Relevant bibliographies by topics / Sp1

Academic literature on the topic 'Sp1'

Author: Grafiati
Published: 4 June 2021
Last updated: 22 February 2023

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Journal articles on the topic "Sp1"

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Dąbrowska, Katarzyna, and Magdalena Zielińska. "Silencing of Transcription Factor Sp1 Promotes SN1 Transporter Regulation by Ammonia in Mouse Cortical Astrocytes." International Journal of Molecular Sciences 20, no. 2 (January 9, 2019): 234. http://dx.doi.org/10.3390/ijms20020234.

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The involvement of the astrocytic SN1 (SNAT3) transporter in ammonia-induced l-glutamine retention was recently documented in mouse-cultured astrocytes. Here we investigated the involvement of specificity protein 1 (Sp1) transcription factor in SN1 regulation in ammonium chloride (“ammonia”)-treated astrocytes. Sp1 expression and its cellular localization were determined using real-time qPCR, Western blot, and confocal microscopy. Sp1 binding to Snat3 promoter was analyzed by chromatin immunoprecipitation. The role of Sp1 in SN1 expression and SN1-mediated [3H]glutamine uptake in ammonia-treated astrocytes was verified using siRNA and mithramycin A. The involvement of protein kinase C (PKC) isoforms in Sp1 level/phosphorylation status was verified using siRNA technology. Sp1 translocation to the nuclei and its enhanced binding to the Snat3 promoter, along with Sp1 dependence of system N-mediated [3H]glutamine uptake, were observed in astrocytes upon ammonia exposure. Ammonia decreased the level of phosphorylated Sp1, and the effect was reinforced by long-term incubation with PKC modulator, phorbol 12-myristate 13-acetate, which is a treatment likely to dephosphorylate Sp1. Furthermore, silencing of the PKCδ isoform appears to enhance the ammonia effect on the Sp1 level. Collectively, the results demonstrate the regulatory role of Sp1 in regulation of SN1 expression and activity in ammonia-treated astrocytes and implicate altered Sp1 phosphorylation status in this capacity.
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Budiarti, Lia Yulia, Isnaini Isnaini, Puteri Dayana, Norma Sari, and Nur Almira R. S. "Antimicrobial Activity of Stenochlaena palustris and Sauropus androgynus in Staphylococcus aureus, Escherichia coli and Candidia albicans." Bioinformatics and Biomedical Research Journal 4, no. 1 (November 29, 2021): 32–38. http://dx.doi.org/10.11594/bbrj.04.01.05.

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Stenochlaena palustris and Sauropus androgynus are known to contains antimicrobial substances such as flavonoids, saponins and tannins compounds.The purpose of this study was to analyzes the antimicrobial activity of young and old leaf infusions of S. palustris and S. androgynus leaves against Staphylococcus aureus, Escherichia coli and Candida albicans. Analyze the antibacterial activity of a single preparations with a combination preparation of S.palustris (SP) and S.androgynus (SA) leaves infusion against S.aureus, E.coli and C.albicans. Leaves of S.palustris young part (SP1) taken 0-10 cm from shoots and old parts (SP2) 11-20 cm from shoots, while leaves of S.androgynus young part (SA1) leaves number 1 - 10 from the top and the old part (SA2) leaves number 11-20 from the top. The results showed that a single infusion of SP1 75% and SP2 75%, SA1 90% and SA2 90%, and a combination of SP1 75% and SA1 75%, SP2 75% and SA2 75% have the same activity as ampicillin in S.aureus. Single infusion of SP1 90% and SP2 90%, SA1 90% and SA2 90%, combination of SP1 75% and SA1 80% and the combination of SP2 80% and SA2 60% have the same activity as ciprofloxacin in E. coli. Single infusion of SP1 90% and SP2 90%, and a combination of SP1 80% and SA1 80%, SP2 80% and SA2 80% have the same activity as ketoconazole in C.albicans. The difference in activity due to differences in leaf parts used only occurred in E. coli, whereas in S.aureus and C.albicans (p <0.05).
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Dąbrowska, Katarzyna, Katarzyna Skowrońska, Mariusz Popek, Jan Albrecht, and Magdalena Zielińska. "The Role of Nrf2 Transcription Factor and Sp1-Nrf2 Protein Complex in Glutamine Transporter SN1 Regulation in Mouse Cortical Astrocytes Exposed to Ammonia." International Journal of Molecular Sciences 22, no. 20 (October 18, 2021): 11233. http://dx.doi.org/10.3390/ijms222011233.

