Academic literature on the topic 'NF-kB activity'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'NF-kB activity.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "NF-kB activity"
Amin, Jakia, Ken-ichiro Otsuyama, Abul Islam, Karim Shamsasenjan, Shamim Mohd Iqbal, and Michio M. Kawano. "The Mechanism of Constitutive NF-kB Activity in Myeloma Cell Lines." Blood 110, no. 11 (November 16, 2007): 4740. http://dx.doi.org/10.1182/blood.v110.11.4740.4740.
Full textGhosh, Sankar, Eijiro Jimi, Jie Dong, and Haihong Zhong. "REGULATION OF NF-KB TRANSCRIPTIONAL ACTIVITY." Shock 21, Supplement (March 2004): 44. http://dx.doi.org/10.1097/00024382-200403001-00176.
Full textOtsuyama, Ken-ichiro, Jakia Amin, Saeid Abroun, Abul Islam, Karim Shamsasenjan, Shamim Mohd Iqbal, and Michio M. Kawano. "The PPARß Activation Mechanism Which Suppresses the Constitutive NF-kB Activity in Human Myeloma Cell Lines." Blood 110, no. 11 (November 16, 2007): 4739. http://dx.doi.org/10.1182/blood.v110.11.4739.4739.
Full textMagrangeas, Florence, Philippe Moreau, Loic Campion, Herve Avet-Loiseau, Catherine Guérin, Wilfried Gouraud, Gérald Marit, et al. "Low Level Of NF-Kb Activity Is Associated With Higher Response Rate To Bortezomib-Based Induction Therapy In Patients With Newly Diagnosed Multiple Myeloma." Blood 122, no. 21 (November 15, 2013): 3106. http://dx.doi.org/10.1182/blood.v122.21.3106.3106.
Full textTsai, Hui-Jen, Seiichiro Kobayashi, Kiyoko Itoh, Takaomi Ishida, Kazuo Umezawa, and Arinobu Tojo. "Microenvironmental Up-Regulation of NF-kB Activity Via P65-Dependent and Independent Pathways in a Bioimaging Model of Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia." Blood 110, no. 11 (November 16, 2007): 723. http://dx.doi.org/10.1182/blood.v110.11.723.723.
Full textBao, Xiaoyong, Deepthi Kolli, Tianshuang Liu, Yichu Shan, Roberto P. Garofalo, and Antonella Casola. "Human Metapneumovirus Small Hydrophobic Protein Inhibits NF-κB Transcriptional Activity." Journal of Virology 82, no. 16 (June 11, 2008): 8224–29. http://dx.doi.org/10.1128/jvi.02584-07.
Full textWang, Xianhuo, Huaqing Wang, Chengfeng Bi, Xiaoyan Zhang, Xin Huang, Xuan Zhang, Javeed Iqbal, et al. "Microrna-17~92 Cluster Upregulates NF-KB Activity Via Suppressing Multiple NF-KB Negative Regulators Mediating Ubiquitination." Blood 126, no. 23 (December 3, 2015): 3638. http://dx.doi.org/10.1182/blood.v126.23.3638.3638.
Full textVassiliev, P. M., A. A. Spasov, L. R. Yanaliyeva, A. N. Kochetkov, V. V. Vorfolomeyeva, V. G. Klochkov, and D. T. Appazova. "Neural network modeling of multitarget RAGE inhibitory activity." Biomeditsinskaya Khimiya 65, no. 2 (2019): 91–98. http://dx.doi.org/10.18097/pbmc20196502091.
Full textNeumann, Manfred, and Michael Naumann. "Beyond IκBs: alternative regulation of NF‐KB activity." FASEB Journal 21, no. 11 (April 12, 2007): 2642–54. http://dx.doi.org/10.1096/fj.06-7615rev.
