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Статті в журналах з теми "Facteurs de transcription NRF2"
Patra, Upayan, Urbi Mukhopadhyay, Arpita Mukherjee, Rakesh Sarkar, and Mamta Chawla-Sarkar. "Progressive Rotavirus Infection Downregulates Redox-Sensitive Transcription Factor Nrf2 and Nrf2-Driven Transcription Units." Oxidative Medicine and Cellular Longevity 2020 (April 6, 2020): 1–48. http://dx.doi.org/10.1155/2020/7289120.
Повний текст джерелаKondratenko, N. D., L. A. Zinovkina, and R. A. Zinovkin. "Transcription Factor NRF2 in Endothelial Functions." Молекулярная биология 57, no. 6 (November 1, 2023): 1058–76. http://dx.doi.org/10.31857/s0026898423060101.
Повний текст джерелаPlafker, Kendra S., and Scott M. Plafker. "The ubiquitin-conjugating enzyme UBE2E3 and its import receptor importin-11 regulate the localization and activity of the antioxidant transcription factor NRF2." Molecular Biology of the Cell 26, no. 2 (January 15, 2015): 327–38. http://dx.doi.org/10.1091/mbc.e14-06-1057.
Повний текст джерелаScoazec, Jean-Yves. "Facteurs de transcription : quelles applications diagnostiques ?" Annales de Pathologie 32, no. 5 (November 2012): S32—S33. http://dx.doi.org/10.1016/j.annpat.2012.08.003.
Повний текст джерелаHe, Feng, Xiaoli Ru, and Tao Wen. "NRF2, a Transcription Factor for Stress Response and Beyond." International Journal of Molecular Sciences 21, no. 13 (July 6, 2020): 4777. http://dx.doi.org/10.3390/ijms21134777.
Повний текст джерелаTamir, Tigist Y., Brittany M. Bowman, Megan J. Agajanian, Dennis Goldfarb, Travis P. Schrank, Trent Stohrer, Andrew E. Hale, et al. "Gain-of-function genetic screen of the kinome reveals BRSK2 as an inhibitor of the NRF2 transcription factor." Journal of Cell Science 133, no. 14 (June 16, 2020): jcs241356. http://dx.doi.org/10.1242/jcs.241356.
Повний текст джерелаMalloy, Melanie Theodore, Deneshia J. McIntosh, Treniqka S. Walters, Andrea Flores, J. Shawn Goodwin, and Ifeanyi J. Arinze. "Trafficking of the Transcription Factor Nrf2 to Promyelocytic Leukemia-Nuclear Bodies." Journal of Biological Chemistry 288, no. 20 (March 29, 2013): 14569–83. http://dx.doi.org/10.1074/jbc.m112.437392.
Повний текст джерелаKondratenko, N. D., L. A. Zinovkina, and R. A. Zinovkin. "Transcription Factor NRF2 in Endothelial Functions." Molecular Biology 57, no. 6 (December 2023): 1052–69. http://dx.doi.org/10.1134/s0026893323060092.
Повний текст джерелаMcIntosh, Deneshia J., Treniqka S. Walters, Ifeanyi J. Arinze, and Jamaine Davis. "Arkadia (RING Finger Protein 111) Mediates Sumoylation-Dependent Stabilization of Nrf2 Through K48-Linked Ubiquitination." Cellular Physiology and Biochemistry 46, no. 1 (2018): 418–30. http://dx.doi.org/10.1159/000488475.
Повний текст джерелаMaruyama, Atsushi, Keizo Nishikawa, Yukie Kawatani, Junsei Mimura, Tomonori Hosoya, Nobuhiko Harada, Masayuki Yamamato, and Ken Itoh. "The novel Nrf2-interacting factor KAP1 regulates susceptibility to oxidative stress by promoting the Nrf2-mediated cytoprotective response." Biochemical Journal 436, no. 2 (May 13, 2011): 387–97. http://dx.doi.org/10.1042/bj20101748.
Повний текст джерелаДисертації з теми "Facteurs de transcription NRF2"
Fourquet, Simon. "Régulation redox des facteurs des transcription de la famille CNC-bZip Nrf2 et Bach2." Phd thesis, Université Paris Sud - Paris XI, 2008. http://tel.archives-ouvertes.fr/tel-00553306.