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Ammonia toxicity in the brain primarily affects astrocytes via a mechanism in which oxidative stress (OS), is coupled to the imbalance between glutamatergic and GABAergic transmission. Ammonia also downregulates the astrocytic N system transporter SN1 that controls glutamine supply from astrocytes to neurons for the replenishment of both neurotransmitters. Here, we tested the hypothesis that activation of Nrf2 is the process that links ammonia-induced OS formation in astrocytes to downregulation and inactivation of SN1 and that it may involve the formation of a complex between Nrf2 and Sp1. Treatment of cultured cortical mouse astrocytes with ammonia (5 mM NH4Cl for 24 h) evoked Nrf2 nuclear translocation, increased its activity in a p38 MAPK pathway-dependent manner, and enhanced Nrf2 binding to Slc38a3 promoter. Nrf2 silencing increased SN1 mRNA and protein level without influencing astrocytic [3H]glutamine transport. Ammonia decreased SN1 expression in Nrf2 siRNA treated astrocytes and reduced [3H]glutamine uptake. In addition, while Nrf2 formed a complex with Sp1 in ammonia-treated astrocytes less efficiently than in control cells, treatment of astrocytes with hybrid-mode inactivated Sp1-Nrf2 complex (Nrf2 silencing + pharmacological inhibition of Sp1) did not affect SN1 protein level in ammonia-treated astrocytes. In summary, the results document that SN1 transporter dysregulation by ammonia in astrocytes involves activation of Nrf2 but does not require the formation of the Sp1-Nrf2 complex.
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Rui, Xianliang, Jennivine Tsao, Joshua O. Scheys, Gary D. Hammer, and Bernard P. Schimmer. "Contributions of Specificity Protein-1 and Steroidogenic Factor 1 to Adcy4 Expression in Y1 Mouse Adrenal Cells." Endocrinology 149, no. 7 (April 3, 2008): 3668–78. http://dx.doi.org/10.1210/en.2008-0203.

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The type 4 adenylyl cyclase, Adcy4, is the least abundant of five different adenylyl cyclase isoforms expressed in the Y1 mouse adrenocortical cell line and is deficient in a Y1 mutant with impaired steroidogenic factor 1 (SF1) activity. This study examines the contributions of SF1 and other DNA promoter/regulatory elements to Adcy4 expression in the Y1 cell line and its derivative Adcy4-deficient mutant. Primer extension and in silico analyses indicate that Adcy4 transcription initiates from multiple sites just downstream of a GC-rich sequence. Luciferase reporter gene assays identify a 124-bp sequence, situated 19 bp upstream of the major transcription start site and highly conserved among several mammalian species, as the major determinant of Adcy4 expression in Y1 cells and as a site of compromised activity in the Adcy4-deficient mutant. EMSAs using competitor nucleotides and specific antibodies indicate that this conserved region contains three specificity protein (Sp)-1/Sp3-binding sites and one SF1-binding site. As determined by site-specific mutagenesis, the 5′-most Sp1/Sp3-site enhances promoter activity, whereas the middle Sp1/Sp3 and SF1 sites each repress Adcy4 promoter activity. In the Adcy4-deficient mutant, mutating the SF1 site restores Adcy4 promoter activity and knocking down SF1 with small interfering RNAs increases Adcy4 expression, confirming the contribution of SF1 to the mutant phenotype. These studies demonstrate roles for Sp1/Sp3 and SF1 in Adcy4 expression in Y1 cells and establish a repressor function for SF1 in certain promoter contexts.
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Barnes, John G. P. "SP1." ACM SIGAda Ada Letters XXVII, no. 3 (November 17, 2007): 3. http://dx.doi.org/10.1145/1315607.1315584.

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Sward, Ricky E. "SP1." ACM SIGAda Ada Letters 28, no. 3 (December 2008): 3–4. http://dx.doi.org/10.1145/1454497.1454477.

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POPPLETON, Helen M., and Rajendra RAGHOW. "Transcriptional activation of the minimal human Proα1(I) collagen promoter: obligatory requirement for Sp1." Biochemical Journal 323, no. 1 (April 1, 1997): 225–31. http://dx.doi.org/10.1042/bj3230225.

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A construct containing human Proα1(I) collagen gene promoter/enhancer-driven chloramphenicol acetyltransferase (CAT), pCOL-KT, failed to be expressed significantly in Sp1-deficient Schneider Drosophila line 2 (SL2) cells. However, CAT expression was induced 200-fold in SL2 cells co-transfected with pCOL-KT and pPACSp1, an Sp1-expression vector driven by the Drosophila actin 5C promoter. Elimination of the four potential Sp1-binding sites from pCOL-KT (pCOL-KTΔI), by removal of the first intron, did not abrogate Sp1-mediated induction of CAT. Even more significantly, a minimal Proα1(I) collagen promoter (-100 to +117 bp), containing a TATA box (-28 to -25 bp) and one putative Sp1-binding site (-87 to -82 bp), elicited strong Sp1-induced transactivation. Furthermore, mutation of the Sp1 motif in the minimal Proα1(I) collagen promoter-CAT construct abolished Sp1-induced expression of the reporter gene. Purified Sp1 protein bound specifically to DNA fragments of the Proα1(I) minimal promoter encompassing the putative Sp1-binding site; Sp1 binding could be competed out by a double-stranded oligonucleotide containing the wild-type Sp1 sequence, while an oligonucleotide containing a mutated Sp1 site failed to compete. Based on these results, we postulate that Sp1 plays an obligatory role in the transcriptional activation of the human Proα1(I) collagen gene. Additionally, we propose that a bona fide Sp1 motif, located most proximal to the TATA box, is necessary and sufficient for Sp1-mediated activation of the minimal Proα1(I) collagen promoter.
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Zhang, Ying, and Maria L. Dufau. "Repression of the Luteinizing Hormone Receptor Gene Promoter by Cross Talk among EAR3/COUP-TFI, Sp1/Sp3, and TFIIB." Molecular and Cellular Biology 23, no. 19 (October 1, 2003): 6958–72. http://dx.doi.org/10.1128/mcb.23.19.6958-6972.2003.

