subject:(NF kappaB)

Université Paris-Sud – Paris XI

1. Hatchi, Emeline. Caractérisation des processus d'ubiquitination régulant le facteur de transcription NF-kappaB au cours de l’activation lymphocytaire Rôle de l’E3 ligase TRIM13 et de la déubiquitinase USP34 : Characterization of ubiquitination processes regulating the transcription factor NF-kappaB During lymphocyte activation Role of the E3 ligase TRIM13 and of the deubiquitinase USP34.

Degree: Docteur es, Immunologie, 2014, Université Paris-Sud – Paris XI

URL: http://www.theses.fr/2014PA11T040

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Le facteur de transcription NF-KB joue un rôle essentiel dans le développement, l’homéostasie, la survie du système immunitaire, mais également dans la propagation de certains… (more)

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Le facteur de transcription NF-KB joue un rôle essentiel dans le développement, l’homéostasie, la survie du système immunitaire, mais également dans la propagation de certains lymphomes. L’activation optimale de NF-ΚB en réponse à l’engagement de nombreux immunorécepteurs repose sur la mise en place de larges signalosomes dans lesquels des adaptateurs spécifiques sont recrutés et poly-Ubiquitinylés de façon non-Dégradative. En réponse à des cytokines pro-Inflammatoires ou à l’activation des récepteurs antigéniques, ces adaptateurs ubiquitinylés s’accumulent sur la face cytoplasmique du réticulum endoplasmique (RE) via la protéine du RE metadherine (MTDH) qui assure la propagation du signal NF-KB. Toutefois, la nature des E3 ligases en charge de relayer NF-KB au niveau des organites intracellulaires reste méconnue. C’est pourquoi j’ai réalisé le crible par bioluminescence d’une librairie de siRNA dirigée contre les 46 E3 ubiquitine ligases humaines pourvues d’un domaine transmembranaire qui les ancrent au niveau de différents compartiments cellulaires afin d’étudier leur impact sur l’activation de NF-KB en réponse à une stimulation antigénique dans un modèle de lymphocytes T immortalisés Jurkat. Nous avons identifié la protéine du RE TRIM13 comme un régulateur positif de la signalisation NF-ΚB. Nos données suggèrent un modèle dans lequel TRIM13 régule l’activation de NF-KB en modulant indépendamment l’activation de deux membres clés de la famille NF-KB au cours de l’activation lymphocytaire, RelA (p65) et c-Rel.Lors de cette thèse, j’ai également participé au crible d’une librairie de siRNA ciblant les 96 déubiquitinases (DUBs) codées par le génome humain afin d’identifier celles en charge de ramener les cellules vers leur état basal. Ceci a permis la caractérisation de la protéase spécifique de l’ubiquitine USP34 (Ubiquitin specific protease 34). La réduction des niveaux endogènes de USP34 potentialise l’activation de NF-KB en réponse à l’engagement du récepteur antigénique T ou du récepteur au TNFa et la liaison de NF-KB à l’ADN est accrue. Collectivement, ces résultats suggèrent que USP34 est un nouvel acteur impliqué dans la régulation négative de NF-KB.Ces résultats illustrent l’importance des processus d’ubiquitination réversibles dans la régulation de la signalisation NF-ΚB et introduisent les cribles génétiques comme un outil efficace pour l’identification de régulateurs de processus biologiques divers.

The transcription factor NF-KappaB plays a critical role in the development, homeostasis, the survival of the immune system, but also in the propagation of certain lymphomas. The optimal activation of NF-KappaB in response to the engagement of many immunoreceptors rely on the implementation of large signalosomes where specific adaptors are recruited and poly-Ubiquitinylated in a non-Degradative manner. In response to proinflammatory cytokines or activation of antigen receptors, these Ubiquitinylated adaptors accumulate on the cytoplasmic leaflet of the endoplasmic reticulum (ER) via the ER protein metadherin…

Advisors/Committee Members: Bidère, Nicolas (thesis director).

