Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Activation of expression of genes encoding transcription factors: c-fos and c-jun and formation of AP1 transcriptional complex in human monocytes was investigated. It was found that lipopolysaccharide induced strongly both c-fos and c-jun expression as well as AP1 formation. Interferon gamma activated strongly c-fos and weakly c-jun and AP1. Tumor necrosis factor induced slightly c-fos and had almost no effect on c-jun and AP1. The data suggest that differences in functional responses elicited in monocytes by all three factors may be dependent on different routes on nuclear signalling employed by the factors.
 ...
PMID:Transcription factor activation and functional stimulation of human monocytes. 131 39

Observations that primary rat astrocytes express high-affinity binding sites for endothelins and, in addition, are capable of producing not only endothelin-3 but also endothelin-1 prompted the investigation of a possible relation between endothelin peptides and receptors in these cells. Sarafotoxin S6b, an endothelin receptor agonist, was used as a tool to study endothelin receptor-mediated changes in the secretion of endothelin-1 and -3. The effects of sarafotoxin S6b and endothelin-1 in stimulating inositolphospholipid turnover as well as in inducing AP1 in primary astrocyte cultures were found to be similar. A low cross-reactivity of sarafotoxin S6b with endothelin-1 and -3 in the endothelin radioimmunoassays used here, along with a distinctly different elution position in high-performance liquid chromatography, allowed a clear discrimination between sarafotoxin and endothelins in the culture media. Stimulation of primary rat astrocytes with 10(-7) M sarafotoxin S6b for 1 hour resulted in a substantial increase in endothelin-1 immunoreactivity in the medium. This immunoreactivity reached a peak at 3 hours and showed no further increase after 8 and 24 hours. Treatment of our cultures with phorbol myristate acetate, lipopolysaccharide, tumor necrosis factor alpha, and norepinephrine for 24 hours led to only a moderate elevation of endothelin-1 immunoreactivity. Immunoreactive endothelin-3 was not affected by any of the treatments tested. Thus, our data suggest that endothelins in primary rat astrocytes are subject to selective autoregulation, as demonstrated by the potentiation of endothelin-1 secretion after activation of glial endothelin receptors.
 ...
PMID:Selective autoregulation of endothelins in primary astrocyte cultures: endothelin receptor-mediated potentiation of endothelin-1 secretion. 164 83

The high-molecular-weight material released into the medium by Escherichia coli AP1, an enterotoxigenic strain of porcine origin, has been isolated and resolved into two clearly distinct fractions, based on sucrose density gradient and differential centrifugation, chemical analysis, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and freeze-fracture electron microscopy. These two fractions, referred to as "medium vesicles" and "medium lipopolysaccharides", were compared with the cellular outer and cytoplasmic membranes, the periplasmic fraction, and the cytoplasmic fraction. The medium vesicles closely resembled outer membrane and accounted for 3 to 5% of the total cellular outer membrane. They contained most of the heat-labile enterotoxin (LT) activity released into the medium by E. coli AP1. The medium lipopolysaccharide consisted mostly of lipopolysaccharide and a small amount of outer membrane and contained relatively little LT activity. Based on experiments with E. coli K-12 strains, in which about 5% of the newly synthesized outer membrane is lost from areas of outer membrane synthesis, it is proposed that enterotoxigenic E. coli strains release LT as part of such newly synthesized outer membrane fragments and that released outer membrane fragments may function as physiologically significant LT carriers.
 ...
PMID:Some characteristics of the outer membrane material released by growing enterotoxigenic Escherichia coli. 701 82

Expression of the kappa immunoglobulin light chain gene requires developmental- and tissue-specific regulation by trans-acting factors which interact with two distinct enhancer elements. A new protein-DNA interaction has been identified upstream of the intron enhancer, within the matrix-associated region of the J-C intron. The binding activity is greatly inducible in pre-B cells by bacterial lipopolysaccharide and interleukin-1 but specific complexes are found at all stages of B cell development tested. The footprinted binding site is homologous to the consensus AP1 motif. The protein components of this complex are specifically competed by an AP1 consensus motif and were shown by supershift to include c-Jun and c-Fos, suggesting that this binding site is an AP1 motif and that the Jun and Fos families of transcription factors play a role in the regulation of the kappa light chain gene. Mutation of the AP1 motif in the context of the intron enhancer was shown to decrease enhancer-mediated activation of the promoter in both pre-B cells induced with LPS and constitutive expression in mature B cells.
 ...
PMID:An AP1 binding site upstream of the kappa immunoglobulin intron enhancer binds inducible factors and contributes to expression. 781 34