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ABSTRACT Transcription of luteinizing hormone receptor (LHR) gene is activated by Sp1/Sp3 at two Sp1 sites and is repressed by nuclear orphan receptors EAR2 and EAR3 through a direct-repeat (DR) motif. To elucidate the mechanism of the orphan receptor-mediated gene repression, we explored the functional connection between the orphan receptors and Sp1/Sp3 complex, and its impact on the basal transcription machinery. The Sp1(I) site was identified as critical for the repression since its mutation reduced the inhibition by EAR2 and abolished the inhibition by EAR3. Cotransfection analyses in SL2 cells showed that both Sp1 and Sp3 were required for this process since EAR3 displayed a complete Sp1/Sp3-dependent inhibitory effect. Functional cooperation between Sp1 and DR domains was further supported by mutual recruitment of EAR3 and Sp1/Sp3 bound to their cognate sites. Deletion of EAR3 N-terminal and DNA-binding domains that reduced its interaction with Sp1 impaired its inhibitory effect on human LHR (hLHR) gene transcription. Furthermore, we demonstrate interaction of TFIIB with Sp1/Sp3 at the Sp1(I) site besides its association with EAR3 and the TATA-less core promoter region. Such interaction relied on Sp1 site-bound Sp1/Sp3 complex and adaptor protein(s) present in the JAR nuclear extracts. We further demonstrated that EAR3 specifically decreased association of TFIIB to the Sp1(I) site without interfering on its interaction with the hLHR core promoter. The C-terminal region of EAR3, which did not participate in its interaction with Sp1, was required for its inhibitory function and may affect the association of TFIIB with Sp1. Moreover, perturbation of the association of TFIIB with Sp1 by EAR3 was reflected in the reduced recruitment of RNA polymerase II to the promoter. Overexpression of TFIIB counteracted the inhibitory effect of EAR3 and activated hLHR gene transcription in an Sp1 site-dependent manner. These findings therefore indicate that TFIIB is a key component in the regulatory control of EAR3 and Sp1/Sp3 on the initiation complex. Such cross talk among EAR3, TFIIB, and Sp1/Sp3 reveals repression of hLHR gene transcription by nuclear orphan receptors is achieved via perturbation of communication between Sp1/Sp3 at the Sp1-1 site and the basal transcription initiator complex.
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NICOLÁS, Marta, Vèronique NOÉ, and Carlos J. CIUDAD. "Transcriptional regulation of the human Sp1 gene promoter by the specificity protein (Sp) family members nuclear factor Y (NF-Y) and E2F." Biochemical Journal 371, no. 2 (April 15, 2003): 265–75. http://dx.doi.org/10.1042/bj20021166.

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We analysed in detail the minimal promoter of transcription factor Sp1, which extends 217bp from the initiation of transcription. Within this sequence we identified putative binding sites for Sp1, nuclear factor Y (NF-Y), activator protein 2 ('AP-2'), CCAAT/enhancer-binding protein ('C/EBP') and E2F transcription factors. In one case, the boxes for Sp1 and NF-Y are overlapping. Gel-shift and supershift assays demonstrated specific binding of Sp1, Sp3 and NF-Y proteins. Transient transfections and luciferase assays revealed activation of the Sp1 minimal promoter upon overexpression of Sp1 itself, NF-Y and E2F. Whereas overexpression of NF-Y or E2F had an additive effect on Sp1 overexpression, the activation of Sp1 transcription due to Sp1 was counteracted by Sp3 overexpression. Mutagenesis analysis of the NFY/Sp1-overlapping box revealed that both factors compete for this box, and that when the NF-Y site of this overlapping box is specifically mutated there is an increase in Sp1 binding, thus increasing transcriptional activity. These results help to explain the complex regulation of the Sp1 gene, which depends on the relative amounts of Sp1, Sp3, E2F and NF-Y proteins in the cell.
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Chen, L. I., T. Nishinaka, K. Kwan, I. Kitabayashi, K. Yokoyama, Y. H. Fu, S. Grünwald, and R. Chiu. "The retinoblastoma gene product RB stimulates Sp1-mediated transcription by liberating Sp1 from a negative regulator." Molecular and Cellular Biology 14, no. 7 (July 1994): 4380–89. http://dx.doi.org/10.1128/mcb.14.7.4380-4389.1994.

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Studies have demonstrated that the retinoblastoma susceptibility gene product, RB, can either positively or negatively regulate expression of several genes through cis-acting elements in a cell-type-dependent manner. The nucleotide sequence of the retinoblastoma control element (RCE) motif, GCCACC or CCACCC, and the Sp1 consensus binding sequence, CCGCCC, can confer equal responsiveness to RB. Here, we report that RB activates transcription of the c-jun gene through the Sp1-binding site within the c-jun promoter. Preincubation of crude nuclear extracts with monoclonal antibodies to RB results in reduction of Sp1 complexes in a mobility shift assay, while addition of recombinant RB in mobility shift assay mixtures with CCL64 cell extracts leads to an enhancement of DNA-binding activity of SP1. These results suggest that RB is directly or indirectly involved in Sp1-DNA binding activity. A mechanism by which RB regulates transactivation is indicated by our detection of a heat-labile and protease-sensitive Sp1 negative regulator(s) (Sp1-I) that specifically inhibits Sp1 binding to a c-jun Sp1 site. This inhibition is reversed by addition of recombinant RB proteins, suggesting that RB stimulates Sp1-mediated transactivation by liberating Sp1 from Sp1-I. Additional evidence for Sp1-I involvement in Sp1-mediated transactivation was demonstrated by cotransfection of RB, GAL4-Sp1, and a GAL4-responsive template into CV-1 cells. Finally, we have identified Sp1-I, a approximately 20-kDa protein(s) that inhibits the Sp1 complexes from binding to DNA and that is also an RB-associated protein. These findings provide evidence for a functional link between two distinct classes of oncoproteins, RB and c-Jun, that are involved in the control of cell growth, and also define a novel mechanism for the regulation of c-jun expression.
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Dissertations / Theses on the topic "Sp1"

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Tuthill, Matthew Charles. "N-myc oncogene expression in neuroblastoma is dependent on Sp1 and Sp3." Thesis, University of Hawaii at Manoa, 2003. http://hdl.handle.net/10125/987.

