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Relevant bibliographies by topics / Inhibitors of NF-κB activation

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Academic literature on the topic 'Inhibitors of NF-κB activation'

Author: Grafiati

Published: 28 May 2022

Last updated: 30 May 2022

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Journal articles on the topic "Inhibitors of NF-κB activation"

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Han, Bing, Baoan Ji та Craig D. Logsdon. "CCK independently activates intracellular trypsinogen and NF-κB in rat pancreatic acinar cells". American Journal of Physiology-Cell Physiology 280, № 3 (2001): C465—C472. http://dx.doi.org/10.1152/ajpcell.2001.280.3.c465.

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In the cholecystokinin (CCK) hyperstimulation model of acute pancreatitis, two early intracellular events, activation of trypsinogen and activation of nuclear factor-κB (NF-κB), are thought to be important in the development of the disease. In this study, the relationship between these two events was investigated. NF-κB activity was monitored by using a DNA binding assay and mob-1 chemokine gene expression. Intracellular trypsin activity was measured by using a fluorogenic substrate. Protease inhibitors including FUT-175, Pefabloc, and E-64d prevented CCK stimulation of intracellular trypsinog

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Hideshima, Teru, Hiroshi Ikeda, Dharminder Chauhan та ін. "Bortezomib induces canonical nuclear factor-κB activation in multiple myeloma cells". Blood 114, № 5 (2009): 1046–52. http://dx.doi.org/10.1182/blood-2009-01-199604.

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Bortezomib is a proteasome inhibitor with remarkable preclinical and clinical antitumor activity in multiple myeloma (MM) patients. The initial rationale for its use in MM was inhibition of nuclear factor (NF)-κB activity by blocking proteasomal degradation of inhibitor of κBα (IκBα). Bortezomib inhibits inducible NF-κB activity; however, its impact on constitutive NF-κB activity in MM cells has not yet been defined. In this study, we demonstrate that bortezomib significantly down-regulated IκBα expression and triggered NF-κB activation in MM cell lines and primary tumor cells from MM patients

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Hsia, Chih-Wei, Wei-Chieh Huang, Chih-Hao Yang та ін. "Comparison of the Potency of Pterostilbene with NF-κB Inhibitors in Platelet Activation: Mutual Activation by Akt-NF-κB Signaling in Human Platelets". Applied Sciences 11, № 13 (2021): 6149. http://dx.doi.org/10.3390/app11136149.

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Myocardial infarction and cerebral ischemic stroke are prominent causes of death worldwide. Platelets play major roles in these diseases, although they are anucleated cells, but also express the NF-κB. Pterostilbene (PTE) possesses some intriguing pharmacological properties, including the capacity to inhibit platelet activation. We investigated the inhibitory role of PTE in NF-κB-mediated signal events and compared the relative potency with that of classical NF-κB inhibitors. PTE and IκB kinase (IKK) inhibitor, BAY11-7082, and proteasome inhibitor, Ro106-9920, inhibited platelet aggregation; t

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Song, Junbin, та Young-Seuk Bae. "CK2 Down-Regulation Increases the Expression of Senescence-Associated Secretory Phenotype Factors through NF-κB Activation". International Journal of Molecular Sciences 22, № 1 (2021): 406. http://dx.doi.org/10.3390/ijms22010406.

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Senescent cells secrete pro-inflammatory factors, and a hallmark feature of senescence is senescence-associated secretory phenotype (SASP). The aim of this study is to investigate the protein kinase CK2 (CK2) effects on SASP factors expression in cellular senescence and organism aging. Here CK2 down-regulation induced the expression of SASP factors, including interleukin (IL)-1β, IL-6, and matrix metalloproteinase (MMP) 3, through the activation of nuclear factor-κB (NF-κB) signaling in MCF-7 and HCT116 cells. CK2 down-regulation-mediated SIRT1 inactivation promoted the degradation of inhibito

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Frazia, Simone La, Carla Amici та M. Gabriella Santoro. "Antiviral Activity of Proteasome Inhibitors in Herpes Simplex Virus-1 Infection: Role of Nuclear Factor-κB". Antiviral Therapy 11, № 8 (2006): 995–1004. http://dx.doi.org/10.1177/135965350601100805.

