Relevant bibliographies by topics / RelA(p65)

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  2. Dissertations / Theses
  3. Conference papers

Academic literature on the topic 'RelA(p65)'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 September 2023

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Journal articles on the topic "RelA(p65)"

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Hansen, S. K., P. A. Baeuerle, and F. Blasi. "Purification, reconstitution, and I kappa B association of the c-Rel-p65 (RelA) complex, a strong activator of transcription." Molecular and Cellular Biology 14, no. 4 (1994): 2593–603. http://dx.doi.org/10.1128/mcb.14.4.2593-2603.1994.

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HeLa cells contain a DNA-binding activity which associates with a kappa B-like DNA element, termed Rel-related protein-binding element (RRBE), localized upstream of the human urokinase promoter. We have purified this activity from the HeLa cell cytosol and have shown that it represents a performed heteromeric complex between p65 (RelA) and c-Rel. Coexpression of c-Rel and p65 (RelA) by in vitro translation formed a DNA-binding complex indistinguishable from purified cellular c-Rel-p65 (RelA) in mobility shift assays. The c-Rel-p65 (RelA) complex was also formed in COS7 cells upon coexpression
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Hansen, S. K., P. A. Baeuerle, and F. Blasi. "Purification, reconstitution, and I kappa B association of the c-Rel-p65 (RelA) complex, a strong activator of transcription." Molecular and Cellular Biology 14, no. 4 (1994): 2593–603. http://dx.doi.org/10.1128/mcb.14.4.2593.

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HeLa cells contain a DNA-binding activity which associates with a kappa B-like DNA element, termed Rel-related protein-binding element (RRBE), localized upstream of the human urokinase promoter. We have purified this activity from the HeLa cell cytosol and have shown that it represents a performed heteromeric complex between p65 (RelA) and c-Rel. Coexpression of c-Rel and p65 (RelA) by in vitro translation formed a DNA-binding complex indistinguishable from purified cellular c-Rel-p65 (RelA) in mobility shift assays. The c-Rel-p65 (RelA) complex was also formed in COS7 cells upon coexpression
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Hoberg, Jamie E., Anita E. Popko, Catherine S. Ramsey та Marty W. Mayo. "IκB Kinase α-Mediated Derepression of SMRT Potentiates Acetylation of RelA/p65 by p300". Molecular and Cellular Biology 26, № 2 (2006): 457–71. http://dx.doi.org/10.1128/mcb.26.2.457-471.2006.

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ABSTRACT Over the last several years, significant progress has been made in identifying chromatin-regulated events that govern NF-κB transcription. Using either laminin attachment or tumor necrosis factor alpha as a physiological stimulus of NF-κB activation, we demonstrate that IκB kinase α (IKKα) is recruited to chromatin in distinct phases. In the initial phase, IKKα is responsible for derepressing the silencing mediator for retinoic acid and thyroid hormone receptor (SMRT)-histone deacetylase 3 (HDAC3) corepressor complex from the p50 homodimer. However, in the latter phase, chromatin-boun
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Hertlein, Erin, Jingxin Wang, Katherine J. Ladner, Nadine Bakkar та Denis C. Guttridge. "RelA/p65 Regulation of IκBβ". Molecular and Cellular Biology 25, № 12 (2005): 4956–68. http://dx.doi.org/10.1128/mcb.25.12.4956-4968.2005.

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ABSTRACT IκB inhibitor proteins are the primary regulators of NF-κB. In contrast to the defined regulatory interplay between NF-κB and IκBα, much less is known regarding the regulation of IκBβ by NF-κB. Here, we describe in detail the regulation of IκBβ by RelA/p65. Using p65 −/− fibroblasts, we show that IκBβ is profoundly reduced in these cells, but not in other NF-κB subunit knockouts. This regulation prevails during embryonic and postnatal development in a tissue-specific manner. Significantly, in both p65 −/− cells and tissues, IκBα is also reduced, but not nearly to the same extent as Iκ
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Lai, J. H., G. Horvath, J. Subleski, J. Bruder, P. Ghosh, and T. H. Tan. "RelA is a potent transcriptional activator of the CD28 response element within the interleukin 2 promoter." Molecular and Cellular Biology 15, no. 8 (1995): 4260–71. http://dx.doi.org/10.1128/mcb.15.8.4260.