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Regulation of N-myc oncogene expression is an important determinant of the biological behavior of neuroblastoma. The N-myc promoter contains several potential binding sites for transcription factors of the Sp1 family. Mutation of a CT-box motif contained within a 26 base pair region required for N-myc downregulation by retinoic acid decreased basal transcriptional activity and altered DNA-protein interactions of the promoter, while mutations flanking this motif did neither. On gel shift this region generated 3 specific DNA-protein complexes that were reliant on wild type sequence of the core CT element within it. Both Spl and Sp3 bound to the wild type probe as distinct complexes in specifically retarded bands, while neither protein was present on mutated sequences. Lysates from Drosophila S2 cells expressing exogenous Sp1 and Sp3 proteins were able to reproduce the gel shift complexes seen with neuroblastoma nuclear extract. Transient transfections of S2 cells showed that individually or together, Sp1 and Sp3 were able to trans-activate a N-myc CT-box-containing luciferase reporter construct in a dose-dependent manner. Conversely, transfection of CT-box oligonucleotide was able to decrease endogenous N-myc expression in neuroblastoma cells. Together these results suggest that the CT-box element serves a critical functional role, and in the basal state allows for N-myc transactivation by Spl and Sp3.
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Kim, KyoungHyun. "Domain analysis for estrogen receptor/Sp1-mediated transactivation and detection of estrogen receptor/Sp1 protein interactions in living cells." Texas A&M University, 2004. http://hdl.handle.net/1969.1/2666.

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Estrogen Receptor ? (ER?)/Sp1 activation of GC-rich gene promoters in breast cancer cells is dependent, in part, on the activation function 1 (AF1) of ER?. This study investigates contributions of the DNA binding domain (C) and AF2 (DEF) regions of ER? on activation of ER?/Sp1. 17Beta-estradiol (E2) and the antiestrogens 4-hydroxytamoxifen and ICI 182,780 induced reporter gene activity in MCF-7 and MDA-MB-231 cells cotransfected with human or mouse ER? (hER? or MOR), but not ER? and GC-rich constructs containing three tandem Sp1 binding sites (pSp13) or other E2-responsive GC-rich promoters. Estrogen and antiestrogen activation of hER?/Sp1 was dependent on overlapping and different regions of the C, D, E, and F domains of ER?. Antiestrogen-induced activation of hER?/Sp1 was lost using hER? mutants deleted in zinc finger 1 (amino acids (aa) 185-205), zinc finger 2 (aa 218-245), and the hinge/helix 1 (aa 265-330) domains. In contrast with antiestrogens, E2-dependent activation of hER?/Sp1 required the C-terminal F domain (aa 579-595), which contains a ?-strand structural motif. Moreover, in peptide competition experiments overexpression of NR-box peptides inhibits E2-induced luciferase activity of pERE3, which contains three tandem repeats of consensus ERE sites, whereas E2-induced hER?/Sp1 action was not inhibited by NR-box peptide expression. In contrast, overexpression of a C-terminal (aa 575-595) F domain peptide specifically blocked E2-dependent activation of hER?/Sp1, but not on activation of pERE3, suggesting that F domain interactions with nuclear cofactors are specifically required for ER?/Sp1 action. Furthermore, direct physical interactions between hER? and Sp1 protein in vivo have been investigated by using Fluorescence Resonance Energy Transfer (FRET) microscopy and image analysis. Consistent with results from transient transfection assay, E2, 4OHT, and ICI enhanced hER?/Sp1 interactions in living cells and these interactions were also confirmed by coimmunoprecipitation. In addition, endogenous hER?/Sp1 action was evaluated by using si RNA for Sp1 and a significant decrease in ligand-induced hER?/Sp1 action was observed after decreased Sp1 expression.
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Menderin, Nathan. "Studies on the Human Sp1 DNA-Binding Domain." Thesis, University of Exeter, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.507135.

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Andrade, João Nilton Barreto. "O SP1 (transcription factor Sp1) participa da regulação transcricional do Slc2a4 mediada pelo receptor de estrógeno ER-alfa em adipócitos 3T3-L1." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5160/tde-17082018-095039/.