The murine macrophage inflammatory protein 1 beta mRNA (MIP-1 beta) is rapidly and transiently induced in macrophages by lipopolysaccharide (LPS), serum or cycloheximide. Functional studies of the MIP-1 beta proximal promoter indicate that it is cell-specific, and serum- and LPS-responsive in macrophages. A 76-bp proximal promoter sequence (-51 to -127 bp) confers cell-specific and LPS-inducible activity when placed upstream from a heterologous promoter in both orientations. One essential cis-regulatory element within the enhancer-like sequence is an activating transcription factor/cAMP response element (CRE)-binding protein (ATF/CREB)-binding site, although the promoter is not cAMP responsive. Electrophoretic mobility shift assays and mutational analyses suggest that the promoter site is bound by nuclear protein complexes containing cAMP-independent members of the ATF/CREB family of proteins and c-Jun, and are functionally distinct from the AP1-related TPA-response element (TRE) binding activity.
 ...
PMID:An ATF/CREB-binding site is essential for cell-specific and inducible transcription of the murine MIP-1 beta cytokine gene. 783 96

When transfected into mouse splenic B cells stimulated with lipopolysaccharide (LPS) the expression of DNA vectors containing the chloramphenicol acetyl transferase gene under the control of a SP6 kappa promoter and the Ig heavy chain intron enhancer could be down-regulated 5- to 10-fold by treatment of the cells with anti-Ig prior to transfection. Exchanging the SP6 kappa promoter by minimal promoters consisting of an octamer or a SP1 motif linked to TATA box did not impair the anti-Ig induced down-regulation while inserting a rabbit beta-globin promoter did. The transcriptional regulation could be observed after replacing the Ig heavy chain intron enhancer with a SV40 enhancer, or duplicated minimal Ig heavy chain enhancers containing or lacking the octamer element. The down-regulation was not dependent on the level of transcriptional stimulation observed. A difference in Oct2 expression could neither be detected at the RNA nor protein level after treatment of LPS stimulated B cells with anti-Ig or phorbol-dibutyrate. Anti-Ig treatment, but not phorbol-di-butyrate treatment, induced increased levels of AP1 and NF kappa B transcription factors. Thus, either differentiation specific transcriptional control of Ig genes is exerted via transcription factors common to several distinct enhancers or via transcriptional adaptor molecules that can interact with several distinct DNA binding proteins.
 ...
PMID:Transcriptional regulation of immunoglobulin gene expression by anti-Ig. 814 26

Tissue factor, the cellular receptor for factor VII/VIIa, activates both the intrinsic and extrinsic pathways of blood coagulation. In this analysis we have used DNase I footprinting to map the sites of protein-DNA interaction along the promoter (-383 to +8) using nuclear extracts prepared from uninduced and lipopolysaccharide-induced THP-1 cells. We have identified six regions that interact with nuclear factors in both uninduced and induced extracts. Four footprints are contained within a region reported to confer base-line high level expression and lipopolysaccharide and serum induction. Two additional footprints map to a region reported to reduce basal transcription by 50%. The only qualitative change in the footprint pattern with uninduced and induced extracts is the appearance of two hypersensitive sites with uninduced extracts. In addition, changes in the level of protein- DNA binding are detected with only one probe by DNA mobility shift analysis. A combination of well characterized transcription factors (AP1), primarily lymphoid cell specific regulatory proteins (NF-kappa B- and/or Ets-1-related proteins), as well as additional, uncharacterized proteins appear to interact with these sequences. Our data suggest that post-translational modification of existing transcription factors, and not induction of new DNA-binding activity, mediates the lipopolysaccharide induction of tissue factor synthesis in THP-1 cells.
 ...
PMID:Lipopolysaccharide induction of tissue factor expression in THP-1 monocytic cells. Protein-DNA interactions with the promoter. 828 2