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T-cell activation requires two different signals. The T-cell receptor's recognition of a specific antigen on antigen-presenting cells provides one, and the second signal comes from costimulatory molecules such as CD28. In contrast, T cells that are stimulated with antigen in the absence of the CD28 costimulatory signal can become anergic (nonresponsive). The CD28 response element (CD28RE) has been identified as the DNA element mediating interleukin 2 (IL-2) gene activation by CD28 costimulation. Our previous work demonstrates that the Rel/NF-kappa B family proteins c-Rel, RelA (p65), and NFKB1
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Liu, Yuan, Philip W. Smith, and David R. Jones. "Breast Cancer Metastasis Suppressor 1 Functions as a Corepressor by Enhancing Histone Deacetylase 1-Mediated Deacetylation of RelA/p65 and Promoting Apoptosis." Molecular and Cellular Biology 26, no. 23 (2006): 8683–96. http://dx.doi.org/10.1128/mcb.00940-06.

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ABSTRACT The antiapoptotic transcription factor NF-κB is constitutively activated in many cancers and is important for cytokine-mediated progression and metastatic movement of tumors. Breast cancer metastasis suppressor 1 (BRMS1) is a metastasis suppressor gene whose mechanisms of action are poorly understood. In this report, we demonstrate that BRMS1 decreases the transactivation potential of RelA/p65 and ameliorates the expression of NF-κB-regulated antiapoptotic gene products. BRMS1 immunoprecipitates with the RelA/p65 subunit of NF-κB with protein-protein interactions occurring at the C te
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Bijli, Kaiser M., Mohd Minhajuddin, Fabeha Fazal, Michael A. O'Reilly, Leonidas C. Platanias, and Arshad Rahman. "c-Src interacts with and phosphorylates RelA/p65 to promote thrombin-induced ICAM-1 expression in endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 2 (2007): L396—L404. http://dx.doi.org/10.1152/ajplung.00163.2006.

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The procoagulant thrombin promotes polymorphonuclear leukocyte (PMN) adhesion to endothelial cells by a mechanism involving expression of intercellular adhesion molecule-1 (ICAM-1) via an NF-κB-dependent pathway. We now provide evidence that activation of c-Src is crucial in signaling thrombin-induced ICAM-1 expression via tyrosine phosphorylation of RelA/p65. Stimulation of human umbilical vein endothelial cells with thrombin resulted in a time-dependent activation of c-Src, with maximal activation occurring at 30 min after thrombin challenge. Inhibition of c-Src by pharmacological and geneti
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Duckett, C. S., N. D. Perkins, T. F. Kowalik, et al. "Dimerization of NF-KB2 with RelA(p65) regulates DNA binding, transcriptional activation, and inhibition by an I kappa B-alpha (MAD-3)." Molecular and Cellular Biology 13, no. 3 (1993): 1315–22. http://dx.doi.org/10.1128/mcb.13.3.1315-1322.1993.

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Inducible expression of human immunodeficiency virus (HIV) is regulated by a cellular transcription factor, nuclear factor kappa B (NF-kappa B). NF-kappa B is composed of distinct subunits; five independent genes, NFKB1(p105), NFKB2(p100), RelA(p65), c-rel and relB, that encode related proteins that bind to kappa B DNA elements have been isolated. We have previously found that NFKB2(p49/p52) acts in concert with RelA(p65) to stimulate the HIV enhancer in Jurkat T-leukemia cells. Here we examine the biochemical basis for the transcriptional regulation of HIV by NFKB2. Using Scatchard analysis,
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Duckett, C. S., N. D. Perkins, T. F. Kowalik, et al. "Dimerization of NF-KB2 with RelA(p65) regulates DNA binding, transcriptional activation, and inhibition by an I kappa B-alpha (MAD-3)." Molecular and Cellular Biology 13, no. 3 (1993): 1315–22. http://dx.doi.org/10.1128/mcb.13.3.1315.

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Inducible expression of human immunodeficiency virus (HIV) is regulated by a cellular transcription factor, nuclear factor kappa B (NF-kappa B). NF-kappa B is composed of distinct subunits; five independent genes, NFKB1(p105), NFKB2(p100), RelA(p65), c-rel and relB, that encode related proteins that bind to kappa B DNA elements have been isolated. We have previously found that NFKB2(p49/p52) acts in concert with RelA(p65) to stimulate the HIV enhancer in Jurkat T-leukemia cells. Here we examine the biochemical basis for the transcriptional regulation of HIV by NFKB2. Using Scatchard analysis,
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CHAPMAN, Neil R., Gill A. WEBSTER, Peter J. GILLESPIE, Brian J. WILSON, Dorothy H. CROUCH та Neil D. PERKINS. "A novel form of the RelA nuclear factor κB subunit is induced by and forms a complex with the proto-oncogene c-Myc". Biochemical Journal 366, № 2 (2002): 459–69. http://dx.doi.org/10.1042/bj20020444.

