · 5.52 Impact Factor
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    ABSTRACT: Ligation of TLR4 with LPS in macrophages leads to the production of proinflammatory cytokines, which are central to eliminate viral and bacterial infection. However, uncontrolled TLR4 activation may contribute to pathogenesis of inflammatory diseases such as septic shock. In this study, we found microRNA-210 was induced in murine macrophages by LPS. Transfection of miR-210 mimics significantly inhibited LPS-induced production of inflammatory cytokines. In contrast, transfection of anti-miR-210 inhibitors increased LPS-induced expression of proinflammatory cytokines. Furthermore, we demonstrated that miR-210 targets NF-κB1. Therefore, our data identify miR-210 as a very important feedback negative regulator for LPS-induced production of proinflammatory cytokines.
    FEBS letters 04/2012; 586(8):1201-7. · 3.54 Impact Factor
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    ABSTRACT: Patients with esophageal squamous cell carcinoma (ESCC) undergoing definitive chemoradiotherapy (CRT) seem to have a disparity in therapeutic response. The identification of CRT sensitivity-related clinicopathological factors would be helpful for selecting patients most likely to benefit from CRT. Cytokeratin 19 fragment antigen 21-1 (CYFRA21-1) and carcinoembryonic antigen (CEA) have been reported as useful tumor markers for esophageal cancer. The aim of this study was to examine the predictive value of CYFRA21-1 in comparison with CEA and other clinicopathological factors in patients with ESCC treated with definitive CRT. Pretreatment serum CYFRA21-1 and CEA levels were measured by immunoradiometric assays. The relationships between pretreatment clinicopathological factors and the efficacy of CRT were analyzed. Overall survival (OS) was estimated by univariate and multivariate analysis. The results from a univariate analysis indicated that the efficacy of CRT was significantly associated with the serum levels of CYFRA21-1 and CEA before treatment (P = 0.001 and P = 0.023, respectively). It also indicated that the efficacy of CRT was significantly associated with the pretreatment tumor location (P = 0.041). By Logistic regression analysis, the independent predictive factor associated with efficacy of CRT was CYFRA21-1 (P = 0.002). The OS of the patients with high CYFRA 21-1 levels was worse than that of those with low CYFRA21-1 levels (P = 0.001). In multivariate analysis, a low level of CYFRA21-1 was the most significant independent predictor of good OS (P = 0.007). CEA and tumor location may be useful in predicting the sensitivity of ESCC to CRT. CYFRA21-1 may be an independent predictor for definitive CRT sensitivity in ESCC.
    Chinese medical journal 04/2012; 125(8):1410-5. · 0.90 Impact Factor
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    ABSTRACT: Activation of TLR signaling in the innate immune cells is critical for the elimination of invading microorganisms. However, uncontrolled activation may lead to autoimmune and inflammatory diseases. In this article, we report the identification of tripartite motif (TRIM) 38 as a negative feedback regulator in TLR signaling by targeting TNFR-associated factor 6 (TRAF6). TRIM38 was induced by TLR stimulation in an NF-κB-dependent manner in macrophages. Knockdown of TRIM38 expression by small interfering RNA resulted in augmented activation of NF-κB and MAPKs, and enhanced expression of proinflammatory cytokines, whereas overexpression of TRIM38 has an opposite effect. As an E3 ligase, TRIM38 bound to TRAF6 and promoted K48-linked polyubiquitination, which led to the proteasomal degradation of TRAF6. Consistently, knockdown of TRIM38 expression resulted in higher protein level of TRAF6 in primary macrophages. Our findings defined a novel function for TRIM38 to prevent excessive TLR-induced inflammatory responses through proteasomal degradation of TRAF6.
    The Journal of Immunology 03/2012; 188(6):2567-74. · 5.52 Impact Factor
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    ABSTRACT: TLR signaling is associated with the transcription of various proinflammatory cytokines, including TNF-α, IL-6, and IL-1β. After transcription, the mRNA of these proinflammatory cytokines needs to be tightly controlled at the posttranscriptional level to achieve an optimal expression. However, the precise mechanism of posttranscriptional regulation is not fully understood. In the current study, we found the expression of heterogeneous nuclear ribonucleoprotein U (hnRNP U), also termed scaffold attachment factor A, was greatly induced by TLR stimulation in macrophages. Knockdown of hnRNP U expression greatly attenuated TLR-induced expression of TNF-α, IL-6, and IL-1β, but not IL-12, whereas hnRNP U overexpression greatly increased TLR-induced expression of TNF-α, IL-6, and IL-1β. Furthermore, hnRNP U knockdown accelerated the turnover and decreased the t(1/2) of TNF-α, IL-6, and IL-1β mRNA. RNA immunoprecipitation demonstrated that hnRNP U bound to the mRNA of these proinflammatory cytokines through the RGG motif. Importantly, we showed that TLR stimulation provided a stimulus for hnRNP U nuclear to cytoplasmic translocation. Therefore, we propose that hnRNP U induced by TLR signaling binds to the mRNA of a subset of proinflammatory cytokines and positively regulates the expression of these cytokines by stabilizing mRNA.
    The Journal of Immunology 02/2012; 188(7):3179-87. · 5.52 Impact Factor

Publication Stats

835 Citations
116.33 Total Impact Points

Institutions

  • 2012–2014
    • University of Jinan (Jinan, China)
      Chi-nan-shih, Shandong Sheng, China
  • 2013
    • General Hospital of Jinan Military Region
      Chi-nan-shih, Shandong Sheng, China
    • Shandong University
      Chi-nan-shih, Shandong Sheng, China
  • 2010
    • Fudan University
      • Department of Oncology
      Shanghai, Shanghai Shi, China
  • 2006–2009
    • Arizona State University
      • • Department of Electrical Engineering
      • • School of Electrical, Computer and Energy Engineering
      Phoenix, Arizona, United States