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Berlin Brandenburg

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  • Signal Transduction
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  • 1
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 22 February 2011, Vol.108(8), pp.3436-41
    Description: In living organisms sugars not only provide energy and carbon skeletons but also act as evolutionarily conserved signaling molecules. The three major soluble sugars in plants are sucrose, glucose, and fructose. Information on plant glucose and sucrose signaling is available, but to date no fructose-specific signaling pathway has been reported. In this study, sugar repression of seedling development was used to study fructose sensitivity in the Landsberg erecta (Ler)/Cape Verde Islands (Cvi) recombinant inbred line population, and eight fructose-sensing quantitative trait loci (QTLs) (FSQ1-8) were mapped. Among them, FSQ6 was confirmed to be a fructose-specific QTL by analyzing near-isogenic lines in which Cvi genomic fragments were introgressed in the Ler background. These results indicate the existence of a fructose-specific signaling pathway in Arabidopsis. Further analysis demonstrated that the FSQ6-associated fructose-signaling pathway functions independently of the hexokinase1 (HXK1) glucose sensor. Remarkably, fructose-specific FSQ6 downstream signaling interacts with abscisic acid (ABA)- and ethylene-signaling pathways, similar to HXK1-dependent glucose signaling. The Cvi allele of FSQ6 acts as a suppressor of fructose signaling. The FSQ6 gene was identified using map-based cloning approach, and FSQ6 was shown to encode the transcription factor gene Arabidopsis NAC (petunia No apical meristem and Arabidopsis transcription activation factor 1, 2 and Cup-shaped cotyledon 2) domain containing protein 89 (ANAC089). The Cvi allele of FSQ6/ANAC089 is a gain-of-function allele caused by a premature stop in the third exon of the gene. The truncated Cvi FSQ6/ANAC089 protein lacks a membrane association domain that is present in ANAC089 proteins from other Arabidopsis accessions. As a result, Cvi FSQ6/ANAC089 is constitutively active as a transcription factor in the nucleus.
    Keywords: Signal Transduction ; Arabidopsis -- Metabolism ; Arabidopsis Proteins -- Physiology ; Fructose -- Metabolism ; Transcription Factors -- Physiology
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 2
    Language: English
    In: Connective Tissue Research, 02 January 2015, Vol.56(1), pp.9-17
    Description: Purpose of the study: Gluteal muscle contracture (GMC) is a chronic fibrotic disease of gluteal muscles which is characterized by excessive deposition of collagen in the extracellular matrix. Transforming growth factor (TGF)-βs have been shown to play an important role in the progression of...
    Keywords: Gluteal Muscle Contracture ; Pai-1 ; Smad2/3 ; Smad7 ; Tgf-Β/Smad Pathway ; Biology ; Anatomy & Physiology
    ISSN: 0300-8207
    E-ISSN: 1607-8438
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  • 3
    Language: English
    In: Virology Journal, 01 September 2012, Vol.9(1), p.202
    Description: Abstract Background Bovine herpesvirus type 1 (BHV-1) is an important pathogen in cattle that is responsible for substantial economic losses. Previous studies suggest that BHV-1 may induce apoptosis in Madin-Darby bovine kidney (MDBK) cells via a mechanism only involving caspases and p53. However,...