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Background Herpes simplex virus type 1 (HSV-1) is a potent inducer of nuclear factor-κB (NF-κB), a cellular transcription factor with a crucial role in promoting inflammation and controlling cell proliferation and survival. Objectives On the basis of the recent demonstration that HSV-1-induced NF-κB is actively recruited to κB-binding sites in the HSV-1 infected-cell protein 0 (ICP0) promoter enhancing viral transcription and replication, we investigated the effect of proteasome inhibitors MG132, MG115 and epoxomicin, which block NF-κB function by preventing the degradation of the inhibitory p

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Nguyen, Anne, Le Su, Belinda Campbell, Neal M. Poulin, and Torsten O. Nielsen. "Synergism of Heat Shock Protein 90 and Histone Deacetylase Inhibitors in Synovial Sarcoma." Sarcoma 2009 (2009): 1–10. http://dx.doi.org/10.1155/2009/794901.

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Current systemic therapies have little curative benefit for synovial sarcoma. Histone deacetylase (HDAC) inhibitors and the heat shock protein 90 (Hsp90) inhibitor 17-AAG have recently been shown to inhibit synovial sarcoma in preclinical models. We tested combinations of 17-AAG with the HDAC inhibitor MS-275 for synergism by proliferation and apoptosis assays. The combination was found to be synergistic at multiple time points in two synovial sarcoma cell lines. Previous studies have shown that HDAC inhibitors not only induce cell death but also activate the survival pathway NF-κB, potentiall

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Kawakami, Atsushi, Tomoki Nakashima, Hideaki Sakai та ін. "Inhibition of Caspase Cascade by HTLV-I Tax Through Induction of NF-κB Nuclear Translocation". Blood 94, № 11 (1999): 3847–54. http://dx.doi.org/10.1182/blood.v94.11.3847.

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Abstract NF-κB is required for prevention of apoptosis. We examined the importance of human T-cell leukemia virus–I (HTLV-I) Tax protein to stimulate NF-κB nuclear translocation, thus preventing apoptosis. Jurkat cells and JPX-9 cells in which the inducible Tax expression plasmid vector was stably transfected were used in the present study. Both Jurkat and Tax− JPX-9 cells had small amounts of basal nuclear NF-κB activity. The addition of NF-κB inhibitors suppressed NF-κB nuclear translocation of the cells, thus inducing apoptosis. Sequential activation of caspases from caspase-8 to caspase-3

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Kawakami, Atsushi, Tomoki Nakashima, Hideaki Sakai та ін. "Inhibition of Caspase Cascade by HTLV-I Tax Through Induction of NF-κB Nuclear Translocation". Blood 94, № 11 (1999): 3847–54. http://dx.doi.org/10.1182/blood.v94.11.3847.423a24_3847_3854.

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NF-κB is required for prevention of apoptosis. We examined the importance of human T-cell leukemia virus–I (HTLV-I) Tax protein to stimulate NF-κB nuclear translocation, thus preventing apoptosis. Jurkat cells and JPX-9 cells in which the inducible Tax expression plasmid vector was stably transfected were used in the present study. Both Jurkat and Tax− JPX-9 cells had small amounts of basal nuclear NF-κB activity. The addition of NF-κB inhibitors suppressed NF-κB nuclear translocation of the cells, thus inducing apoptosis. Sequential activation of caspases from caspase-8 to caspase-3 was shown

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Sizemore, Nywana, Stewart Leung та George R. Stark. "Activation of Phosphatidylinositol 3-Kinase in Response to Interleukin-1 Leads to Phosphorylation and Activation of the NF-κB p65/RelA Subunit". Molecular and Cellular Biology 19, № 7 (1999): 4798–805. http://dx.doi.org/10.1128/mcb.19.7.4798.

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ABSTRACT The work of Reddy et al. (S. A. Reddy, J. A. Huang, and W. S. Liao, J. Biol. Chem. 272:29167–29173, 1997) reveals that phosphatidylinositol 3-kinase (PI3K) plays a role in transducing a signal from the occupied interleukin-1 (IL-1) receptor to nuclear factor κB (NF-κB), but the underlying mechanism remains to be determined. We have found that IL-1 stimulates interaction of the IL-1 receptor accessory protein with the p85 regulatory subunit of PI3K, leading to the activation of the p110 catalytic subunit. Specific PI3K inhibitors strongly inhibit both PI3K activation and NF-κB-dependen

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Bitko, Vira, та Sailen Barik. "Persistent Activation of RelA by Respiratory Syncytial Virus Involves Protein Kinase C, Underphosphorylated IκBβ, and Sequestration of Protein Phosphatase 2A by the Viral Phosphoprotein". Journal of Virology 72, № 7 (1998): 5610–18. http://dx.doi.org/10.1128/jvi.72.7.5610-5618.1998.