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Members of both Myc and nuclear factor κB (NF-κB) families of transcription factors are found overexpressed or inappropriately activated in many forms of human cancer. Furthermore, NF-κB can induce c-Myc gene expression, suggesting that the activities of these factors are functionally linked. We have discovered that both c-Myc and v-Myc can induce a previously undescribed, truncated form of the RelA(p65) NF-κB subunit, RelA(p37). RelA(p37) encodes the N-terminal DNA binding and dimerization domain of RelA(p65) and would be expected to function as a trans-dominant negative inhibitor of NF-κB. S
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Dissertations / Theses on the topic "RelA(p65)"

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Latreche-Carton, Céline. "Rôle oncogénique des fragments de p65/RelA Nf-kB générés par l'activité de RIPK3." Thesis, Lille 2, 2017. http://www.theses.fr/2017LIL2S048/document.

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L'utilisation d'un agent déméthylant induit la réexpression de la protéine RIP3, une sérine-thréonine kinase, dans un modèle leucémique murin exprimant BCR-ABL humain. La réexpression de RIP3 conduit rapidement les cellules vers la nécroptose. Le mutant délété du domaine kinase est de façon surprenante plus "apoptogène" et induit le clivage de p65/RelA sur le résidu d'acide aspartique D361 par la caspase 6. Pour déterminer l'impact de ce clivage, nous avons construit un mutant non clivable p65/RelA D361E, ainsi que des plasmides exprimant chacun des fragments p65/RelA 1-361 ou p65/RelA 362-549
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Pejanovic, Nadja. "Identification of mechanisms controlling the transcriptional activity of nuclear factor kappa B (NF-κB) p65/RelA". Doctoral thesis, Instituto de Tecnologia Química e Biológica. Universidade Nova de Lisboa, 2011. http://hdl.handle.net/10362/9919.

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Dissertação para a obtenção do grau de doutor em Biologia pelo Instituto de Tecnologia Química e Biológica. Universidade Nova de Lisboa.<br>Living in an ever-changing environment, cells have evolved numerous mechanisms that allow their assessment of the environment, their communication with each other and the integration of the information in order to adapt to the environmental changes and to maintain their homeostasis. In the presence of harmful stimuli, such as infection or tissue damage, a series of defensive sequential events, including the activation of vascular endothelial cells (E
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Bu, Yiwen. "PHOSPHORYLATION OF NF-ΚB RELA/P65 ON SER536 SIGNALS CANCER CELLS TO DEATH AND ENHANCES CHEMOSENSITIVITY". OpenSIUC, 2014. https://opensiuc.lib.siu.edu/dissertations/801.

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RelA/p65 is a main subunit of nuclear factor-kappaB (NF-kappaB) that regulates expression of genes involved in cell growth and survival, stress response, and inflammation, but its oncogenic or tumor-suppressive function in tumorigenesis has been highly controversial. Hundreds of NF-kappaB inhibitors have been developed for targeted cancer therapy, but fail to achieve anticipated anticancer efficacy. Complexity of posttranslational modifications may contribute to tumorigenic diversity of RelA/p65, but mechanisms of action remain unclear. Here we show that phosphorylation of RelA/p65 at Ser536 f
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Leavenworth, Jianmei Wu. "Understanding T cells in type 1 diabetes: a role for c-Maf and characterization of intracellular signaling following engagement of transgenic Ly49A." OpenSIUC, 2008. https://opensiuc.lib.siu.edu/dissertations/269.

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Activated islet specific T cells are central to the destructive autoimmune response observed in type 1 diabetes (T1D). Not surprisingly, intense focus is placed on understanding how autoreactive T cell responses arise and contribute to disease pathology in the hope of using this information to develop novel therapeutic strategies for treatment of T1D. Here we investigate the mechanisms underlying defective c-Maf binding to the IL-4 promoter in T cells from diabetes prone mice and identify the mechanisms responsible for suppression of T cells by the inhibitory receptor Ly49A. It is not cle
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Lesina, Marina [Verfasser], Michael [Akademischer Betreuer] Schemann, Hana [Akademischer Betreuer] Algül та Roland M. [Akademischer Betreuer] Schmid. "Charakterisierung der Funktion des Transkriptionsfaktors RelA/p65 im Ela-TGFα transgenen Mausmodell der pankreatischen Karzinogenese / Marina Lesina. Gutachter: Hana Algül ; Roland M. Schmid ; Michael Schemann. Betreuer: Michael Schemann". München : Universitätsbibliothek der TU München, 2013. http://d-nb.info/1036974758/34.