Повний текст джерелаGenard, Romain. "Rôle du facteur de transcription Nrf2 dans l'immunomodulation induit par les adjuvants vaccinaux." Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS230/document.
Повний текст джерелаVaccine adjuvants are able to boost immune response toward antigens when there are simultaneously injected. Some of these adjuvant mimic danger signals, such as Toll like receptors (TLR) agonists or NOD-like receptors agonists, required for dendritic cell (DC) activation. DC are essentiales for adaptative immune response against antigens : they acquire mature phenotype, controlled by MAPK and NF-kB signaling pathway, leading to antigen presentation and specific immune response. The Nrf2/keap1 signaling pathway, mainly involves in xenobiotics detoxication and oxidative stress control, can be activate by TLR agonists, such as LPS (TLR 4 agonist).We showed that R848 (TLR 7/8 agonist) and MDP (NOD2 agonist) could induce Nrf2’s target genes transcription in murines dendritic cells (BMDC). Nrf2 seems also to be part of inflammatory cytokines production in response to LPS or R848 and modulated T lymphocyte proliferation induced by MDP pre-treated BMDC. Moreover, Nrf2 appears to play a role in specific antibodies response against an antigen in mice. . In fact, Tetanus toxoid (TT) injection induces higher titer of antibodies anti-TT in nrf2-/- mice compared to nrf2+/+ mice. This increase is also correlated with more specific B lymphocytes in bone marrow and spleen after TT immunisation
Saliou, Alexa. "Study of cellular senescence in Glioblastoma : Application for the development of companion therapies." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL036.
Повний текст джерелаDiffuse gliomas are the most common primary tumor of the adult central nervous system. Glioblastoma (GBM) accounts for the most aggressive subtype. Conventional treatments remain ineffective as the vast majority of tumors relapse and patient survival remains limited (15 months). Due to a highly immunosuppressive microenvironment, immunotherapies also fail to treat GBM. Thus, the development of novel therapies is crucial to increase patient survival. To this end, we investigate the role of cellular senescence during gliomagenesis. In the first part of my project, we demonstrated the pro-tumoral action of malignant senescent cells in GBM using patient tumor specimens and a mouse GBM model. Indeed, partial removal of malignant senescent cells modulates the immune compartment and improves survival of GBM-bearing mice. In addition, we identified the NRF2 transcription factor, as a determinant of the senescent phenotype. Based on mouse GBM transcriptomic data, we defined a 31-gene senescence signature which is conserved in human lesions. Its high expression correlates with poor outcomes in patients. These findings highlight senolytics as a potential adjuvant therapy to treat GBM. In the light of these findings, we hypothesized that (i) exploring NRF2 signaling may provide new therapeutic insights and that (ii) senolytic-driven modulation of the immune compartment may prime GBM to respond to immunotherapy. Single cell analysis of malignant and immune paired fractions from control (miR-ctl) and NRF2-KD (miR-NRF2) immunocompetent mouse GBMs showed a decrease in the malignant senescent cluster upon NRF2-KD, strengthening NRF2 as a determinant of senescence. NRF2-KD in tumoral cells enhances cellular plasticity and enables the emergence of clusters, characterized by differential upregulation of genes coding for major histocompatibility complex (MHC) molecules. This suggests that NRF2 indirectly promotes immunogenicity in GBM. Immune transcriptomic analysis and immunophenotyping by flow cytometry will help confirming these results. Furthermore, we observed that GBM-bearing mice treated with a genetic senolytic (p16-3MR+GCV) displayed an upregulation of gene signatures associated to the antigen presentation machinery. Thus, we hypothesized that senolytic and immune checkpoint blockade (ICB) might synergize and delay tumor growth. We subjected mouse cohorts to different combination of senolytic and ICBs and highlighted a specific cocktail which positively benefited mouse survival. Thus, our preliminary results suggest that senolytic might potentiates immune checkpoint blockade to hinder GBM progression. Further work is needed to immunophenotype control and treated tumors, investigate treatment-related microenvironment modifications as well as identify the immune subtype driving the response to immunotherapy. Altogether, these results open promising avenues for personalized therapies in the context of senescence enriched GBMs. Also, identification of novel senolytics associated to NRF2 could beneficiate several pathologies in which senescence role is critical
Fourquet, Simon. "Régulation redox des facteurs des transcriptions de la famille CNC-bZip Nrf2 et Bach2." Paris 11, 2008. http://www.theses.fr/2008PA112305.
