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#29114247   2017/10/24 To Up

Elusive Role of the CD94/NKG2C NK Cell Receptor in the Response to Cytomegalovirus: Novel Experimental Observations in a Reporter Cell System.

Human cytomegalovirus (HCMV) infection promotes the differentiation and persistent expansion of a mature NK cell subset, which displays high surface levels of the activating CD94/NKG2C NK cell receptor, together with additional distinctive phenotypic and functional features. The mechanisms underlying the development of adaptive NK cells remain uncertain but some observations support the involvement of a cognate interaction of CD94/NKG2C with ligand(s) displayed by HCMV-infected cells. To approach this issue, the heterodimer and its adaptor (DAP12) were expressed in the human Jurkat leukemia T cell line; signaling was detected by transfection of a reporter plasmid encoding for Luciferase (Luc) under NFAT/AP1-dependent control. Engagement of the receptor by solid-phase bound CD94- or NKG2C-specific monoclonal antibodies (mAbs) triggered Luc expression. Moreover, reporter activation was detectable upon interaction with HLA-E+ 721.221 (.221-AEH) cells, as well as with 721.221 cells incubated with synthetic peptides, which stabilized surface expression of endogenous HLA-E; the response was specifically antagonized by soluble NKG2C- and HLA-E-specific mAbs. By contrast, activation of Jurkat-NKG2C+ was undetectable upon interaction with Human Fetal Foreskin Fibroblasts (HFFF) infected with HCMV laboratory strains (i.e., AD169, Towne), regardless of their differential ability to preserve surface HLA-E expression. On the other hand, infection with two clinical isolates or with the endotheliotropic TB40/E strain triggered Jurkat-NKG2C+ activation; yet, this response was not inhibited by blocking mAbs and was independent of CD94/NKG2C expression. The results are discussed in the framework of previous observations supporting the hypothetical existence of specific ligand(s) for CD94/NKG2C in HCMV-infected cells.
Aldi Pupuleku, Marcel Costa-García, Domènec Farré, Hartmut Hengel, Ana Angulo, Aura Muntasell, Miguel López-Botet

2017 related Products with: Elusive Role of the CD94/NKG2C NK Cell Receptor in the Response to Cytomegalovirus: Novel Experimental Observations in a Reporter Cell System.

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#28274746   2017/03/06 To Up

Transcription factors SF1 and cJUN cooperate to activate the Fdx1 promoter in MA-10 Leydig cells.

The Ferredoxin 1 (FDX1) protein supports steroid biosynthesis in steroidogenic cells through electron transfer to the rate-limiting steroidogenic enzyme, CYP11A1. The latter catalyzes the conversion of cholesterol to pregnenolone through side chain cleavage inside the mitochondria. Thus far, only several transcription factors have been implicated in the regulation of mouse Fdx1 promoter activity in Leydig cells. These include the nuclear receptor SF1 and SP1. Since two conserved regulatory elements for AP1 transcription factors have been located at -764 and -617bp of the Fdx1 promoter, we hypothesized that cJUN may cooperate with other partners to regulate Fdx1 in Leydig cells. Indeed, we report that SF1 and cJUN interact and cooperate to activate the Fdx1 promoter in MA-10 and TM3 Leydig cells. Furthermore, we found that such activation requires different regulatory elements located between -124 and -306bp of the Fdx1 promoter and involves recruitment of SF1 to this region. Using RNA interference, the importance of SF1 in transcriptional regulation of Fdx1 was confirmed, whereas cJUN was dispensable even though it cooperated with SF1 to upregulate Fdx1 expression in MA-10 cells. Thus, our data provides new insights in the molecular mechanisms that control mouse Fdx1 transcription, possibly leading to regulation of CYP11A1 enzyme activation, in Leydig cells.
Pauline Roumaud, Arlette Rwigemera, Luc J Martin

1295 related Products with: Transcription factors SF1 and cJUN cooperate to activate the Fdx1 promoter in MA-10 Leydig cells.