    Keywords: Bhv-1 ; Mdbk Cells ; Apoptosis ; Caspase Cascades ; Fas ; Mitochondria ; Medicine ; Biology
    ISSN: 1743-422X
    E-ISSN: 1743-422X
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  • 4
    Language: English
    In: International journal of molecular medicine, January 2019, Vol.43(1), pp.127-142
    Description: Accumulating evidence has suggested that circular RNAs (circRNAs), a novel class of non‑coding RNAs, have crucial roles in tumor progression. However, the significance of circRNAs in hypopharyngeal cancer (HCa) remains to be investigated. The present study has identified aberrantly expressed circRNAs by performing circRNA sequencing analyses of three pairs of tumor and adjacent normal samples from patients with HCa. The results demonstrated that 173 circRNAs were differentially expressed (DE), including 71 upregulated and 102 downregulated circRNAs (FDR〈0.05 and fold changes of ≥2 or ≤0.5 by Mann‑Whitney U test followed by Benjamini‑Hochberg correction for multiple testing). Pathway analyses of the genes producing DE circRNAs revealed that many of them were involved in cancer‑related pathways. To further illustrate the roles of circRNAs in HCa progression, a competing endogenous RNA (ceRNAs) network was constructed, consisting of circRNAs, miRNA, and miRNA targeted genes. The results demonstrated that multiple cancer‑related pathways were affected by performing enrichment analyses of the targeted genes. Of note, a ceRNA subnetwork was isolated, consisting of two circRNAs (hsa_circ_0008287 and hsa_circ_0005027) and one miRNA (hsa‑miR‑548c‑3p), which significantly affect both ErbB and Hippo signaling pathways. In conclusion, the present study identified a set of circRNAs that are potentially implicated in the tumorigenesis of HCa and may serve as potential biomarkers for the diagnosis of HCa.
    Keywords: Rna -- Research ; Cellular Signal Transduction -- Research ; Pharyngeal Cancer -- Development And Progression ; Pharyngeal Cancer -- Research ; Pharyngeal Cancer -- Genetic Aspects;
    ISSN: 11073756
    E-ISSN: 1791-244X
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  • 5
    Language: English
    In: Free radical biology & medicine, 15 April 2006, Vol.40(8), pp.1281-92
    Description: gamma-Glutamyl transpeptidase (GGT) plays key roles in glutathione homeostasis and metabolism of glutathione S-conjugates. Rat GGT is transcribed via five tandemly arranged promoters into seven transcripts. The transcription of mRNA V is controlled by promoter 5. Previously we found that GGT mRNA V-2 was responsible for the induction of GGT in rat alveolar epithelial cells by 4-hydroxynonenal (HNE). In the current study, the underlying mechanism was investigated. Reporter deletion and mutation analysis demonstrated that an electrophile-response element (EpRE) in the proximal region of GGT promoter 5 (GP5) was responsible for the basal- and HNE-induced promoter activity. Gel-shift assays showed an increased binding activity of GP5 EpRE after HNE exposure. The nuclear content of NF-E2-related factor 2 (Nrf2) was significantly increased by HNE. The recruitment of Nrf2 to GP5 EpRE after HNE treatment was demonstrated by supershift and chromatin immunoprecipitation assays. The tissue expression pattern of GGT mRNA V was previously unknown. Using polymerase chain reaction, we found that GGT mRNA V-2 was expressed in many tissues in rat. Taken together, GGT mRNA V-2 is widely expressed in rat tissues and its basal and HNE-induced expression is mediated through EpRE/Nrf2 signaling.
    Keywords: Aldehydes -- Pharmacology ; Epithelial Cells -- Drug Effects ; Nf-E2-Related Factor 2 -- Metabolism ; Signal Transduction -- Drug Effects ; Gamma-Glutamyltransferase -- Metabolism
    ISSN: 0891-5849
    E-ISSN: 18734596
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  • 6
    Language: English
    In: Molecular Medicine Reports, 12/2015, Vol.12(6), pp.8282-8288
    Description: Cardiomyocyte hypertrophy is a threat to human health due to the probability of sudden heart failure-induced mortality. Previous studies have demonstrated that nuclear factor of activated T cells cytoplasmic 3 (NFATC3) is important in the process of cardiomyocyte hypertrophy. However, the molecular mechanism underlying the alteration in the expression levels of NFATC3 during cardiomyocyte hypertrophy has remained to be fully elucidated. In order to shed light on the molecular mechanism, the present study employed several approaches, including the measurement of the cell surface area, analysis of the protein/DNA ratio, western blot analysis and a Luciferase reporter assay using isolated rat cardiomyocytes as model. The results showed that expression of microRNA-1 ( miR-1 ) was reduced in patients diagnosed with cardiac hypertrophy and rat cardiomyocytes treated with pro-hypertrophic stimuli. The increase in the expression of miR-1 was able to inhibit the hypertrophic remodeling of cardiomyocytes. The suppression of miR-1 was sufficient to induce cardiomyocyte hypertrophy, and further experiments confirmed that NFATC3 was a target of miR-1 in cardiomyocytes. Forced expression of NFATC3 inhibited the protective activity of miR-1 against hypertrophic stimuli in the cardiomyocytes. These findings provided clarification of the regulatory signaling pathway underlying cardiac hypertrophy, and provided evidence that targeting the miR-1 /NFATC3 pathway may be a promising strategy for the prevention and treatment of heart hypertrophy.