Повний текст джерелаIn mammalian cells, CNC-bZip family members Nrf2 and Bach2 participate in the cellular control of prooxidant species. Many classes of electrophilic compounds allow Nrf2 to transactivate ARE cis-regulated genes coding for detoxifying enzymes, so as to achieve a homeostatic control at non toxic levels for these compounds. Activation of Bach2, which is a transcriptional repressor, participate in cell killing in response to some electrophilic species, especially in B cell. We sought to determine the mechanisms involved in Nrf2 and Bach2 activation by oxidant molecules produced by activated macrophages during inflamation, such as hydrogen peroxide and nitric oxide. We described the oxidation through disulfide bonds of Bach2 and Keap1, the main regulator of Nrf2 activation. Mutagenesis experiment identified the cysteines engaged in disulfides in the different oxidation forms of Keap1. We also showed that Keap1 oxidation leads to a derepression of Nrf2, thereby to its activation. The nature and function of Bach2 oxidation couldn't be completely understood. We described a positive regulation of peroxiredoxin Prx1 of Nrf2 and Bach2 oxidation, which as unexpected since the peroxidase activity sould have hampered other oxidation reactions. We propose a mechanistic model based on the Orp1-Yap1 peroxyde sensing system of S. Cerevisiae to rationalize this observation
Tertil, Magdalena. "Role of thymidine phosphorylase and Nrf2 transcription factor in non-small cell lung carcinoma growth and angiogenesis." Thesis, Orléans, 2013. http://www.theses.fr/2013ORLE2043.
Повний текст джерелаNrf2, heme oxygenase-1 (HO-1) and thymidine phosphorylase (TP) are considered as potential targets for combinatorial anti-cancer therapies. The aim of the study was to investigate the interplay of these proteins in regulation of growth and angiogenesis in non-small cell lung carcinoma (NSCLC) cells NCI-H292. Stable overexpression of Nrf2 (NCI-Nrf2 cell line) resulted in decreased cell proliferation and migration in vitro, upregulation of tumor suppressor microRNAs and downregulation of oncogenic miR-378 and many MMPs. Silencing of HO-1 in NCI-Nrf2 cells partially reversed the effect on MMP-1, MMP-3 and miR-378. NCI-Nrf2 cells exhibited increased expression of proangiogenic factors IL-8, angiopoietin-1 and TP, which was also upregulated in cell overexpressing HO-1. In both models, the effect was TP reversible by siRNA targeted at HO-1 and possibly mediated by modulation of oxidative status of the cell. Moreover, it was observed that overexpression of TP in vitro attenuated proliferation and migration of NSCLC cells, but increased their angiogenic potential. In vivo, NCI-TP tumors tended to grow faster, were better oxygenated and exhibited increased expression of inflammatory cytokines IL-1β and IL-6. Correlation of TP with IL-1β and IL-6 was also confirmed in clinical samples from NSCLC patients. Overall, our results enforce the notion of targeting TP for treatment of NSCLC
Olagnier, David. "Rôle des facteurs de transcription PPARgamma et Nrf2 dans la modulation de l'expression du récepteur scavenger CD36 des macrophages : implication dans la physiopathologie du paludisme." Toulouse 3, 2011. http://thesesups.ups-tlse.fr/1308/.