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#27264312   2016/06/06 To Up

Novel CHOP activator LGH00168 induces necroptosis in A549 human lung cancer cells via ROS-mediated ER stress and NF-κB inhibition.

C/EBP homologous protein (CHOP) is a transcription factor that is activated at multiple levels during ER stress and plays an important role in ER stress-induced apoptosis. In this study we identified a novel CHOP activator, and further investigated its potential to be a therapeutic agent for human lung cancer.
Yi-Ming Ma, Yan-Min Peng, Qiong-Hua Zhu, An-Hui Gao, Bo Chao, Qiao-Jun He, Jia Li, You-Hong Hu, Yu-Bo Zhou

2649 related Products with: Novel CHOP activator LGH00168 induces necroptosis in A549 human lung cancer cells via ROS-mediated ER stress and NF-κB inhibition.

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#24440756   2014/01/15 To Up

Role of ERK/NFκB in vanadium (IV) oxide mediated osteoblast differentiation in C3H10t1/2 cells.

Vanadium (V) compounds are reported to have insulin mimicking action, which render them to show excellent osteogenic activity. In the current study we investigated the effect of various vanadium compounds on osteoblast differentiation of mouse mesenchymal stem cells, C3H10t1/2 cells, and analyzed the underlying mechanism of vanadium for this action. Our data showed that treatment of C3H10t1/2 cells with V (IV) oxide complex (at 7-25 μM concentrations) induced osteoblast differentiation maximally as compared to V2O5. On the other hand, ammonium vanadate was found to dampen the osteoblast differentiation process. Based on this data, V (IV) oxide was investigated further to analyze its probable mode of action as an osteoblastic agent. The key factors implicated in osteoblast differentiation i.e., NFκB, ERK ½, AP1 and CRE were examined in response to V (IV) oxide exposure. Exposure to V (IV) oxide caused 2- and 5-folds induction of luciferase activities in cells transfected with SRE-luc and NFκB-luc reporter vectors respectively (p < 0.05). Further, exposure to V (IV) oxide enhanced the phosphorylation of ERK ½, IκB and NFκBp65 proteins. In addition, RT-PCR analysis, alizarin red staining and immunoblot analysis showed that inhibition of osteoblast differentiation in presence of PD98059 and parthenolide (inhibitors of ERK and NFκB pathways respectively) was rescued in presence of V (IV) oxide. These results suggest that V (IV) oxide up regulates osteoblast differentiation through ERK and NFκB pathways and hence could be utilized as an agent for bone formation after further analysis and validation.
Swati Srivastava, Narender Kumar, Partha Roy

1667 related Products with: Role of ERK/NFκB in vanadium (IV) oxide mediated osteoblast differentiation in C3H10t1/2 cells.

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#21617851   2011/05/20 To Up

Overexpression of EGR-1 modulates the activity of NF-κB and AP-1 in prostate carcinoma PC-3 and LNCaP cell lines.

To address elements that might uniquely characterize EGR-1 mediated signaling, the expression of two transcription factors, namely, nuclear factor kappa B (NF-κB) and activator protein-1 (AP-1) were studied. PC-3 and LNCaP prostate carcinoma cell lines were transiently transfected with wild-type Egr-1 expression plasmid (pCMV-Egr-1) and treated with cisplatin and TPA. Overexpression of EGR-1 was found to induce nuclear expression of both, NF-κB and AP1. However, the intensity of the induced AP-1 and NF-κB was diminished after cisplatin treatment, but not after TPA. Our findings confirm that the overexpression of wild-type Egr-1 caused a marked increase in cell proliferation in PC-3 and LNCaP proliferation in a 14-day soft agar colony forming assay. In addition, luciferase reporter gene assay showed that the transcriptional activity of AP-1 and NF-κB in PC-3 and LNCaP prostate carcinoma cell lines was also modulated by the overexpression of EGR-1 in these cells using tandem repeated Luc-AP-1 and Luc-NF-κB. The activation of both NF-κB and AP-1 are key steps in the cascade of events following the activation of the EGR-1 gene. It was revealed that overexpression of EGR-1 selectively increased AP-1 and NF-κB activation, and that the activation of these nuclear factors appears to be essential for the induction of proliferation and anchorage independence in activated PC-3 and LNCaP cells. However, the mechanism underlying the modulation of AP-1 and NF-κB by the overexpression of EGR-1 is still unknown.
Eduardo Parra, Jorge Ferreira, Arnaldo Ortega