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ABSTRACT Respiratory syncytial virus (RSV) activated the RelA (p65) subunit of nuclear factor kappa B (NF-κB) over many hours postinfection. The initial activation coincided with phosphorylation and degradation of IκBα, the cytoplasmic inhibitor of RelA. During persistent activation of NF-κB at later times in infection, syntheses of inhibitors IκBα as well as IκBβ were restored. However, the resynthesized IκBβ was in an underphosphorylated state, which apparently prevented inhibition of NF-κB. Use of specific inhibitors suggested that the pathway leading to the persistent—but not the initial—a

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Dissertations / Theses on the topic "Inhibitors of NF-κB activation"

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Xu, Lu. "New quinazoline analogues as NF-κB activation inhibitors". Scholarly Commons, 2013. https://scholarlycommons.pacific.edu/uop_etds/152.

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NF-κB is a transcription factor protein complex that plays an important role in some cancers and inflammatory responses. It can enhance the proliferation rate, reduce apoptosis, as well as create more blood flow to ensure the survival of cancer. Thus blocking the NF-κB pathway has potential therapeutic benefit. We designed a series of compounds based on quinazoline scaffold pharmacophore model which may have high binding affinity with p50 subunit of NF-κB. The compound series with phenyl substitution at position 2 of quinazoline proved to be more effective at inhibiting NF-κB function both the

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Takeuchi, Junko. "Thioredoxin Inhibits Tumor Necrosis Factor-or Interleukin-1-induced NF-κB activation at the Level Upstream of NF-κB-inducing Kinase". Kyoto University, 2000. http://hdl.handle.net/2433/151398.

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Ember, Stuart William John. "Vaccinia virus protein C4 is an inhibitor of NF-κB activation and contributes to virulence". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/14495.

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Vaccinia virus (VACV) expresses many proteins that subvert the host innate immune response and this thesis describes the characterisation of C4, a VACV protein unstudied hitherto, which was hypothesised to have such a role. C4 is conserved in six orthopoxvirus species and shares 43.7% amino acid identity to VACV protein C16, a known virulence factor. C4 is an intracellular protein that is expressed early during infection and localises to both the cytoplasm and nucleus. Functional screens revealed C4 is an inhibitor of IFNβ promoter activation via the inhibition of NF-κB activation. Mechanistic

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McCoy, Laura Ellen. "Vaccinia virus protein B14, an inhibitor of NF-κB activation, and its counterpart in MVA". Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/5590.

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Vaccinia virus (VACV) encodes multiple proteins which modulate NF-[kappa]B activation to evade the host immune response. One example is B14, a virulence factor that reduces NF-[kappa]B activation via interaction with IKK [Beta]. B14 has orthologues in many VACV strains, including modified virus Ankara (MVA), which lacks many of the immunomodulators present in other VACV strains. Here, the MVA counterpart of B14, protein 183, was characterised. 183R was both removed from MVA and inserted into the B14R locus of a VACV strain Western Reserve (WR) lacking B14R, but in each case there was no change

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Шаталін, Б. О. "Роль активних форм кисню та азоту в механізмах ушкодження сім'яників і сперматозоїдів при поєднаній дії на організм рентгенівського опромінення та нітрату натрію". Thesis, Українська медична стоматологічна академія, 2017. http://essuir.sumdu.edu.ua/handle/123456789/55181.

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В роботі проведена оцінка результатів експериментальних досліджень поєднаної дії на організм лабораторних щурів рентгенівського опромінення та нітрату натрію за показниками розвитку окисно-нітративного стресу в сім’яниках та спермі. На основі проведених досліджень встановлено особливості поєднаної дії на організм лабораторних щурів фракційного рентгенівського опромінення в сумарній дозі 0,24 Гр та нітрату натрію, що виражається в розвитку негативних ефектів у сім’яниках утворенні пероксинітриту, розвитку декомпенсованого пероксидного окиснення ліпідів, зменшенні активності цитохромок

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Geldmeyer-Hilt, Kerstin Verfasser], та Roland [Akademischer Betreuer] [Lauster. "Vitamin D inhibits NF-κB activation in B cells and controls the humoral immune response / Kerstin Geldmeyer-Hilt. Betreuer: Roland Lauster". Berlin : Universitätsbibliothek der Technischen Universität Berlin, 2011. http://d-nb.info/1014619734/34.