Повний текст джерелаMalaria remains the deadliest parasitic disease in the world. The introduction of new pharmacological approaches in the fight against this pathogen is essential. Macrophages through the expression of CD36 receptor play a crucial role in the recognition and the elimination of P. Falciparum infected erythrocytes. Therefore, maintaining an elevated level of CD36 receptor on the surface of macrophages is a crucial element in the struggle against the parasite. The establishment of malaria infection is always associated with an excessive production of pro-inflammatory mediators. In this work, we show in vitro that inflammatory processes negatively regulate the expression of CD36 receptor on the surface of human and mouse macrophages and hence decrease the clearance of parasitized erythrocytes. In these inflammatory conditions, we demonstrate that PPARgamma activators are ineffective to promote CD36 expression on macrophages, a phenomenon directly associated with a defect of both PPARgamma expression and activation. However, we highlight here for the first time that the activation of the Nrf2 transcription factor controls independently of PPARgamma the expression of CD36 receptor and its antiplasmodial function. All these results have been reproduced in vivo in a murine malaria model where only Nrf2 activators and not PPARgamma ligands contribute to improve the outcome of infection. Collectively, these data highlight the important role of the Nrf2 transcription factor in the control of malaria through the modulation of CD36 expression on macrophages
El, ali Zeina. "Rôle du facteur de transcription Nrf2 dans le contrôle de l'allergie cutanée en réponse aux molécules allergisantes." Thesis, Paris 11, 2013. http://www.theses.fr/2013PA114847/document.
Повний текст джерелаAllergic reactions such as contact hypersensitivity (CHS) are a problem of public health occurring after repeated exposures to contact sensitizers. CHS is a common skin disease involving dendritic cells (DC) playing a key role in this pathology. Contact sensitizers, like dinitrochlorobenzene (DNCB) or cinnamaldehyde (CinA) are known to induce reactive oxygen species (ROS) production. The Nrf2/Keap1 pathway is central for detoxification. In the absence of a chemical stress, Keap1 associates with Nrf2 and leading to its degradation. In the presence of an electrophilic compound like contact sensitizers, Keap1’s conformation is modified leading to Nrf2 translocation to the nucleus and transcription of its target genes [heme-oxygénase 1 (ho-1), NADPH quinone oxydoreductase (nqo1), glutathione-s-transferase (gst)]. We showed, for the first time, that Nrf2 controls the loss of mitochondrial membrane potential and caspase-3/7 activity in DC activated by contact sensitizers. In the absence of Nrf2, DNCB and CinA induced DC apoptosis via caspase activation involved in intrinsic pathway of apoptosis also called ‘mitochondrial pathway’. This apoptosis was mainly mediated by the production of ROS in response to DNCB. However, ROS faintly control CinA-induced cell death. We also showed that Nrf2 controls the transcription of the anti-apoptotic gene bcl-2 in response to DNCB or CinA and also the transcription of immune related and antioxidant genes that could be implicated in DC apoptosis.Otherwise, we also showed that Nrf2 plays a key role in sensitization and elicitation phases of CHS and even in the irritation phase. Adoptive transfer experiments showed that Nrf2 plays a crucial role in DC during CHS.Finally, we showed that Nrf2 regulates skin Treg and participates to skin tolerance
Helou, Doumet. "Rôle du facteur de transcription Nrf2 dans la régulation des fonctions du neutrophile in vitro et dans l’allergie cutanée." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS305/document.
Повний текст джерелаNeutrophils form the first line of defense against infectious agents. However, their uncontrolled activation may exacerbate certain inflammatory conditions such as cutaneous allergies. Our team has previously shown that Nrf2 transcription factor known for its antioxidant role, regulates skin inflammation in contact hypersensitivity (CHS). Thus, our work was carried out to evaluate in vitro the involvement of Nrf2 pathway in neutrophil functions and to identify Nrf2 role in neutrophil recruitment and activation in CHS.In vitro, we showed that the protein Nrf2 was highly expressed in bone marrow neutrophils. Nrf2 is functional in stimulated neutrophils: it activates the transcription of cytoprotective genes and downregulates that of inflammatory genes. Thus, pretreatment of neutrophils with an Nrf2 activator such as sulforaphane reduces the production of reactive oxygen species (ROS) in response to stimulation. In parallel, Nrf2 does not affect two key functions of neutrophil, phagocytosis and netosis.Finally, Nrf2 is essential for optimal migration of neutrophils toward chemokines. In CHS induced by the dinitrochlorobenzene (DNCB), Nrf2 indirectly regulates the recruitment of neutrophils, through regulation of skin oxidant stress and inflammatory pathways that are involved in chemokines production, including CCL2, CCL4 and CCL11. In addition, Nrf2 induces the up-regulation of scavenger CD36 in macrophages and thus increases their ability to eliminate apoptotic neutrophils leading to the resolution of inflammation.In conclusion, Nrf2 activation in neutrophils participates in the control of ROS production and migration. In addition, Nrf2 emerges as an important effector in the control of neutrophil recruitment and clearance during the skin inflammatory response to allergenic molecules. The demonstration of Nrf2 protective mechanisms leads us to suggest this protein as a new therapeutic target in the control of chronic skin inflammations
Raffalli, Chloé. "Les allergies cutanées aux fragrances : mécanisme d'action et rôle du facteur de transcription Nrf2. Du modèle 2D au modèle 3D." Thesis, Université Paris-Saclay (ComUE), 2018. http://www.theses.fr/2018SACLS045/document.