2212 related Products with: Overexpression of EGR-1 modulates the activity of NF-κB and AP-1 in prostate carcinoma PC-3 and LNCaP cell lines.

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#20466060   2010/05/11 To Up

Leptin upregulates VEGF in breast cancer via canonic and non-canonical signalling pathways and NFkappaB/HIF-1alpha activation.

High levels of VEGF and leptin are strongly linked to worse prognosis of breast cancer. Leptin signalling upregulates VEGF in human and mouse mammary tumor cells (MT), but the specific molecular mechanisms are largely unknown. Pharmacologic and genetic approaches were used to dissect the mechanism of leptin regulation of VEGF protein and mRNA in MT (4T1, EMT6 and MMT). A series of VEGF-promoter Luc-reporters (full-length and transcription factor-binding deletions) were transfected into MT to analyze leptin regulation of VEGF transcription. Deletion analysis of VEGF promoter and RNA knockdown shows that HIF-1alpha and NFkappaB are essentials for leptin regulation of VEGF. Leptin activation of HIF-1alpha was mainly linked to canonic (MAPK, PI-3K) and non-canonic (PKC, JNK and p38 MAP) signalling pathways. Leptin non-canonic signalling pathways (JNK, p38 MAP and to less extent PKC) were linked to NFkappaB activation. SP1 was involved in leptin regulation of VEGF in 4T1 cells. AP1 was not involved and AP2 repressed leptin-induced increase of VEGF. Overall, these data suggest that leptin signalling regulates VEGF mainly through HIF-1alpha and NFkappaB. These results delineate a comprehensive mechanism for leptin regulation of VEGF in MT. Disruption of leptin signalling could be used as a novel way to treat breast cancer.
Ruben R Gonzalez-Perez, Yanbo Xu, Shanchun Guo, Amber Watters, Weiqiang Zhou, Samuel J Leibovich

2743 related Products with: Leptin upregulates VEGF in breast cancer via canonic and non-canonical signalling pathways and NFkappaB/HIF-1alpha activation.



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#17994337   // To Up

Activation of human period-1 by PKA or CLOCK/BMAL1 is conferred by separate signal transduction pathways.

Circadian clocks are self-sustained biochemical oscillators that autonomously generate a near-24 h cycle in the absence of external signals. The process of synchronization to the environment involves the transcriptional activation of several genes. Photic input signals from the retina are transduced via the retinohypothalamic tract to the central pacemaker located in the suprachiasmatic nuclei (SCN) of the hypothalamus. It is known that cells of peripheral organs possess similar molecular organizations, but the signal transductional pathways lack direct light entrainment. It has been assumed that the adaptation of peripheral organs to the SCN phase is achieved by the alternate usage of promoter elements. This question has been addressed by characterizing the signal transductional pathways regulating human Period-1 gene expression in human hepatoma cells (HuH-7). Plasmids coding for key modulators of circadian rhythm, hCLOCK, hBMAL1, and hCRY2 were used to analyze the activation of a human period-1 promoter luciferase (hPER1-luc) construct. Beside classical CLOCK/BMAL1 activation, hPER1-luc was also inducible by the overexpression of the catalytic subunit of PKA (Calpha). The cotransfection of dominant negative constructs to c-FOS, CREB, PKA, and C/EBP were used to characterize both regulatory pathways. It was found that hCLOCK/hBMAL1-mediated hPER1 activation was influenced by AP1, but not significantly by other regulators. Conversely, PKA-induced activation of hPER1 was reduced by the inhibition of CREB and the CCAAT-box binding protein C/EBP, but not by AP1. The present findings imply that CLOCK/BMAL1-mediated activation of hPER1 by AP1 and E-Box elements is distinct from peripheral transcriptional modulation via cAMP-induced CREB and C/EBP.
Dirk Motzkus, Sabine Loumi, Christina Cadenas, Charles Vinson, Wolf-Georg Forssmann, Erik Maronde