    Keywords: Microrna-1 ; Nuclear Factor Of Activated T Cells Cytoplasmic 3 ; Cardiomyocyte ; Hypertrophy
    ISSN: 1791-2997
    E-ISSN: 1791-3004
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  • 7
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 06 November 2018, Vol.115(45), pp.E10682-E10691
    Description: Immune thrombocytopenia (ITP) is an autoimmune disorder characterized by low platelet count which can cause fatal hemorrhage. ITP patients with antiplatelet glycoprotein (GP) Ib-IX autoantibodies appear refractory to conventional treatments, and the mechanism remains elusive. Here we show that the platelets undergo apoptosis in ITP patients with anti-GPIbα autoantibodies. Consistent with these findings, the anti-GPIbα monoclonal antibodies AN51 and SZ2 induce platelet apoptosis in vitro. We demonstrate that anti-GPIbα antibody binding activates Akt, which elicits platelet apoptosis through activation of phosphodiesterase (PDE3A) and PDE3A-mediated PKA inhibition. Genetic ablation or chemical inhibition of Akt or blocking of Akt signaling abolishes anti-GPIbα antibody-induced platelet apoptosis. We further demonstrate that the antibody-bound platelets are removed in vivo through an apoptosis-dependent manner. Phosphatidylserine (PS) exposure on apoptotic platelets results in phagocytosis of platelets by macrophages in the liver. Notably, inhibition or genetic ablation of Akt or Akt-regulated apoptotic signaling or blockage of PS exposure protects the platelets from clearance. Therefore, our findings reveal pathogenic mechanisms of ITP with anti-GPIbα autoantibodies and, more importantly, suggest therapeutic strategies for thrombocytopenia caused by autoantibodies or other pathogenic factors.
    Keywords: Akt ; Apoptosis ; Immune Thrombocytopenia ; Phosphatidylserine Exposure ; Platelet ; Apoptosis ; Blood Platelets -- Cytology ; Proto-Oncogene Proteins C-Akt -- Metabolism ; Purpura, Thrombocytopenic, Idiopathic -- Pathology
    ISSN: 00278424
    E-ISSN: 1091-6490
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  • 8
    Language: English
    In: Life Sciences, 22 May 2012, Vol.90(19-20), pp.721-727
    Description: In the present study, we explored the hypothesis that initiation of PH involves the upregulation of monocyte chemoattractant protein-1 (MCP-1) in acute PTE. We evaluated the effects of resveratrol and the role of p38 mitogen-activated protein kinase (MAPK) in this process. A rat model of acute PTE was established by infusion of an autologous blood clot into the pulmonary artery through a polyethylene catheter. Rats were randomly divided into 1, 4, and 8 hour time groups. Resveratrol, C1142 (a rodent chimeric mAb that neutralizes rat MCP-1) or SB203580 (a p38MAPK specific inhibitor) was administered to the animals beginning 1 h prior to the start of the acute PTE protocol. At each time point, the mean pulmonary artery pressure (mPAP), mRNA and protein expressions of MCP-1 were measured. The phosphorylation of p38 MAPK (p-pMAPK) was also detected. Acute PTE elicited significant increases in mean pulmonary artery pressure (mPAP), and up-regulated the expression of monocyte chemoattractant protein-1 (MCP-1) and phosphorylation of p38 mitogen-activated protein kinase (p-p38 MAPK). Administration of C1142 markedly reduced mPAP. Furthermore, pre-treatment of rats with resveratrol significantly reduced mPAP and down-regulated the expression of MCP-1, which was associated with robustly suppressed acute PTE-induced p-p38MAPK expression. These findings suggested that MCP-1 was involved in the formation of acute PTE-induced PH, and resveratrol down-regulated the expression of MCP-1 by inhibiting acute PTE-induced p-p38MAPK activation, which contributed to the decrease in PH.