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Watanabe, Kenichiro. "Prevention of etoposide-induced apoptosis by Proteasome inhibitors in a human leukemic cell line but not in fresh acute leukemia blasts : A differential role of NF-κB activation". Kyoto University, 2000. http://hdl.handle.net/2433/151424.

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Alsayeqh, Abdullah Fayez. "Activation of the transcription factor NF-κB by Campylobacter jejuni". Thesis, University of Nottingham, 2007. http://eprints.nottingham.ac.uk/27855/.

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Campylobacter is currently the most frequently isolated food-borne bacterial pathogen worldwide. Infections caused by C. jejuni may be self-limiting enteritis or chronic conditions such as Guillain-Barre' syndrome (GBS). Although the mechanisms by which C. jejuni causes disease are not clearly understood, the activation of the transcription factor NF-KB, which controls pro-inflammatory responses, is thought to be an important contributing mechanism for initiating the host's immune responses to C. jejuni infection. Signaling pathways leading to NF-KB by pathogens and/or their products include t

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Oruganti, Sreenivasa Rao. "Regulation of activation of NF-κB by Calmodulin in T-lymphocytes". Doctoral thesis, Umeå universitet, Institutionen för molekylärbiologi (Medicinska fakulteten), 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-46561.

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Nuclear factor kappa B (NF-kB) is a widely expressed family of transcription factors that are involved in a diverse number of processes. These include inflammation or differentiation, survival or apoptosis, and proliferation or cell cycle arrest. NF-kB is usually associated with inhibitory kB proteins (IkB), which mask the nuclear localisation sequence (NLS) of NF-kB and renders it in the cytoplasm. Various stimuli result in the activation of the I kappa B kinase (IKK) protein complex, which phosphorylates IκB proteins and thereby marks them for degradation by the ubiquitin-proteasome pathway.

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Krumbach, Rebekka Luise. "A genetic screen to study NF-κB activation by CpG DNA". Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611106.

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Book chapters on the topic "Inhibitors of NF-κB activation"

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Cusack, James C. "Proteasome-Dependent Regulation of NF-κB Activation." In Proteasome Inhibitors in Cancer Therapy. Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-794-9_11.

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Verstrepen, Lynn, Isabelle Carpentier, and Rudi Beyaert. "The Biology of A20-Binding Inhibitors of NF-κB Activation (ABINS)." In Advances in Experimental Medicine and Biology. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0398-6_2.

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Wrighton, C., R. Hofer-Warbinek, T. Moll, E. Hofer, F. H. Bach, and R. DeMartin. "Inhibition of Endothelial Cell Activation by -Mediated Expression of IκBα, an Inhibitor of the Transcription Factor NF-κB." In Vascular Endothelium. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4899-0133-0_44.

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Chen, Fei, Min Ding, Vince Castranova, and Xianglin Shi. "Carcinogenic metals and NF-κB activation." In Molecular Mechanisms of Metal Toxicity and Carcinogenesis. Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-0793-2_19.

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Poyet, J. L., та E. S. Alnemri. "NF-κB Activation by Card Proteins". У Nuclear Factor кB. Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-010-0163-2_3.

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Courtois, Gilles, Alessandra Pescatore, Jérémie Gautheron, Francesca Fusco, Matilde Valeria Ursini та Anna Senegas. "Genetic Diseases Affecting the Canonical Pathway of NF-κB Activation". У NF-κB-Related Genetic Diseases. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-25850-8_2.

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Qu, Zhaoxia, and Gutian Xiao. "Systematic Detection of Noncanonical NF-κB Activation." In Methods in Molecular Biology. Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2422-6_8.

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Lawrence, Toby. "Role of NF-κB Activation in Macrophages." In Macrophages: Biology and Role in the Pathology of Diseases. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1311-4_21.

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Yamamoto, Y., U. N. Verma та R. B. Gaynor. "Tools to Interfere with NF-κB Activation". У Nuclear Factor кB. Springer Netherlands, 2003. http://dx.doi.org/10.1007/978-94-010-0163-2_9.

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Courtois, Gilles, Alessandra Pescatore, Jérémie Gautheron, Francesca Fusco, Matilde Valeria Ursini та Anna Senegas. "Genetic Diseases Affecting the Non-canonical Pathway of NF-κB Activation". У NF-κB-Related Genetic Diseases. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-25850-8_3.

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Conference papers on the topic "Inhibitors of NF-κB activation"

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Wolfe, Valerie M., Seonghun Park, Marjana Tomic, Peter A. Torzilli, and C. T. Christopher Chen. "Load Down-Regulates TNF-Alpha Induced Cartilage Degradation in Part Through NF-KB and P38 Pathways." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176541.