1154 related Products with: Activation of human period-1 by PKA or CLOCK/BMAL1 is conferred by separate signal transduction pathways.

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#17988550   // To Up

[The effect of adenoviral E1A on inflammatory mediator expression of rat alveolar epithelial cells].

The relationship between latent adenvorius infection and airway inflammation has not been well documented. The aim of this study is to illustrate the roles of adenovirus E1A protein on the inflammation mediator expression in response to lipopolysaccharide and tumor necrosis factor alpha (TNF-alpha) in rat alveolar epithelial cells.
Juan Chen, Bing Li, Jian-dong Luo, Dan-dan Zhang, Pi-xin Ran

1183 related Products with: [The effect of adenoviral E1A on inflammatory mediator expression of rat alveolar epithelial cells].

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#17951536   // To Up

Expression and role of estrogen receptor alpha and beta in medullary thyroid carcinoma: different roles in cancer growth and apoptosis.

Medullary thyroid carcinoma (MTC) originates from parafollicular C cells. Estrogen receptor beta(ERbeta) expressionwas detected in normal parafollicular C cells and MTC tumor tissue, but ERalpha expression in MTC tumors still remains undetermined. The appearance and loss of ERalpha or ERbeta expression has been known to play a role in the development and progression of many human cancers. We performed immunohistochemical studies of ERalpha, ERbeta, and Ki67, a mitotic index, in 11 human MTC tissue samples. ERalpha was detected in 10 cases (91%), and ERbeta expression was observed in 8 cases (72.7%). A majority (8/10) of ERalpha-positive tumors showing ERbeta Ki67 expression was detected in three cases (27.3%). Neither clinical parameters nor tumor node metastasis (TNM) tumor staging was correlated with the positivity for ERs or Ki67. To investigate the biological role of each ER, we used ER-negative MTC TT cells and adenoviral vectors carrying ERalpha (Ad-ERalpha), ERbeta (Ad-ERbeta), estrogen response element (ERE)-Luc (Ad-ERE-Luc), and activator protein 1 (AP1)-Luc (Ad-AP1-Luc). Estrogen stimulated and anti-estrogen, ICI 182 780, suppressed ERE reporter activity in TT cells expressing ERalpha or ERbeta, suggesting that both ERs use the same classical ERE-mediated pathway. Ad-ERalpha infection stimulated TT cell growth; in contrast, Ad-ERbeta infection suppressed their growth. Apoptosis was detected in Ad-ERbeta-infected TT cells. Estrogen and anti-estrogen suppressed AP1 activity in Ad-ERalpha-infected cells, whereas upon Ad-ERbeta infection estrogen further stimulated AP1 activity which in turn is suppressed by anti-estrogen, suggesting that each ER acts differently through a non-ERE-mediated pathway. Our results suggest that ERalpha and ERbeta may play different roles in MTC tumor growth and progression.
Mi Ae Cho, Mi Kyung Lee, Kee-Hyun Nam, Woung Youn Chung, Cheong Soo Park, Ju Hyeong Lee, Taewoong Noh, Woo Ick Yang, Yumie Rhee, Sung-Kil Lim, Hyun Chul Lee, Eun Jig Lee

2042 related Products with: Expression and role of estrogen receptor alpha and beta in medullary thyroid carcinoma: different roles in cancer growth and apoptosis.

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