Повний текст джерелаAllergic contact dermatitis (ACD) represents a severe health problem. It is a dendritic cells (DCs) mediated skin disease caused by repeated exposure to an allergenic compound. ACD cases of fragrances in general population is estimated from 1.7 % to 4.1%. Contact sensitizers are compounds termed haptens and they will form a conjugate with epidermis and dermis proteins. Example is cinnamaldehyde (CinA), a molecule found in cinnamon. Linalool and limonene are terpenes found in lavender and oranges. In contact with the air, they will autoxidize to form highly allergenic compounds: allylic hydroperoxides. The first aim of this thesis was to study the mechanism of action of those terpenes and their respective allylic hydroperoxides on THP-1 cell-line, described as a surrogate of DCs. The transcription factor Nrf2 is playing a major role in oxidative stress and was also investigated.Consumers of cosmetic products are exposed to low quantities of allergenic compounds, but several times a day or a week. We wanted to study repeated exposure of low concentration of haptens on the skin.KCs also play a key role in ACD: they are the first cells that will encounter the allergenic compound in the skin. The second aim of this thesis was to study the impact of repeated exposure of low concentrations of CinA on those KCs and more particularly on the epidermis differenciation, using a 3D organotypic culture of skin
Salamito, Mélanie. "Le facteur de transcription antioxydant NRF2 comme nouveau régulateur de la matrice extracellulaire des fibroblastes de peau humaine." Thesis, Lyon, 2020. http://www.theses.fr/2020LYSEN058.
Повний текст джерелаThe nuclear factor-erythroid 2-related factor 2 (NRF2) is a transcription factor involved in cell defense against oxidative and xenobiotic stresses. SKN-1, the nematode homologue of NRF2 is a master regulator of longevity that, under specific metabolic conditions, surprisingly acts through the activation of collagens expression. Fibroblasts are the major producers and organizers of collagen-rich tissues and, as such, play a key role in dermis homeostasis. Therefore, we investigated the potential new role of NRF2 in regulating extracellular matrix (ECM) expression in human skin fibroblasts. Dysregulation of NRF2 was realized using siRNA and shRNA. A global transcriptomic analysis of siNrf2 human skin fibroblasts performed by RNA-seq revealed that, in addition to known NRF2 targets, matrisome and tissue skeleton genes were the most represented gene sets, including some key ECM genes. Analysis of ECM production and organization was further conducted in cultured shNrf2 fibroblasts using a combination of microscopies (SHG, confocal, TEM and AFM). Long-term effect of silencing NRF2 in fibroblasts (shNrf2) resulted in defects in collagen expression and fibril formation, likely due to a disturbed collagen I to collagen V ratio. Interestingly, a transcription factor involved in connective tissue disease and described as a regulator of collagen expression was identified as a novel target of NRF2. Immunofluorescence staining of silenced NRF2 fibroblasts (siRNA and shRNA) strikingly revealed that NRF2 downregulation impacts its translocation rate into the nucleus. Our results demonstrate that silencing NRF2 impacts ECM and especially collagens in human skin fibroblasts. A transcription factor known to regulate collagen expression, could act as a specific cofactor of NRF2 in the regulation of ECM gene expression. NRF2 can thus be considered as a novel regulator of ECM genes in human skin fibroblasts and represents a new target to maintain dermis homeostasis
Книги з теми "Facteurs de transcription NRF2"
Stephen, Goodbourn, ed. Eukaryotic gene transcription. Oxford: IRL Press at Oxford University Press, 1996.