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Pro-inflammatory cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF), can induce cartilage degradation after acute injury or in inflammatory diseases [1,2,3,7]. The degradative events are coordinated through the elevation and activation of two classes of enzymes, namely matrix metalloproteinases (MMPs) and aggrecanases (ADAMTS-4 and −5) [1,6]. Prior studies suggested that pro-inflammatory responses induced by IL-1β can be inhibited by tensile load [2] and more recently by cyclic compression [8]. It is, however, not clear whether load affects other cytokines, such as TNF-α.

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Gates, KL, N. Wang, H. Trejo, JI Sznajder та PH Sporn. "Hypercapnia Inhibits IL-6 Expression Independently of Acidosis and Downstream of NF-κB Activation." 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.a1318.

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Mebratu, Y. A., J. T. Jones, D. Tassew, T. J. Mariani та Y. Tesfaigzi. "Noxa in Airway Epithelia Inhibits NF-κB Activation and the Development of Cigarette Smoke-induced Emphysema". У American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3785.

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Zhang, Laiqun, Ken Blackwell, Zhaohui Shi та Hasem Habelhah. "Abstract 1267: The RING domain of TRAF2 inhibits TNFα-induced cell death independent of NF-κB activation". У Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1267.

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Rymaszewski, Amy, Michael Straza, Anne Frei та Carmen Bergom. "Abstract 3678: The tumor suppressive small GTPase DiRas3 (ARHI) inhibits proliferation and activation of NF-κB in glioblastoma". У 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.am2016-3678.

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Lee, Sin-Rong, Zhao-Lin Tan, Yuan Chang, I.-Tsang Chiang та Fei-Ting Hsu. "Abstract 978: Magnolol induces apoptosis and inhibits metastasis via suppression of NF-κB activation in human bladder cancer". У Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-978.

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Chen, C. T., S. Park, M. Bhargava, and P. A. Torzilli. "Inhibitory Effect of Mechanical Load on IL-1 Induced Cartilage Degradation Is Mediated by Interferon-Gamma and IL-1 Receptor 1." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193230.

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Matrix remodeling in articular cartilage is regulated by the elevation and activation of aggrecanases (ADAMTS-4 and ADAMTS-5) and matrix metalloproteinases (MMPs) [2–4, 7–9, 10]. Several recent studies from our and other groups have shown that mechanical loading can counteract interleukin 1 (IL-1) induced pro-inflammatory and catabolic events by down-regulating aggrecanases, MMPs, and pro-inflammatory genes [1, 3, 5, 6], but the molecular mechanism is not clear. Many previous studies have shown that the regulation of pro-inflammatory effect of IL-1 come from several aspects: anti-inflammatory

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Yang, Chao, та Qing Jiang. "Abstract 2242: Vitamin E δ-tocotrienol inhibits NF-κB activation by up-regulating A20 in macrophages and suppresses colitis-promoted colon tumorigenesis in mice". У 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.am2017-2242.

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Zhou, Liang, Shuang Chen, Hui Lin та ін. "Abstract 3346: A20/TNFAIP3, a novel target of histone deacetylase inhibitor-induced NF-κB activation, functionally disables the extrinsic apoptotic pathway in human leukemia cells." У Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3346.

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Son, Phil-Soon, Sin-Aye Park, Hye-Kyung Na та Young-Joon Surh. "Abstract 5670: Piceatannol, a catechol-type polyphenol, inhibits phorbol ester-induced NF-κB activation and cyclooxygenase-2 expression in human breast epithelial cells: Cys179 of IKKβ as a potential target". У Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5670.

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Reports on the topic "Inhibitors of NF-κB activation"

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Schwartz, Bertha, Vaclav Vetvicka, Ofer Danai, and Yitzhak Hadar. Increasing the value of mushrooms as functional foods: induction of alpha and beta glucan content via novel cultivation methods. United States Department of Agriculture, 2015. http://dx.doi.org/10.32747/2015.7600033.bard.

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During the granting period, we performed the following projects: Firstly, we differentially measured glucan content in several pleurotus mushroom strains. Mushroom polysaccharides are edible polymers that have numerous reported biological functions; the most common effects are attributed to β-glucans. In recent years, it became apparent that the less abundant α-glucans also possess potent effects in various health conditions. In our first study, we explored several Pleurotus species for their total, β and α-glucan content. Pleurotuseryngii was found to have the highest total glucan concentrati

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