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O diabetes mellitus tipo 2 (DM2) é caracterizado pela presença de resistência à insulina, a qual pode ser modulada pelo estrógeno, tanto em fêmeas como em machos. Nesse processo, o transportador de glicose GLUT4 (gene Slc2a4, solute carrier family 2 member 4) desempenha papel importante, pois aumento da expressão do GLUT4 melhora o controle glicêmico. Estradiol (E2) regula a expressão do Slc2a4 por meio do balanço dos efeitos contrários de seus receptores (ERs): ER-alfa estimula e ER-beta inibe a expressão. Efeitos transcricionais dos ERs envolvem a participação de co-reguladores, destacadamente o SP1 (transcription factor Sp1), potente estimulador do Slc2a4. Entretanto, o papel do SP1 na regulação do Slc2a4 mediada pelos ERs é desconhecido; e este foi o objetivo do presente estudo. Investigou-se adipócitos maduros 3T3-L1, tratados por 24 horas com E2, agonista de ER-alfa (PPT) ou agonista de ER-beta (DPN). Avaliou-se: a expressão gênica (RT-qPCR) de Slc2a4 e Sp1; o conteúdo (Western blotting) total de GLUT4 e o nuclear de ER-alfa/beta e SP1; a atividade de ligação do SP1 no Slc2a4 (ensaio de mobilidade eletroforética); e a formação de complexos SP1/ER-alfa (imunoprecipitação). Os resultados confirmaram que E2 aumenta a expressão de Slc2a4/GLUT4 pela ação preponderante do ER-alfa. O agonista PPT aumentou: o conteúdo nuclear de SP1, a interação SP1/ER-alfa e a atividade de ligação do SP1 no Slc2a4. O agonista DPN indicou que a ação repressora do ER-beta não envolve o SP1. Conclui-se que o efeito estimulador do ER-alfa na expressão do Slc2a4 envolve mecanismo de transativação gênica via SP1. Essas observações colocam a cooperação ER-alfa/SP1 como um novo alvo para o desenvolvimento de medidas terapêuticas para resistência à insulina e diabetes mellitus tipo 2
Type 2 diabetes mellitus (T2DM) is characterized by insulin resistance, which can be modulated by estrogen in both females and males. In this process, the glucose transporter GLUT4 (solute carrier family 2 member 4 gene - Slc2a4) plays an important role, since increasing GLUT4 expression improves glycemic control. Estradiol (E2) regulates the expression of Slc2a4, by a mechanism in which estrogen receptors (ERs) play opposite effects: ER-alpha stimulates, whereas ER-beta inhibits the expression. Transcriptional effects of ERs involve co-regulators, notably the transcription factor SP1, a powerful enhancer of Slc2a4. However, the role of SP1 in the ERs-mediated regulation of Slc2a4 is unknown; and that was the aim of the present study. Differentiated adipocytes 3T3-L1 were treated (24 hours) with E2, ER-alpha agonist (PPT) or ER-beta agonist (DPN). It was analyzed: gene expression (RT-qPCR) of Slc2a4 and Sp1; total content o GLUT4 and nuclear content of ER-alpha/beta and SP1 (Western blotting); binding activity of SP1 into Slc2a4 promoter (electrophoretic mobility shift assay); and content of nuclear SP1/ER-alpha complexes (immunoprecipitation). Results confirmed that E2 increases the expression of Slc2a4/GLUT4, by the dominant effect of ER-alpha. The ER-alpha agonist PPT increased the nuclear content of SP1, the interaction of SP1/ER-alpha, and the binding activity of SP1 into the Slc2a4. The agonist DPN evinced that ER-beta activity does not involve the SP1. In conclusion, the enhancer effect of ER-alpha upon Slc2a4 gene expression involves a transactivation mechanism via SP1. This observation point outs the cooperation of ER-alpha/SP1 as a new target for the development of approaches to treat insulin resistance and T2DM
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Broad, William. "Elucidating the function of the suppressor of ppi1 locus 2." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:81cb5fb1-e735-453c-9c4b-332a5aa16b27.

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MURATE, TAKASHI, YOSHINORI NOZAWA, YOSHIKO BANNO, MOTOSHI SUZUKI, TETSUHITO KOJIMA, AKIRA TAKAGI, KAZUMI HAGIWARA, et al. "Mutated RAS Induced PLD1 Gene Expression through Increased Sp1 Trascription Factor." Nagoya University School of Medicine, 2009. http://hdl.handle.net/2237/16765.

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Darragh, Molly Rose. "Targeting the active serine protease MT-SP1 for tumor detection in vivo." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2010. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3398875.

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Deniaud, Emmanuelle. "Etude des conséquences fonctionnelles de la surexpression du facteur de transcription Sp1." Phd thesis, Ecole normale supérieure de lyon - ENS LYON, 2008. http://tel.archives-ouvertes.fr/tel-00288383.

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Le facteur de transcription Sp1 régule la transcription de nombreux gènes à partir des sites riches en GC. Mon projet a été d'étudier le rôle de Sp1 dans la régulation de l'apoptose et du cycle cellulaire, qui est encore mal défini à l'heure actuelle. Nous avons montré que la surexpression de Sp1 induit un ralentissement du cycle cellulaire en phase G1 et l'apoptose. L'étude du transcriptome a permis d'identifier les mécanismes qui pourraient être à l'origine du ralentissement du cycle cellulaire : la répression de la cycline D2 et l'induction de p18 et cycline G2. Concernant l'induction de l'apoptose, les mécanismes mis en jeu sont spécifiques du type cellulaire et sont différents de ceux décrits jusqu'à ce jour. De façon inattendue, nos résultats montrent que l'ensemble de ces perturbations cellulaires requièrent la liaison de Sp1 à l'ADN mais pourrait être indépendant de son activité transcriptionnelle.
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Cain, Henry James. "A study of transcription factors STAT3, SP1 and NFkB in breast cancer." Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1333.