Знайти повний текст джерелаLatchman, David S. Eukaryotic transcription factors. 5th ed. Great Britain: Academic Press, 2008.
Знайти повний текст джерелаLatchman, David S. Eukaryotic transcription factors. 5th ed. Amsterdam: Elsevier/Academic Press, 2008.
Знайти повний текст джерелаE, Angel Peter, and Herrlich Peter 1940-, eds. The fos and jun families of transcription factors. Boca Raton: CRC Press, 1994.
Знайти повний текст джерелаT, Smale Stephen, and NetLibrary Inc, eds. Transcriptional regulation in eukaryotes: Concepts, strategies, and techniques. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press, 2000.
Знайти повний текст джерелаB, La Thangue Nicholas, and Bandara Lasantha R, eds. Targets for cancer chemotherapy: Transcription factors and other nuclear proteins. Totowa, N.J: Humana Press, 2002.
Знайти повний текст джерелаB, La Thangue Nicholas, and Bandara Lasantha R, eds. Targets for cancer chemotherapy: Transcription factors and other nuclear proteins. Totowa, N.J: Humana Press, 2002.
Знайти повний текст джерелаNATO Advanced Study Institute on Molecular Mechanisms of Signal Transduction (1999 Spetsai Island, Greece). Molecular mechanisms of signal transduction. Amsterdam: IOS Press, 2000.
Знайти повний текст джерелаMorales-Gonzalez, Jose Antonio, Angel Morales-Gonzalez, and Eduardo Osiris Madrigal-Santillan, eds. A Master Regulator of Oxidative Stress - The Transcription Factor Nrf2. InTech, 2016. http://dx.doi.org/10.5772/62743.
Повний текст джерелаEukaryotic transcription factors. 4th ed. Oxford: Academic, 2004.
Знайти повний текст джерелаЧастини книг з теми "Facteurs de transcription NRF2"
Reddy, Narsa M., Wajiha Qureshi, Haranath Potteti, Dhananjaya V. Kalvakolanu, and Sekhar P. Reddy. "Regulation of Mitochondrial Functions by Transcription Factor NRF2." In Mitochondrial Function in Lung Health and Disease, 27–50. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0829-5_2.
Повний текст джерелаPfefferlé, Marc, and Florence Vallelian. "Transcription Factor NRF2 in Shaping Myeloid Cell Differentiation and Function." In Transcription factors in blood cell development, 159–95. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-62731-6_8.
Повний текст джерелаDinkova-Kostova, Albena T., Ying Zhang, Sharadha Dayalan Naidu, Rumen V. Kostov, Ashley Pheely, and Vittorio Calabrese. "Sulfhydryl-Reactive Phytochemicals as Dual Activators of Transcription Factors NRF2 and HSF1." In 50 Years of Phytochemistry Research, 95–119. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-00581-2_6.
Повний текст джерелаLambros, Mandy L., and Scott M. Plafker. "Oxidative Stress and the Nrf2 Anti-Oxidant Transcription Factor in Age-Related Macular Degeneration." In Retinal Degenerative Diseases, 67–72. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_10.
Повний текст джерелаFlorczyk, Urszula, Alicja Józkowicz, and Józef Dulak. "Nrf2 Transcription Factor and Heme Oxygenase-1 as Modulators of Vascular Injury and Angiogenesis." In Angiogenesis and Vascularisation, 213–39. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1428-5_10.
Повний текст джерелаMendonca, Patricia, and Karam F. A. Soliman. "Nutraceutical Activation of the Transcription Factor Nrf2 as a Potential Approach for Modulation of Aging." In Nutraceuticals for Aging and Anti-Aging, 113–31. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003110866-6.
Повний текст джерелаVerma, Neeraj. "NRF2 in Neurological Disorders: A Molecular Beacon for Therapeutics." In The Role of NRF2 Transcription Factor [Working Title]. IntechOpen, 2024. http://dx.doi.org/10.5772/intechopen.1004774.