Full textNakagawa, Masahiro, Munetake Shimabe, Nahoko Nishimoto, Naoko Watanabe-Okochi, Motoshi Ichikawa, Yasuhito Nannya, Yoichi Imai, and Mineo Kurokawa. "AML1/Runx1 Is a Cytoplasmic Attenuator of NF-Kb Signaling: Implication in Pathogenesis and Targeted Therapy of AML1-Related Leukemia." Blood 114, no. 22 (November 20, 2009): 1962. http://dx.doi.org/10.1182/blood.v114.22.1962.1962.
Full textDissertations / Theses on the topic "NF-kB activity"
Lippolis, Davide Giosuè. "Stochastic modeling of fluctuations in the NF-kB activity of neoplastic cells." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2020. http://amslaurea.unibo.it/20550/.
Full textGuo, Canhui. "Mechanism of Anti-Cancer Activity of 9-Aminoacridine Based Drugs." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1216215825.
Full textLunazzi, Giulia 1981. "Analysis of NFAT5 expression and activity in response to toll-like receptors." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/666120.
Full textEn las células del sistema inmunitario innato, la estimulación de los receptores de tipo Toll (TLR) activa la expresión de un programa génico pro-inflamatorio y antimicrobiano que está controlado por una red de reguladores transcripcionales. Hemos demostrado que el NFAT5, perteneciente a la familia de factores de transcripción Rel y previamente caracterizado como un factor de respuesta a estrés osmótico, es importante para la expresión de un grupo de genes de respuesta a TLRs, entre ellos Nos2, Il6 y Tnf. El reclutamiento del NFAT5 a sus genes diana requiere la actividad de IKKβ, la síntesis de novo de proteínas y es sensible a la acción de las deacetilasas de histonas. Resulta interesante el hecho de que el NFAT5 es esencial para responder a bajas dosis de ligando de los TLRs, y que regula grupos de genes específicos dependiendo de la intensidad del estímulo. También mostramos que NFAT5 facilita la accesibilidad de la cromatina en macrófagos, permitiendo el reclutamiento de reguladores transcripcionales como p65/NF-kB, c-Fos y p300 a sus regiones diana. Utilizando Nos2 como un gen cuya inducción es más dependiente de NFAT5 a bajas dosis de LPS, demostramos que el NFAT5 controla el reclutamiento de p65 gracias a que facilita la actividad de las demetilasas de H3K27, pero sin influir en la unión del complejo Polycomb 2 ni JMJD3. En conclusión, esta tesis caracteriza al NFAT5 como un nuevo regulador del sistema inmunitario implicado en el control de la accesibilidad local de la cromatina en respuesta a baja carga de patógenos.
FORLONI, MATTEO. "Immunogenicity of neuroblastoma tumors is controlled by impaired activity of NF-kB and IRF1 transcription factors." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/1424.
Full textLow expression of major histocompatibility complex class I (MHC I) molecules on the cell surface allows tumors to evade the host T cell-based immune response. These abnormalities are often related to either genetic defects of MHC I genes or aberrant expression of antigen processing machinery (APM) components. Neuroblastoma (NB), the most common solid extracranial cancer of childhood, is not an exception. MHC I surface expression is virtually undetectable in the most NB cell lines and primary tumors, and upregulated by gamma-interferon (IFN-γ). This phenotype is compatible with defects in the regulation of antigen processing and presentation components. In this study, the molecular mechanism underlying low immunogenicity in neuroblastoma was investigated. Amplification of the MYCN oncogene characterizes the most aggressive forms of NB and is believe to downregulate expression of MHC class I molecules. Although an inverse correlation between MYCN and MHC I has been reported in human NB cell lines, a direct demonstration of the MYCN-mediated down-regulation of MHC I expression has been questioned. Herein, we demonstrate that MYCN is not responsible for low MHC I, ERAP1 and ERAP2 protein levels in human NB cell lines, since their expression is not affected by neither transfection-mediated overexpression nor siRNA suppression of MYCN. Instead, we identified NF-kB and IRF1 as the main factors involved in the transcriptional regulation of