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Background and Aims: Breast cancer is the second most common cause of cancer deaths in women. It is a tumour which has been extensively studied at a molecular level and, compared to other solid tissue tumours, our understanding of its biology is extensive. There are however some patients who are considered to have good prognostic feature of their tumours who go on to die from their disease. Transcription factors are the end point of many cell signalling pathways. They form the link between exogenous hormones and growth factors and DNA transcription. For the purpose of this study 3 different transcription factors have been selected for investigation. STAT3 is activated by various growth factors and cytokines including EGF. It is classified as an oncoprotein as its activation can mediate tumorgenisis in nude mice. STAT3 has been shown to confer resistance to apoptosis in breast cancer cells and it is associated with poor outcome in high risk breast cancers. SP1 is a transcription factor which is essential in the expression and the action of estrogen receptors (ER). It is known to be over expressed in other solid tissue tumours but there has been little work into its role in breast cancer. NFkB is activated in many cell survival settings. It is involved in the transcription of anti-apoptotic genes and also plays a role in cell proliferation, angiogenisis and cell adhesion. It is associated in breast cancers with an over expression of the oncogene Bcl-2. It has not been show to be a marker of prognosis but does appear to identify breast cancers with a poor response to chemotherapy. The aim of this study is to investigate the role of these transcription factors in the behaviour of breast cancers and the outcome of the disease. It will also investigate the affect of EGF and estogen stimulation on STAT3 activation in breast cancer cell lines. Methods: This study consists of 2 elements. Firstly an assessment of transcription factor expression in breast cancer samples and secondly a cell model experiment to investigate the stimulation of STAT3 activation. A cohort of 213 patients who presented to the Queen Elizabeth Hospital with invasive breast cancer in 1999 was selected. Tumour samples from these patients were retrieved and using immunohistochemistry were tested for the expression of STAT3, SP1 and NFkB. These results were then correlated with pathological features of the tumours, tumour receptor status (ER, PR HER2 and EGFR) and outcome of the disease. Two cell lines, MCF7 and SKBr3, were cultured in depleted medium. These cells were then stimulated with estrogen and EGF alone and in combination. Flow-cytometry was then used to quantify the levels of phosphorylated STAT3 in the 2 cell lines over a 3 day time course. The level of phosphorylation was then compared to the control lines to asses the effect of stimulation. Results: 209 breast cancers were successfully analysed for the expression of STAT3, 27% of these cancers expressed nuclear STAT3. The results demonstrated a significant correlation of STAT3 expression with cancers of a high grade (p=<0.001), increasing tumour size (p=0.004), vessel space invasion (p=0.034) and lymph node metastases (p=0.015). STAT3 expression was shown to be significantly correlated to high Nottingham prognostic index (NPI) scores. With regards to receptor status it was show that STAT3 expression was significantly associated with ER negative and PR negative cancers (p=0.003), whereas there was no relationship with HER2 status. The results did show that there was a significant relationship between STAT3 expression and EGFR positive cancers (p=0.007). When disease outcome was investigated it was shown that there was a trend towards improved survival in the STAT3 negative group and a significant relationship between STAT3 expression and disease recurrence at 5 years (p=0.04). SP1 expression was determined in 208 of the cancer samples with 33% of the tumours having strong nuclear staining. There was no significant relationship between SP1 expression and any of the pathological features mentioned. SP1 expression was related to ER positive tumours (p=0.015). Though there was no relationship with 5 year survival it appears that SP1 expression does reduce the risk of late (>2yr) disease recurrence (p=0.005). NFkB was over expressed in 15% of the 208 cancers samples. Again a significant correlation was shown with high grade tumours (p=0.001) and large tumours (p=0.014). NFkB expression was also shown to be more prevalent in ER negative cancers (p=0.006) and EGFR positive tumours (p=0.007). There was no significant relationship between NFkB expression and disease outcome. The cell model results showed that in the EGFR positive ER negative cell line (SKBr3), EGF stimulation resulted in a biphasic response of STAT3 phosphorylation, whereas estrogen had no effect on phosphorylation. In the ER positive MCF7 cells, which express low levels of EGFR, again EGF stimulation resulted in a biphasic response curve. Estrogen stimulation does cause an increase in activation but when estrogen is added to EGF stimulation there is an inhibition of STAT3 phosphorylation. Conclusions: This study has demonstrated that STAT3 and SP1 expression is important in disease outcome in breast cancer patients. Though there are differences in levels of expression, NFkB does not appear to have a role in breast cancer outcome. The cell model has show that EGF stimulation of EGFR positive cell lines results in increased STAT3 activation and also that this effect is inhibited by the addition of estrogen stimulation. These results raise important questions which are discussed in the study and suggest areas for further investigation.
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Deniaud, Emmanuelle. "Étude des conséquences fonctionnelles de la surexposition du facteur de transcription Sp1." Lyon, École normale supérieure (sciences), 2008. http://www.theses.fr/2008ENSL0455.

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Books on the topic "Sp1"

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Trefethen, Anne E. Implementing the NAS CG benchmark on the SP1/SP2. Ithaca, N.Y: Cornell Theory Center, Cornell University, 1995.

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Windows 7 SP1 quicksteps. New York: McGraw-Hill, 2011.

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Evjen, Bill. Professional ASP.NET 3.5 SP1 Edition. New York: John Wiley & Sons, Ltd., 2010.

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Juergen, Hasslauer, ed. Designing storage for Exchange 2007 SP1. Amsterdam: Digital Press/Elsevier, 2008.

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Wesselius, Jaap, and Michel de Rooij. Pro Exchange 2013 SP1 PowerShell Administration. Berkeley, CA: Apress, 2014. http://dx.doi.org/10.1007/978-1-4302-6847-5.