Subjects/Keywords: NF-kappaB; Ubiquitination; Activation lymphocytaire; NF-kappaB; Ubiquitinylation; Lymphocyte activation

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APA (6^th Edition):

Hatchi, E. (2014). Caractérisation des processus d'ubiquitination régulant le facteur de transcription NF-kappaB au cours de l’activation lymphocytaire Rôle de l’E3 ligase TRIM13 et de la déubiquitinase USP34 : Characterization of ubiquitination processes regulating the transcription factor NF-kappaB During lymphocyte activation Role of the E3 ligase TRIM13 and of the deubiquitinase USP34. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2014PA11T040

Chicago Manual of Style (16^th Edition):

Hatchi, Emeline. “Caractérisation des processus d'ubiquitination régulant le facteur de transcription NF-kappaB au cours de l’activation lymphocytaire Rôle de l’E3 ligase TRIM13 et de la déubiquitinase USP34 : Characterization of ubiquitination processes regulating the transcription factor NF-kappaB During lymphocyte activation Role of the E3 ligase TRIM13 and of the deubiquitinase USP34.” 2014. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed March 03, 2021. http://www.theses.fr/2014PA11T040.

MLA Handbook (7^th Edition):

Hatchi, Emeline. “Caractérisation des processus d'ubiquitination régulant le facteur de transcription NF-kappaB au cours de l’activation lymphocytaire Rôle de l’E3 ligase TRIM13 et de la déubiquitinase USP34 : Characterization of ubiquitination processes regulating the transcription factor NF-kappaB During lymphocyte activation Role of the E3 ligase TRIM13 and of the deubiquitinase USP34.” 2014. Web. 03 Mar 2021.

Vancouver:

Hatchi E. Caractérisation des processus d'ubiquitination régulant le facteur de transcription NF-kappaB au cours de l’activation lymphocytaire Rôle de l’E3 ligase TRIM13 et de la déubiquitinase USP34 : Characterization of ubiquitination processes regulating the transcription factor NF-kappaB During lymphocyte activation Role of the E3 ligase TRIM13 and of the deubiquitinase USP34. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2014. [cited 2021 Mar 03]. Available from: http://www.theses.fr/2014PA11T040.

Council of Science Editors:

Hatchi E. Caractérisation des processus d'ubiquitination régulant le facteur de transcription NF-kappaB au cours de l’activation lymphocytaire Rôle de l’E3 ligase TRIM13 et de la déubiquitinase USP34 : Characterization of ubiquitination processes regulating the transcription factor NF-kappaB During lymphocyte activation Role of the E3 ligase TRIM13 and of the deubiquitinase USP34. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2014. Available from: http://www.theses.fr/2014PA11T040

Texas A&M University

2. Laible, Allyson Marie. Modeling green fluorescent protein transcription, translation and modification as a method to obtain NF-kappaB activation profiles.

Degree: MS, Chemical Engineering, 2009, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-1443

► Cellular response to inflammatory cytokines involves concerted changes in gene expression. Cytokines, such as IL-6 and TNF-α, regulate gene expression through multiple intracellular signaling pathways.… (more)

▼ Cellular response to inflammatory cytokines involves concerted changes in gene expression. Cytokines, such as IL-6 and TNF-α, regulate gene expression through multiple intracellular signaling pathways. The activation of transcription factors is one of the important mechanisms through which these cytokines regulate gene expression, and NF-κB is a key transcription factor that is activated by TNF-α during inflammation. In this study, we have utilized green fluorescent protein reporter cells along with fluorescence microscopy, image analysis and mechanistic modeling to determine the activation dynamics of NF-κB in H35 rat hepatoma cells upon TNF-α stimulation. NF-κB reporter cells were monitored for induction of GFP expression for 24 hours following continuous stimulation with 2.5ng/mL, 10ng/mL and 25ng/mL TNF-α. As expected, TNF-α addition resulted in a significant increase in fluorescence. Relative fluorescence profiles were generated from the fluorescence intensity data, and indicated that fluorescence increases up to 24 hours after an initial delay of approximately four hours. The fluorescence data was also used to develop a model describing significant events leading to NF-κB activation and GFP expression. In addition, a model describing regulatable expression of GFP upon stable integration into the genome was also developed. Comparing these two models led to the construction of a third model depicting NF-κB activation dynamics. Simulation of the model representing NF-κB activation dynamics yielded an NF- κB activation profile, which demonstrated that in the presence of constant TNF-α stimulation, there is an approximate 90 minute hour time delay followed by a rapid increase in nuclear NF-κB, that reaches a steady state value at approximately two hours. This study establishes a method to derive NF-κB activation from reporter cell fluorescence data, and can be used to infer dynamics of activation of other transcription factors using GFP reporter cell lines. Advisors/Committee Members: Jayaraman, Arul (advisor), Hahn, Juergen (committee member), McShane, Mike (committee member).