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Ringelhan, Marc [Verfasser], Fabian K. [Akademischer Betreuer] Geisler, Jörg H. [Akademischer Betreuer] Kleeff та Ernst J. [Akademischer Betreuer] Rummeny. "Charakterisierung der Funktion der transaktivierenden NF-κB Untereinheit RelA/p65 in der Leberregeneration nach partieller Hepatektomie in der Maus / Marc Ringelhan. Gutachter: Jörg H. Kleeff ; Fabian K. Geisler ; Ernst J. Rummeny. Betreuer: Fabian K. Geisler". München : Universitätsbibliothek der TU München, 2013. http://d-nb.info/1042578176/34.

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Santos, Patricia Rabelo dos. "Expressão do fator de transcrição nuclear kB (NF-kB) em neurônios ocitocinérgicos de ratos submetidos à sobrecarga salina : influência da dexametasona." Universidade Federal de Sergipe, 2014. https://ri.ufs.br/handle/riufs/4004.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES<br>The hypothalamic-neurohypophysial system is the main system through which the brain maintains homeostasis of bodily fluids. Specifically, the supraoptic (SON) and paraventricular (PVN) hypothalamic nuclei are directly involved with hydroelectrolytic equilibrium and are specialized in the synthesis and secretion of vasopressin and oxytocin (OT). Changes in the milieu intérieur are conceived as stressors by the central nervous system (CNS) and are modulated by the hypothalamic-pituitary-adrenal axis (HPA). Nuclear transcripti
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Wasal, Karanvir. "The Role of RELA (p65) in Regulation of NF-kappaB Homeostasis: Implications for Atherosclerosis." Thesis, 2011. http://hdl.handle.net/1807/31629.

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The NF-κB/Rel family of transcription factors and IκB inhibitors play a key role in regulation of gene expression in inflammation and immunity. Previous studies from our laboratory suggested that steady-state levels of p65 and other NF-κB components in the normal mouse aorta determine the magnitude of NF-κB target gene expression in response to pro-inflammatory stimuli, however, the mechanism(s) by which steady-state levels of NF-κB components are set is not clear. This study aims at elucidating the mechanisms behind NF-κB homeostasis and how that affects atherosclerosis susceptibility. In He
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Lessard, Laurent. "Rôle de NF-kappaB dans la progression du cancer de la prostate : études clinicopathologiques et moléculaires." Thèse, 2007. http://hdl.handle.net/1866/15606.

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Labouba, Ingrid. "Implication de la voie alternative NF-kappa B dans le cancer de la prostate." Thèse, 2013. http://hdl.handle.net/1866/10867.

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Le cancer de la prostate (CaP) est le plus diagnostiqué chez les hommes au Canada et représente le troisième cancer le plus meurtrier au sein de cette population. Malgré l’efficacité des traitements de première ligne, de nombreux patients finiront par développer une résistance et, le cas échéant, verront leur CaP progresser vers une forme plus agressive. Plusieurs paramètres, essentiellement cliniques, permettent de prédire la progression du CaP mais leur sensibilité, encore limitée, implique la nécessité de nouveaux biomarqueurs afin de combler cette lacune. Dans cette optique nous nous intér
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Conference papers on the topic "RelA(p65)"

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Bijli, KM, M. Minhajuddin, F. Fazal, and A. Rahman. "Recruitment of p300 by Syk Regulates ICAM-1 Expression in Endothelial Cells Via Acetylation of RelA/p65." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2320.

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Fazal, F., K. Levy, M. Minhajuddin, KM Bijli, JN Finkelstein та A. Rahman. "Importin α4 Mediates Thrombin-Induced ICAM-1 Expression in Endothelial Cells by Facilitating RelA/p65 Nuclear Translocation." У American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2329.

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Nugues, Anne-Lucie, Hassiba Bouafia, Dominique Hetuin, et al. "Abstract 1342: RIP3 is downregulated in human myeloid leukemia cells and modulates apoptosis and caspase-mediated p65/RelA cleavage." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1342.

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Bond, Mark, Joseph Hawkins, Madeleine McNeill, Reza Ebrahimighaei, Harry Mellor, and Andrew Newby. "BS33 Cyclic-amp increases nuclear actin monomer which promotes proteasomal degradation of rela/p65 leading to anti-inflammatory effects." In British Cardiovascular Society Annual Conference, ‘100 years of Cardiology’, 6–8 June 2022. BMJ Publishing Group Ltd and British Cardiovascular Society, 2022. http://dx.doi.org/10.1136/heartjnl-2022-bcs.213.

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Adeeb, F., E. R. Dorris, S. Tariq та ін. "THU0002 Novel pathogenic stop codon mutation in the nf-Κb p65 subunit (RELA) associated with both behÇet’s disease like syndrome and neuromyelitis optica in an irish family". У Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.3889.

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