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Mastering Microsoft Exchange server 2007 SP1. 2nd ed. Indianapolis, Ind: Wiley Pub., 2009.

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Feldman, Arlen S. WPF in action with Visual Studio 2008: Covers Visual Studio 2008 SP1 and .Net 3.5 SP1. Greenwich, CT: Manning Publications Co., 2009.

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McBee, Jim. Mastering Microsoft® Exchange Server 2007 SP1. Indianapolis, IN, USA: Wiley Publishing, Inc., 2009. http://dx.doi.org/10.1002/9781118257425.

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Shapiro, Jeffrey. Windows Server 2003 Bible, R2 and SP1 edition. Hoboken, NJ: Wiley Technology Pub., 2006.

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Wally, Mead, ed. System center 2012 configuration manager SP1: Mastering the fundamentals. 2nd ed. [S.l.]: Deployment Artist, 2013.

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Book chapters on the topic "Sp1"

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Koizume, Shiro, and Yohei Miyagi. "Sp1." In Encyclopedia of Signaling Molecules, 5100–5106. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101923.

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Koizume, Shiro, and Yohei Miyagi. "Sp1." In Encyclopedia of Signaling Molecules, 1–6. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101923-1.

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Gara, Alan, José E. Moreira, Tejas S. Karkhanis, José E. Moreira, José E. Moreira, Michael Flynn, Yoichi Muraoka, et al. "IBM SP1." In Encyclopedia of Parallel Computing, 912. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-09766-4_2280.

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Wesselius, Jaap, and Michel de Rooij. "Introduction to Exchange 2013 SP1." In Pro Exchange 2013 SP1 PowerShell Administration, 1–41. Berkeley, CA: Apress, 2014. http://dx.doi.org/10.1007/978-1-4302-6847-5_1.

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Abali, Bülent, and Cevdet Aykanat. "Routing algorithms for IBM SP1." In Parallel Computer Routing and Communication, 161–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/3-540-58429-3_35.

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Johnson, Matthew, Giacomo Paesani, and Daniël Paulusma. "Connected Vertex Cover for $$(sP_1+P_5)$$(sP1+P5)-Free Graphs." In Graph-Theoretic Concepts in Computer Science, 279–91. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-00256-5_23.

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Tillu, Himanshu, and Pallaval Veera Bramhachari. "Role of Sp1 in Liver Cancer." In Role of Transcription Factors in Gastrointestinal Malignancies, 495–508. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-6728-0_37.

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Szelényi, Ferenc. "Scalable POWERparallel Systems IBM 9076 SP1." In Supercomputer ’93, 77–84. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-78348-7_9.

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Wesselius, Jaap, and Michel de Rooij. "Security." In Pro Exchange 2013 SP1 PowerShell Administration, 489–525. Berkeley, CA: Apress, 2014. http://dx.doi.org/10.1007/978-1-4302-6847-5_10.

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Wesselius, Jaap, and Michel de Rooij. "Office 365 and Exchange Online." In Pro Exchange 2013 SP1 PowerShell Administration, 527–99. Berkeley, CA: Apress, 2014. http://dx.doi.org/10.1007/978-1-4302-6847-5_11.

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Conference papers on the topic "Sp1"

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Sward, Ricky E. "SP1." In the 2008 ACM annual international conference. New York, New York, USA: ACM Press, 2008. http://dx.doi.org/10.1145/1454474.1454477.

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Barnes, John G. P. "SP1." In the 2007 ACM international conference. New York, New York, USA: ACM Press, 2007. http://dx.doi.org/10.1145/1315580.1315584.

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Lidbury, David, Elisabeth Keim, Bernard Marini, Lorenzo Malerba, Asmahana Zeghadi, Dominique Moinereau, and Abderrahim Al Mazouzi. "Overview of RPV Sub-Project of Perform 60." In ASME 2011 Pressure Vessels and Piping Conference. ASMEDC, 2011. http://dx.doi.org/10.1115/pvp2011-57551.

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PERFORM 60 (Prediction of the effects of radiation for reactor pressure vessel and in-core materials using multi-scale modelling — 60 years foreseen plant lifetime) is a 48-month project of the 7th Framework of the European Atomic Energy Community (EURATOM) being carried out under the auspices of the Directorate General Research, Technology and Development (DG.RTD) of the European Commission. Launched in March 2009, and building on the achievements of PERFECT, a EURATOM 6th Framework project, PERFORM 60 has as its main objective the development of multi-scale modelling tools integrated onto a common software platform, aimed at predicting for PWRs (i) the effects of irradiation on RPV materials (low alloy bainitic steels), (ii) the combined effects of irradiation and corrosion on internals (austenitic stainless steels). Accordingly, PERFORM 60 is based on two main technical sub-projects: SP1 (RPV) and SP2 (Internals). An integration work package within both SP1 and SP2 serves to facilitate software development. A Users’ Group (SP3) supports the main technical sub-projects and allows representatives of constructors, utilities, regulators and research organizations from Europe and further afield to receive the information and training needed to make their own appraisal as to the validity of the developed tools. A significant effort is also being made to train young researchers in the field of physical modelling of materials degradation due to neutron irradiation. Against this background, the paper provides an overview of SP1, highlighting the various models and methods being developed, building on the achievements of PERFECT, to describe the evolution of flow properties of low-alloy steels with irradiation and address their subsequent effects on cleavage fracture behaviour.
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"Session SP1: Signal processing I." In 2009 International Conference on Computer Engineering & Systems (ICCES 2009). IEEE, 2009. http://dx.doi.org/10.1109/icces.2009.5383289.