MHC I and ERAPs proteins. By chromatin immunoprecipitation assay, we show a recruitment of p65 NF-kB to the MHC I, ERAP1 and ERAP2 promoters that is proportional with the expression of these genes. Moreover, low nuclear activity of both NF-kB and IRF1 factors correlated with the MHC I, ERAP1 and ERAP2-low phenotype of the most aggressive NB cell lines. Overexpression of either the transcription factors alone rescued the MHC I, ERAP1 and ERAP2-low phenotype, but only partially and in a cell-type depending manner. Important, the co-transfection of both NF-kB and IRF1 cooperated to strongly enhance the transactivation of MHC I, ERAP1 and ERAP2 in any cell lines. Notheworthy, NF-kB and IRF1 acted in a synergistic manner. We found an intriguing parallel in primary NB tumors, in fact, nuclear p65 was detected in the maturing neuroblastic cells (i.e. ganglionic cells) which express higher levels of MHC I molecules in human NB specimens. These findings provide molecular insight into defective MHC I expression in NB tumors and indicate that activating NF-kB and IRF1 in MHC I-low, aggressive NB cells could be instrumental for successful application of T cell-based immunotherapy.
Gadd, Samantha. "Acetaminophen-induced proliferation of estrogen-responsive breast cancer cells is associated with increased c-mcy RNA expression and NF-kB activity." Morgantown, W. Va. : [West Virginia University Libraries], 2001. http://etd.wvu.edu/templates/showETD.cfm?recnum=2016.
Full textTitle from document title page. Document formatted into pages; contains xi, 147 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 128-143).
Tong, Lingying. "The Role of Nitric Oxide Synthase and Carnosol in UVB-induced NF-κB Activity and Skin Damage." Ohio University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1412768175.
Full textBrittain, George C. IV. "A Novel Role for the TRAFs as Co-Activators and Co-Repressors of Transcriptional Activity." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/451.
Full textQin, Zhihua. "SAMHD1 Negatively Regulates the Innate Immune Responses to Inflammatory Stimuli and Viral Infection." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1587587968104986.
Full textMOL, MARCO HENDRIKUS ADRIANUS. "Analytical Strategies for the Identification and Characterization of RAGE Binders of Proinflammatory mediators. AGEs and ALES." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/675044.
Full textTadlaoui, Hbibi Ali. "Détection de facteurs de transcription actifs dans le cancer colorectal et inhibition spécifique de leur activité par des oligonucléotides leurres : applications à STAT3 et NF-kB." Paris 13, 2008. http://www.theses.fr/2008PA132023.
Full textThe important role of transcription factors such as STAT3 and Nf-kB in biological processes, and their involvement in oncogenesis, justifies the numerous studies on these factors. To inhibit and control their activities appears to be promising therapeutic approach. Firstly, we have shown that STAT3 is constitutively activated in colon cancer and is associated with histopronostics features. In secondly, we inhibited the transcription factors STAT3 and NF-kB in cancer cell lines, we using decoy oligonucleotide containing the consensus target ssequences of these two factors. The decoy oligonucleotides induce the death of a cell line of colon cancer (SW480), however, the decoy ODN of STAT3 was found to interact with STAT1 and prevent IFNy action. Thus, it's of interest to inhibit transcription factors in tumor cells but specific issues are not resolved
Book chapters on the topic "NF-kB activity"
Goh, Fui G., Helen Banks, and Irina A. Udalova. "Detecting and Modulating the NF-kB Activity in Human Immune Cells: Generation of Human Cell Lines with Altered Levels of NF-κB." In Methods in Molecular Biology™, 39–54. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-530-9_4.
Full textConference papers on the topic "NF-kB activity"
Hartley, Antja-Voy, Benlian Wang, Masaru Miyagi, Rasika Mundade, James Hamilton, and Tao Lu. "Abstract 3346: PRMT5-mediated methylation of YBX1 regulates NF-kB activity in colorectal cancer." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3346.
