Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UNIPROT:P05412 (c-Jun)
11,453 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was carried out to investigate the chemopreventive potentials of plant originated glycoprotein (UDN glycoprotein, 116 kDa) isolated from the stems of Ulmus davidiana Nakai (UDN) on aberrant crypt foci (ACF) formation in 1,2-dimethylhydrazine (DMH)-treated ICR mice. UDN glycoprotein was administered to mice at 0.01% and 0.02% levels for 5 weeks. The mice were treated with 20 mg/kg DMH twice a week for 2 weeks in presence of UDN glycoprotein and killed at week 6. We found that UDN glycoprotein has inhibitory effects on the frequency of colonic aberrant crypt foci (ACF), activation of colonic proliferating cell nuclear antigen (PCNA), and release of plasma lactate dehydrogenase (LDH) in DMH-treated mice. In addition, UDN glycoprotein has anti-oxidative effects on the formation of plasma thiobarbituric acid reactive substances (TBARS) and the production of plasma inducible nitric oxide (NO) in DMH-treated mouse. Also, 0.02% UDN glycoprotein suppressed the DNA binding activities of nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1), accompanying the inhibitions of its subunits (p50, p65, c-Jun, and c-Fos), pro-inflammatory proteins [inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2)], and pro-inflammatory cytokines [tumor necrosis factor (TNF)-alpha and interleukin (IL)-6] on DMH-stimulated ACF formation. On the basis of these results, we assume that UDN glycoprotein may be useful for colon cancer prevention at initiation stage.
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PMID:Inhibitory effect of phytoglycoprotein on tumor necrosis factor-alpha and interleukin-6 at initiation stage of colon cancer in 1,2-dimethylhydrazine-treated ICR mice. 1786 52

alpha2-Heremans Schmid glycoprotein (AHSG), also designated fetuin-A, is an abundant plasma protein that is expressed in hepatocytes. AHSG/fetuin-A has diverse biological functions including regulation of calcium homeostasis and inhibition of insulin receptor tyrosine kinase activity. The aim of this study was to detect single nucleotide polymorphisms (SNPs) of the AHSG gene that can be involved in regulation of AHSG/fetuin-A expression. By a cycle sequencing method, two common SNPs in the promoter region of AHSG gene, -799A/T (rs2248690, dbSNP ID) and -425G/T (rs2077119), were identified. A reporter gene assay using HepG2 cells showed that the -799A allele had significantly higher promoter activity compared with the -799T allele. The overexpression of c-Fos/c-Jun significantly repressed transcriptional activity and a gel shift assay showed that the -799T DNA fragment had a greater affinity for transcription factor AP-1 than the -799A. In 40 unrelated healthy subjects, serum AHSG/fetuin-A levels increased with the following order of genotypes: -799TT<-799AT<-799AA (mean+/-S.E.M.; 222.1+/-11.0, 291.8+/-8.1, and 349.0+/-13.0 microg/ml, respectively, P<0.001). In conclusion, SNP rs2248690 in the promoter region of the AHSG gene affects the AHSG gene transcription, possibly by producing different association with AP-1.
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PMID:A promoter polymorphism of the alpha2-HS glycoprotein gene is associated with its transcriptional activity. 1788 58

This study was carried out to investigate the anti-inflammatory effects of 30-kDa glycoprotein isolated from Dioscorea batatas Decne (DBD glycoprotein), which consists of carbohydrate content (61%) and protein content (39%) on lipopolysaccharide (LPS, 2 microg/ml)-stimulated RAW 264.7 cells. We found that DBD glycoprotein (200 microg/ml) has an inhibitory effect on the production of intracellular hydrogen peroxide (H(2)O(2)), on the phosphorylation of p38 mitogen-activated protein (MAP) kinase, on the DNA binding activity of activator protein-1 (AP-1), and on c-Jun and c-Fos protein expression, respectively. In addition, DBD glycoprotein treatment markedly suppressed the interleukin (IL)-1beta, IL-6, and inducible nitric oxide synthase (iNOS) expression and the production of nitric oxide (NO) in LPS-stimulated RAW 264.7 cells. Interestingly, IL-1beta, IL-6, and iNOS expression was significantly attenuated by treatment with protein kinase C (PKC) inhibitor (staurosporine) as well as p38 MAP kinase inhibitor (SKF86002) in LPS-stimulated RAW 264.7 cells. On the basis of these results, we assume that DBD glycoprotein has anti-inflammatory potential, which can modulate proinflammatory signal transduction in LPS-stimulated RAW 264.7 cells.
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PMID:Phytoglycoprotein inhibits interleukin-1beta and interleukin-6 via p38 mitogen-activated protein kinase in lipopolysaccharide-stimulated RAW 264.7 cells. 1820 96