The molecular mechanisms regulating human immunodeficiency virus (HIV) persistence in a major cell reservoir such as the macrophage remain unknown. NF-kappa B is a transcription factor involved in the regulation of the HIV long terminal repeat and is selectively activated following HIV infection of human macrophages. Although little information as to what signal transduction pathways mediate NF-kappa B activation in monocytes-macrophages is available, our previous work indicated that classical protein kinase C (PKC) isoenzymes were not involved in the HIV-mediated NF-kappa B activation. In this study, we have focused on atypical PKC isoenzymes. PKC-zeta belongs to this family and is known to be an important step in NF-kappa B activation in other cell systems. Immunoblotting experiments with U937 cells demonstrate that PKC-zeta is present in these cells, and its expression can be downmodulated by antisense oligonucleotides (AO). The HIV-mediated NF-kappa B activation is selectively reduced by AO to PKC-zeta. In addition, cotransfection of a negative dominant molecule of PKC-zeta (PKC-zeta mut) with NF-kappa B-dependent reporter genes selectively inhibits the HIV- but not phorbol myristate acetate- or lipopolysaccharide-mediated activation of NF-kappa B. That PKC-zeta is specific in regulating NF-kappa B is concluded from the inability of PKC-zeta(mut) to interfere with the basal or phorbol myristate acetate-inducible CREB- or AP1-dependent transcriptional activity. Lastly, we demonstrate a selective inhibition of p24 production by HIV-infected human macrophages when treated with AO to PKC-zeta. Altogether, these results suggest that atypical PKC isoenzymes, including PKC-zeta, participate in the signal transduction pathways by which HIV infection results in the activation of NF-kappa B in human monocytic cells and macrophages.
 ...
PMID:Protein kinase C-zeta mediates NF-kappa B activation in human immunodeficiency virus-infected monocytes. 852 29

The CD11c/CD18 integrin binds lipopolysaccharide, fibrinogen, and heparin, and mediates leukocyte adhesion, spreading, and migration. CD11c/CD18 is primarily found on myeloid cells and its expression is regulated during myeloid differentiation by transcriptional mechanisms acting on the CD11c gene promoter. We now describe that CCAAT/enhancer-binding proteins (C/EBP) contribute to the basal, tissue-specific and developmentally regulated activity of the CD11c promoter. A C/EBP-binding site within the CD11c promoter (CEBP-80) is bound by CEBPalpha in undifferentiated U937 cells and by C/EBPalpha- and C/EBPbeta-containing dimers in phorbol 12-myristate 13-acetate-differentiating cells, and its disruption decreased the CD11c promoter activity in a cell type-dependent manner. C/EBPalpha transactivated the CD11c promoter through the CEBP-80 element, and C/EBPalpha transactivation was also dependent on the Sp1-70- and Sp1-120 Sp1-binding sites. The -90/-50 fragment from the CD11c promoter, containing the adjacent CEBP-80, Sp1-70, and AP1-60 sites, differentially enhanced the activity of the minimal prolactin promoter in hematopoietic and epithelial cells. Altogether, these results demonstrate that C/EBP factors participate in the tissue-restricted and regulated expression of the CD11c/CD18 integrin through functional interactions with Sp1, suggest that Sp1-related factors modulate C/EBPalpha transcriptional activity on the CD11c promoter, and demonstrate the existence of a composite regulatory element recognized by C/EBP, Sp1, and AP-1 factors and whose enhancing effects are cell-type dependent.
 ...
PMID:CCAAT-enhancer-binding proteins (C/EBP) regulate the tissue specific activity of the CD11c integrin gene promoter through functional interactions with Sp1 proteins. 936 Sep 88

P-selectin, an adhesion receptor for leukocytes, is constitutively expressed in megakaryocytes and endothelial cells. Tumor necrosis factor-alpha (TNF-alpha) or lipopolysaccharide (LPS) increases synthesis of P-selectin in murine but not in human endothelial cells. To identify potential species-specific and conserved mechanisms for regulation of expression of P-selectin, we cloned the 5'-flanking region of the murine P-selectin gene and compared its features with those previously reported for the human gene. The murine and human genes shared conserved Stat-like, Hox, Ets, GATA, and GT-IIC elements. In the murine gene, a conserved GATA element bound to GATA-2 and functioned as a positive regulatory element, whereas a conserved Ets element bound to GA-binding protein and functioned as a negative regulatory element. Significantly, the murine P-selectin gene had several features not found in the human gene. These included an insertion from -987 to -649 that contained tandem GATA and tandem AP1-like sequences, which resembled enhancers in beta-globin locus control regions. Both tandem elements bound specifically to nuclear proteins. The murine gene lacked the unique kappaB site specific for p50 or p52 homodimers found in the human gene. Instead, it contained two tandem kappaB elements and a variant activating transcription factor/cAMP response element site, which closely resembled sites in the E-selectin gene that are required for TNF-alpha- or LPS-inducible expression. TNF-alpha or LPS augmented expression of a reporter gene driven by the murine, but not the human, P-selectin promoter in transfected endothelial cells. Deletional analysis of the murine 5'-flanking region revealed several sequences that were required for either constitutive or inducible expression. These data suggest that both species-specific and conserved mechanisms regulate transcription of the human and murine P-selectin genes.
 ...
PMID:Comparison of promoters for the murine and human P-selectin genes suggests species-specific and conserved mechanisms for transcriptional regulation in endothelial cells. 954 53


1 2 3 Next >>