    Keywords: Resveratrol ; Acute Pulmonary Thromboembolism ; Pulmonary Artery Hypertension ; Monocyte Chemoattractant Protein-1 ; Phosphorylated P38 Mitogen-Activated Protein Kinase ; Sciences (General) ; Biology
    ISSN: 0024-3205
    E-ISSN: 1879-0631
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  • 9
    Language: English
    In: The Biochemical journal, 01 November 2014, Vol.463(3), pp.383-92
    Description: p27Kip1 is a potent inhibitor of cyclin-dependent kinases that drive G1-to-S cell-cycle transition. Reduced p27Kip1 expression is prevalent in a wide range of human tumours; however, the exact mechanism(s) of p27Kip1-mediated tumour suppression remains obscure. In the present study, we identified a close inverse relationship between p27Kip1 and EGFR (epidermal growth factor receptor) expression: the parental T24 human bladder cancer cells had high p27Kip1 expression but low EGFR expression and, in striking contrast, the metastatic derivative of T24 (T24T) had low p27Kip1 expression but high EGFR expression. This relationship was also found in various human cancer tissues, and was not only just correlative but also causal; depletion of p27Kip1 in MEF (mouse embryonic fibroblast) cells resulted in markedly elevated EGFR expression, a result reproducible with an Egfr promoter-luciferase reporter in both T24 and MEF cells, suggesting transcriptional repression of EGFR by p27Kip1. Indeed, p27Kip1 was found to regulate EGFR expression via the JNK (c-Jun N-terminal kinase)/c-Jun transcription factor: p27Kip1 deficiency activated JNK/c-Jun, whereas inhibition of JNK/c-Jun by dominant-negative mutants dramatically repressed Egfr transcription. Furthermore, the proximal promoter of the Egfr gene was crucial for its transcription, where the recruiting activity of c-Jun was much greater in p27Kip1-/- cells than in p27Kip1+/+ cells. Introduction of GFP-p27Kip1 into T24T cells suppressed JNK/c-Jun activation, EGFR expression and anchorage-independent growth. The results of the present study demonstrate that p27Kip1 suppresses JNK/c-Jun activation and EGFR expression in MEFs and human bladder cancer cells, and the results obtained are consistent with those from human cancer specimens. The present study provides new insights into p27Kip1 suppression of cancer cell growth, migration and metastasis.
    Keywords: Cyclin-Dependent Kinase Inhibitor P27 -- Metabolism ; Erbb Receptors -- Metabolism ; Jnk Mitogen-Activated Protein Kinases -- Metabolism ; Proto-Oncogene Proteins C-Jun -- Metabolism ; Urinary Bladder Neoplasms -- Metabolism
    ISSN: 02646021
    E-ISSN: 1470-8728
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  • 10
    Language: English
    In: Molecular and Cellular Biochemistry, 2014, Vol.389(1), pp.25-33
    Description: NF-kappaB pathway has been proven to be critical to survival of lung cancer cells, and many natural products from plants were shown to inhibit the activation of this pathway. In this study, we investigated the effects of two cardamonin analogs, 4,4′-dihydroxylchalcone (DHC) and 4,4′-dihydroxy-2′-methoxychalcone (DHMC), on survival of lung cancer cells and the involved mechanisms. MTT assay revealed that the two compounds potently decreased the survival of immortalized and primary lung cancer cells. DHC and DHMC were able to induce apoptosis in A549 and NCI-H460 cells. Immunoblotting, immunofluorescent staining, and luciferase reporter further demonstrated that the two compounds suppressed the activation of NF-kappaB pathway in lung cancer cells. PMA-mediated NF-kappaB reactivation abrogated the effect of DHC and DHMC on lung cancer cells. DHC and DHMC were also shown to suppress the growth of A549 xenograft in mice. Collectively, we verified two cardamonin analogs as novel compounds suppressing NF-kappaB signaling for lung cancer therapy.
    Keywords: Cardamonin ; Lung cancer ; NF-kappaB ; Natural product
    ISSN: 0300-8177
    E-ISSN: 1573-4919
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