The purpose of this study was to investigate the inhibitory effect of 24-kDa glycoprotein isolated from Zanthoxylum piperitum DC fruit (ZPDC glycoprotein) on glucose/glucose oxidase (G/GO)- or hypoxanthine/xanthine oxidase (HX/XO)-induced cell proliferation in Chang liver cells. We found that ZPDC glycoprotein has significant scavenging effect on the production of intracellular H2O2 without cytotoxicity in G/GO- or HX/XO-treated in Chang liver cells. In the G/GO or HX/XO-stimulated protein kinases activity, ZPDC glycoprotein inhibited translocation of protein kinase C alpha (PKCalpha) to membrane and phosphorylation of extracellular signal-regulated kinase, p38 MAP kinase and c-Jun N-terminal kinase, respectively. In the G/GO or HX/XO-stimulated transcriptional activity, ZPDC glycoprotein also blocked the DNA binding activities of nuclear factor-kappa B and activator protein-1 and attenuated the activities of p50, p65, c-Jun and c-Fos, respectively. Finally, in the G/GO or HX/XO-stimulated cell proliferation, the activity of proliferating cell nuclear antigen was significantly blocked by treatment with ZPDC glycoprotein as well as protein kinase C inhibitor and mitogen-activated protein kinase inhibitors. On the basis of these results, we speculate that this glycoprotein is one of the natural antioxidants and of the modulators on abnormal activation of cell proliferation-related molecules in Chang liver cells.
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PMID:Phytoglycoprotein (24 kDa) inhibits expression of PCNA via PKCalpha and MAPKs in oxygen radical-stimulated Chang liver cells. 1850 55

The purpose of this study was to investigate the preventive effect of glycoprotein (SNL glycoprotein, 150 kDa) isolated from Solanum nigrum Linne fruits on dextran sulfate sodium (DSS, 3%)-induced colitis in A/J mice. To determine the physiological change by SNL glycoprotein, we first evaluated nitric oxide production, lactate dehydrogenase release and thiobarbituric acid reactive substances formation in the mice serum. After that, we tested the activity of inflammation-related signals such as transcriptional factor [nuclear factor-kappa B (NF-kappaB) and activator protein-1 (AP-1)], inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the mice colon tissues. Our results showed that SNL glycoprotein has a dose-dependent inhibitory effect on nitric oxide production, lactate dehydrogenase release, and thiobarbituric acid reactive substances formation. In the inflammation-related signal, our finding showed that SNL glycoprotein (20 mg kg(-1)) has a suppressive effect on activities of NF-kappaB (p50) and AP-1 (c-Jun), and regulates the expression of iNOS and COX-2 in the downstream of signal pathway. Taken together, the results in this study indicated that SNL glycoprotein has potential for prevention of colitis caused by DSS in A/J mice.
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PMID:Phytoglycoprotein (150 kDa) isolated from Solanum nigrum Linne has a preventive effect on dextran sodium sulfate-induced colitis in A/J mouse. 1898 4

RECK, a glycosylphosphatidylinositol-anchored glycoprotein, inhibits the enzymatic activities of some matrix metalloproteinases (MMP), thereby suppressing tumor cell metastasis; however, the detailed mechanism is still obscure. In this study, we compared the gene expression profiles between mock- and RECK-transfected HT1080 cells and showed that RECK decreases MMP-9 mRNA levels but not other MMP mRNA levels. Moreover, treatment with RECK-specific siRNA increased MMP-9 mRNA in RECK-expressing cells. The promoter assay showed that MMP-9 promoter activity was suppressed by RECK and that RECK-mediated suppression of MMP-9 promoter activity requires 12-O-tetradecanoylphorbol-13-acetate-responsive element (TRE) and kappaB sites. Moreover, the binding ability of Fra-1 and c-Jun to TRE within the MMP-9 promoter region was suppressed by RECK. Thus, these results show that RECK is a negative regulator of MMP-9 transcription.
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PMID:RECK negatively regulates matrix metalloproteinase-9 transcription. 1920 44

Interleukin-10 is the most important anti-inflammatory cytokine that controls the progress of the immune response. The molecular mechanisms driving the IL10 gene regulation are not well understood. To gain insight into this process we studied the IL-10 expression on mRNA and protein levels, together with c-Jun, FOXP3 and RelA transcription factors gene expression in human monocytes. We investigated also, the involvement of JNK and p38 transduction pathways in IL-10, c-Jun, FOXP3 and RelA gene expression. The quantity determination of IL-10 was performed by ELISA. qRT-PCR was performed for the detection of mRNA transcripts. The pharmacological inhibitors SP600125 and SB202190 were used to explore JNK and p38 MAPKs involvement in IL10, c-Jun, FOXP3 and RelA gene expression. The measurement of IL-10 mRNA synthesis, triggered by lipopolysaccharide (LPS) or C3 binding glycoprotein (C3bgp) showed that stimulation with both inducers led to similar high level of IL-10 mRNA synthesis, whereas C3bgp was the stronger inducer of IL-10 production than LPS. JNK and p38 inhibition significantly decreased IL-10 expression in stimulated cells. C3bgp and LPS induced comparatively low expression of FOXP3, RelA and c-Jun mRNA in monocytes. The inhibition of p38 MAPK in stimulated monocytes resulted in significant enhancement of c-Jun mRNA synthesis suggesting the functional relation between p38 MAPK and c-Jun gene expression. We concluded that the IL10 gene transcription did not associate with enhancement of c-Jun, RelA and FOXP3 gene expression and strictly depended on the JNK and p38 MAPKs activation in stimulated human monocytes.
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PMID:The inhibition of JNK and p38 MAPKs downregulates IL-10 and differentially affects c-Jun gene expression in human monocytes. 1923 39