Повний текст джерелаBruneska Gondim Martins, Danyelly, Ananda Cristina de Aguiar, Francielle Maria de Araújo Barbosa, and Glauber Moreira Leitão. "The Dual Role of NRF2 Transcription Factor in Female Cancer." In The Role of NRF2 Transcription Factor [Working Title]. IntechOpen, 2024. http://dx.doi.org/10.5772/intechopen.1005041.
Повний текст джерелаA. Samak, Mai. "Nrf2: The Guardian of Cellular Harmony – Unveiling Its Role in Cell Biology and Senescence." In The Role of NRF2 Transcription Factor [Working Title]. IntechOpen, 2024. http://dx.doi.org/10.5772/intechopen.1005182.
Повний текст джерелаBruneska Gondim Martins, Danyelly, Thaysa Walleria Aragão Santos, Maria Helena Menezes Estevam Alves, and Rosângela Ferreira Frade de Araújo. "The Role of NRF2 Transcription Factor in Metabolic Syndrome." In The Role of NRF2 Transcription Factor [Working Title]. IntechOpen, 2024. http://dx.doi.org/10.5772/intechopen.1005035.
Повний текст джерелаТези доповідей конференцій з теми "Facteurs de transcription NRF2"
Tian, Yijun, Qian Liu, Shengnan Yu, Qian Chu, Yuan Chen, Kongming Wu, and Liang Wang. "Abstract 3587: NRF2-driven KEAP1 transcription in human lung cancers." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-3587.
Повний текст джерелаKweider, N., J. Lambertz, T. Pufe, and W. Rath. "Activation of the Transcription factor Nrf2 involved in human trophoblast syncytialization (in vitro study)." In 28. Deutscher Kongress für Perinatale Medizin. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1607808.
Повний текст джерелаAbalenikhina, Y. V., A. A. Seidkuliyeva, E. D. Rokunov, D. S. Nemtinov, A. V. Shchulkin, and E. N. Yakusheva. "PARTICIPATION OF NUCLEAR FACTOR OF ERYTHROID ORIGIN-2 IN REGU-LATION P-GLYCOPROTEIN IN MODELING ENDOGENOUS OXIDATIVE STRESS." In NOVEL TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2022. http://dx.doi.org/10.47501/978-5-6044060-2-1.251-257.
Повний текст джерелаKweider, N., J. Hock, B. Altunay, U. Pecks, C. Wruck, T. Pufe, and W. Rath. "The transcription factor Nrf2 and the placental inflammatory response; potential implication in the pathogenesis of IUGR." In 28. Deutscher Kongress für Perinatale Medizin. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1607684.
Повний текст джерелаBarker, Emily, John J. Letterio, and Gregory P. Tochtrop. "Abstract 2258: Celastrol shows chemopreventive properties in an inflammatory driven model for colon cancer via induction of Nrf2 transcription." In 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.am2013-2258.
Повний текст джерелаKorfei, M., T. Luboeinski, C. Ruppert, R. Schmidt, M. Wygrecka, W. Seeger, A. Guenther, and P. Markart. "Alveolar Oxidative Stress in Patients with Sporadic Idiopathic Pulmonary Fibrosis Is Associated with Oxidant-Antioxidant Imbalance Despite Induction of the Antioxidant Transcription Factor Nrf2." 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.a2733.
Повний текст джерелаDey, Souvik, Carly M. Sayers, Stacey L. Lehman, Yi Cheng, George J. Cerniglia, Stephen W. Tuttle, Michael D. Feldman, et al. "Abstract 1262: The transcription factor ATF4 regulates resistance to anoikis and promotes metastasis in fibrosarcoma via cooperative upregulation of Heme Oxygenase-1 with Nrf2." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1262.
Повний текст джерелаNovik, Victoria, Irene Bobilev, Andrzej Kutner, Itai Levi, Ofer Shpilberg, Yoav Sharoni, George P. Studzinski, and Michael Danilenko. "Abstract 282A: The Nrf2 transcription factor is a positive regulator of differentiation of acute myeloid leukemia cells induced by vitamin D derivatives and plant polyphenols." 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.am2011-282a.
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