Full textGamboa-Cedeño, Angélica María, Mariángeles castillo, Victoria Otero, Natalia Schutz, Dorotea Fantl, Federico Jauk Vitali, Hernán García Rivello, Myriam Nuñez, and Stella Maris Ranuncolo. "Abstract 4032: The alternative NF-kB pathway activity in refractory and relapsed Hodgkin lymphoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4032.
Full textGamboa-Cedeño, Angélica María, Mariángeles castillo, Victoria Otero, Natalia Schutz, Dorotea Fantl, Federico Jauk Vitali, Hernán García Rivello, Myriam Nuñez, and Stella Maris Ranuncolo. "Abstract 4032: The alternative NF-kB pathway activity in refractory and relapsed Hodgkin lymphoma." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4032.
Full textPayne, Julia G., Emily L. Porter, Darrell N. Kotton, and Andrew P. Wilson. "In Vivo NF-kB Activity In A Mouse Model With RelA-Deficient, Lentivirally Transduced Alveolar Macrophages." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1366.
Full textZhang, Daoxiang, Lin Li, Hongmei Jiang, Jinsheng Yu, Brett Knolhoff, Richard Head, Albert C. Lockhart, et al. "Abstract 181: Constitutive IRAK1/4 kinase activation contributes to NF-kB activity and chemoresistance in pancreatic cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-181.
Full textMao, Sun-Zhong, Xiaobing Ye, and Shu F. Liu. "LPS Down-Regulates Specificity Protein 1 DNA Binding Activity Through Nf-&kB Signaling Pathway In Endotoxemic Mice." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5772.
Full textRamos, K. S., E. Wilson, E. S. Williams, and A. Ridall. "OXIDATIVE INJURY ACTIVATES OSTEOPONTIN SIGNALING AND INDUCES MATRIX-DEPENDENT CHANGES OF NF-kB ACTIVITY IN VASCULAR SMOOTH MUSCLE CELLS." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.311.
Full textPantaleon-Garcia, J., V. Kulkarni, T. C. Reese, S. Wase, Y. Wang, and S. E. Evans. "Transcriptional Cooperation Between RelA and Jun/Fos Promotes Differential NF-kB Activity Required for Inducible Epithelial Resistance Against Viral Pneumonia." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1180.
Full textYee, Michelle Y., Stephen J. Chong, and Shazib Pervaiz. "Abstract 440: The oncogenic activity of a pro-oxidant intracellular milieu is associated with redox dependent activation of NF-kB." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-440.
Full textHussain, Showket, Neha Singh, Irfana Salam, Mohammad A. Bhat, Nandita Kakkar, Mohammad M. Mir, Mushtaq A. Siddiqi, et al. "Abstract 2722: Transcription factor NF-kB in esophageal squamous cell carcinoma: Alterations in activity and expression during Human Papillomavirus infection." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2722.
Full textReports on the topic "NF-kB activity"
Nettles, Kendall W., and Geoffrey Greene. Estrogen Receptor Inhibition of NF-kB Activity in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada437786.
Full textBeg, Amer A. Potentiation of T Lymphocyte Responses by Modulating NF-kB Activity in Dendritic Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada437633.
Full textGuo, Shangqin, and Gail Sonenshein. Role of TGR-B1-Mediated Down Regulation of NF-kB/Rel Activity During Growth Arrest of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2001. http://dx.doi.org/10.21236/ada396154.
Full textGuo, Shangqin. Role of TGF-1B1-Mediated Down Regulation of NF-kB/Rel Activity During Growth Arrest of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, November 2002. http://dx.doi.org/10.21236/ada413313.
Full textKim, Dong. Role of TGF-B1-Mediated Down Regulation of NF-kB/Rel Activity During Growth Arrest of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2000. http://dx.doi.org/10.21236/ada393055.
Full text