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"Session SP1: Signal processing I." In Systems (ICCES). IEEE, 2010. http://dx.doi.org/10.1109/icces.2010.5674878.

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"Session SP1: Signal processing (I)." In 2014 9th International Conference on Computer Engineering & Systems (ICCES). IEEE, 2014. http://dx.doi.org/10.1109/icces.2014.7030939.

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"Technical session SP1: Signal processing I." In 2008 International Conference on Computer Engineering & Systems. IEEE, 2008. http://dx.doi.org/10.1109/icces.2008.4772961.

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Jin, Hong-Qing, and Li-Wu Fan. "Melting of a Phase Change Material Filled in a Metal Foam: A Visualized Study at the Pore-Scale Using Infrared Imaging." In ASME 2016 Heat Transfer Summer Conference collocated with the ASME 2016 Fluids Engineering Division Summer Meeting and the ASME 2016 14th International Conference on Nanochannels, Microchannels, and Minichannels. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/ht2016-7338.

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The thermal imaging technique was applied in this work to measure the transient temperature fields during melting of a phase change material (PCM) in a metal foam. A paraffin wax was used as the PCM that was filled in an open-celled copper foam. Melting of a paraffin wax in the presence of copper foam was studied in a rectangular cavity that was heated from one lateral side wall, while the top surface was exposed to an infrared (IR) camera. A thermocouple (TC) was also employed to validate the accuracy of temperature measurements by IR thermal imaging. The relative deviation of measured temperature by the TC and IR camera was found to be under 2% in steady state and under 4% during the entire course of melting. The resolution of IR thermal imaging with the aid of a macro lens allowed for temperature measurements at pore-scale of the copper foam. Local thermal imaging was captured through a minor window on the top plate of the container. Three points (Sp1–3) inside a selected individual pore were marked to quantify the temperature variations of melting process within metal foam/PCM at pore-scale. The average temperature differences between Sp1 and Sp2, Sp3 were found to be about 1 °C over the entire course of melting, and the maximum value was up to nearly 10 °C around the melting point. These preliminary results clearly highlighted the effect of metal ligaments on the temperature distributions at pore-scale.
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Verza, Flávia, Ana Saltoratto, and Mozart Marins. "Screening system development for HDAC1/Sp1 complex inhibitors." In International Symposium on Immunobiologicals. Instituto de Tecnologia em Imunobiológicos, 2022. http://dx.doi.org/10.35259/isi.2022_52294.

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Lee, Jong-Joo, Joo-Hong Park, Keunhee Park, Min-Ji Song, Wook-Jin Yang, and Hyoung-Pyo Kim. "Abstract 2211: Accessible chromatin structure permits factors Sp1 and Sp3 to regulate human TGFBI gene expression." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2211.

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Reports on the topic "Sp1"

1

Gropp, W., E. Lusk, and S. C. Pieper. Users guide for the ANL IBM SP1. Office of Scientific and Technical Information (OSTI), October 1994. http://dx.doi.org/10.2172/10115009.

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Gropp, W. Early experiences with the IBM SP1 and the high-performance switch. Office of Scientific and Technical Information (OSTI), November 1993. http://dx.doi.org/10.2172/10119584.

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CIE. CIE S 025-SP1/E:2019 Test Method for OLED Luminaires and OLED Light Sources. International Commission on Illumination (CIE), 2019. http://dx.doi.org/10.25039/s025-sp1.2019.

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Robinson, Rodney A. Benefit Analysis of SPC Panel SP-3 Projects and Evaluation of SPC Panel SP-3 Management and Administration. Fort Belvoir, VA: Defense Technical Information Center, September 1993. http://dx.doi.org/10.21236/ada458642.

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Robinson, Rodney A. Benefit Analysis of SPC Panel SP-4 Projects and Evaluation of SPC Panel SP-4 Management and Administration. Fort Belvoir, VA: Defense Technical Information Center, September 1993. http://dx.doi.org/10.21236/ada458643.

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Robinson, Rodney A. Benefit Analysis of SPC Panel SP-5 Projects and Evaluation of SPC Panel SP-5 Management and Administration. Fort Belvoir, VA: Defense Technical Information Center, September 1993. http://dx.doi.org/10.21236/ada458644.

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Robinson, Rodney A. Benefit Analysis of SPC Panel SP-8 Projects and Evaluation of SPC Panel SP-8 Management and Administration. Fort Belvoir, VA: Defense Technical Information Center, October 1993. http://dx.doi.org/10.21236/ada458645.

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Robinson, Rodney A. Benefit Analysis of SPC Panel SP-1 Projects & Evaluation of SPC Panel SP-1 Management and Administration. Fort Belvoir, VA: Defense Technical Information Center, September 1993. http://dx.doi.org/10.21236/ada458696.

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Robinson, Rodney A. Benefit Analysis of SPC Panel SP-10 Projects. Fort Belvoir, VA: Defense Technical Information Center, December 1995. http://dx.doi.org/10.21236/ada454983.

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Lopez, Juan J. Characterization of Semi-Insulating InP Wafers by Scanning Luminescence (SPL), Scanning Photocurrent (SPC) and Cathodoluminescence (CL). Study of the Wafer Homogeneity. Fort Belvoir, VA: Defense Technical Information Center, October 2000. http://dx.doi.org/10.21236/ada387598.

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