For Kaposi's sarcoma-associated herpesvirus (KSHV; also called human herpesvirus 8 [HHV8]), the switch from latency to active lytic replication requires RTA, the product of open reading frame 50 (ORF50). RTA activates transcription from nearly 40 early and delayed-early viral promoters, mainly through interactions with cellular DNA binding proteins, such as CSL/RBP-Jkappa, Oct-1, C/EBPalpha, and c-Jun. Reliance on cellular coregulators may allow KSHV to adjust its lytic program to suit different cellular contexts or interpret signals from the outside. CSL is a key component of the Notch signaling pathway and is targeted by several viruses. A search with known CSL binding sequences from cellular genes found at least 260 matches in the KSHV genome, many from regions containing known or suspected lytic promoters. Analysis of clustered sites located immediately upstream of ORF70 (thymidylate synthase), ORF19 (tegument protein), and ORF47 (glycoprotein L) uncovered RTA-responsive promoters that were validated using mRNAs isolated from KSHV-infected cells undergoing lytic reactivation. Notably, ORF19 behaves as a true late gene, indicating that RTA regulates all three phases of the lytic program. For each new promoter, the response to RTA was dependent on CSL, and 5 of the 10 candidate sites were shown to bind CSL in vitro. Analysis of individual sites highlighted the importance of a cytosine residue flanking the core CSL binding sequence. These findings broaden the role for CSL in coordinating the KSHV lytic gene expression program and help to define a signature motif for functional CSL sites within the viral genome.
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PMID:Wide-scale use of Notch signaling factor CSL/RBP-Jkappa in RTA-mediated activation of Kaposi's sarcoma-associated herpesvirus lytic genes. 1990 14

Basal-like carcinomas and human epidermal growth factor receptor 2 (HER-2/neu) overexpression carcinomas are the subgroups of breast cancers that have the most aggressive clinical behavior. Phosphorylation/activation of c-Jun NH2-terminal kinase is characterized as a stress-activated protein kinase, which regulates apoptosis after cellular stress. The aim of this study was to evaluate the association of phosphorylated c-Jun NH2-terminal kinase expression with phenotypes and clinicopathologic parameters of breast cancer. Phosphorylated c-Jun NH2-terminal kinase was immunohistochemically measured in a cohort of 160 patients with invasive breast cancer treated with therapeutic surgery followed by anthracycline or docetaxel-based chemotherapy. These results were further correlated with the phenotypes and clinicopathologic characteristics of breast cancers. Increased phosphorylated c-Jun NH2-terminal kinase expression was significantly associated with lack of estrogen receptor expression (P < .0001), positivity for cytokeratins 5/6 (P = .029), epidermal growth factor receptor (P = .035), basal-like phenotype (P = .015), and "triple-negative" phenotype (P = .01). Furthermore, the positive expression of phosphorylated c-Jun NH2-terminal kinase was positively correlated with p-glycoprotein (r = 0.54, P < .0001) and multidrug resistance-associated protein 1(r = 0.38, P < .0001) but not with lung resistance protein (r = -0.02, P = .78). Our results indicate that the activation of phosphorylated c-Jun NH2-terminal kinase may play a role in the carcinogenesis of basal-like and triple-negative breast carcinoma.
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PMID:Elevated expression of phosphorylated c-Jun NH2-terminal kinase in basal-like and "triple-negative" breast cancers. 1991 78

Bone sialoprotein (BSP) is a major non-collagenous, extracellular matrix glycoprotein associated with mineralized tissues. Fibroblast growth factor 2 (FGF2) is recognized as a potent mitogen for a variety of mesenchymal cells. FGF2 produced by osteoblasts accumulates in the bone matrix and acts as an autocrine/paracrine regulator of osteoblasts. We previously reported that FGF2 regulates BSP gene transcription through the FGF2 response element (FRE) and activator protein 1 (AP1) binding site overlapping with the glucocorticoid response element in the rat BSP gene promoter. In the present study, FGF2 (10 ng/ml) increased BSP and Runx2 mRNA levels at 6 h in MCF7 human breast cancer cells. Transient transfection analyses were performed using chimeric constructs of the human BSP gene promoter linked to a luciferase reporter gene. Treatment of MCF7 cells with FGF2 (10 ng/ml) increased the luciferase activity of the constructs between -84LUC and -927LUC. Gel mobility shift analyses showed that FGF2 increased the binding of AP1 and CRE2. The CRE2- and AP1-protein complexes were disrupted by antibodies against CREB1, c-Fos, c-Jun, Fra2, p300 and Runx2. These studies demonstrate that FGF2 stimulates BSP transcription in MCF7 human breast cancer cells by targeting the AP1 and CRE2 elements in the human BSP gene promoter.
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PMID:Fibroblast growth factor 2 regulates bone sialoprotein gene transcription in human breast cancer cells. 2033 43


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