Subjects/Keywords: Inflammation; NF-kappaB

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APA (6^th Edition):

Laible, A. M. (2009). Modeling green fluorescent protein transcription, translation and modification as a method to obtain NF-kappaB activation profiles. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-1443

Chicago Manual of Style (16^th Edition):

Laible, Allyson Marie. “Modeling green fluorescent protein transcription, translation and modification as a method to obtain NF-kappaB activation profiles.” 2009. Masters Thesis, Texas A&M University. Accessed March 03, 2021. http://hdl.handle.net/1969.1/ETD-TAMU-1443.

MLA Handbook (7^th Edition):

Laible, Allyson Marie. “Modeling green fluorescent protein transcription, translation and modification as a method to obtain NF-kappaB activation profiles.” 2009. Web. 03 Mar 2021.

Vancouver:

Laible AM. Modeling green fluorescent protein transcription, translation and modification as a method to obtain NF-kappaB activation profiles. [Internet] [Masters thesis]. Texas A&M University; 2009. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-1443.

Council of Science Editors:

Laible AM. Modeling green fluorescent protein transcription, translation and modification as a method to obtain NF-kappaB activation profiles. [Masters Thesis]. Texas A&M University; 2009. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-1443

Harvard University

3. Zhou, Alicia. Elucidating the Regulation and Effectors of the Breast Cancer Oncogene, IKKepsilon.

Degree: PhD, Biological and Biomedical Sciences, 2012, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:10086028

► The IkappaB kinase epsilon (IKKepsilon, IKKi, IKBKE) is both a regulator of innate immunity and a breast cancer oncogene that is amplified and overexpressed in… (more)

▼ The IkappaB kinase epsilon (IKKepsilon, IKKi, IKBKE) is both a regulator of innate immunity and a breast cancer oncogene that is amplified and overexpressed in ~30% of breast cancers. IKKepsilon promotes malignant transformation through the activation of NF-kappaB signaling. In addition, breast cancers that harbor amplifications in the IKBKE gene are dependent on IKKepsilon protein expression for survival. IKKepsilon has been characterized as a non-canonical inhibitor of kappaB kinase (IKK) that activates both the interferon response pathway and NF-kappaB signaling in innate immunity. In this dissertation, I explore both the regulation and effectors of the IKKepsilon kinase in the context of malignant transformation. I found that IKKepsilon is modified and regulated by K63-linked polyubiquitination, a proteasome- and degradation-independent form of ubiquitination, at Lysine 30 and Lysine 401. This modification is essential for IKKepsilon-induced kinase function and IKKepsilon-mediated NF-kappaB activation and malignant transformation. Furthermore, I identified TRAF2 as the K63 ubiquitin E3 ligase that associates with and modifies IKKepsilon. I also found that TBK1, a close family member of IKKepsilon, is also regulated by K63-linked ubiquitination. In collaborative work, we used an unbiased positional scanning peptide library screen to identify two novel downstream targets of IKKepsilon phosphorylation in the context of cancer. Specifically, we found IKKepsilon phosphorylates the tumor suppressor CYLD at Serine 418. CYLD phosphorylation at Ser418 downregulates its deubiquitinase activity and is necessary for IKKepsilon-driven transformation. IKKepsilon also phosphorylates TRAF2 at Serine 11. This activity promotes K63-linked TRAF2 ubiquitination, NF-kappaB activation and is also essential for IKKepsilon-transformation. In addition, breast cancer cells that depend on IKKepsilon expression for survival are also dependent on TRAF2. Together, these observations define an oncogenic network that promotes NF-kappaB-mediated cell transformation through the K63-linked ubiquitination of IKKepsilon and subsequent phosphorylation of two novel substrates, TRAF2 and CYLD. Advisors/Committee Members: Hahn, William C. (advisor), Meyerson, Matthew (committee member), McAllister, Sandra (committee member), Weinberg, Robert (committee member).

Subjects/Keywords: IKKepsilon; NF-kappaB; ubiquitination; biology; pathology; biochemistry

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Zhou, A. (2012). Elucidating the Regulation and Effectors of the Breast Cancer Oncogene, IKKepsilon. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:10086028

Chicago Manual of Style (16^th Edition):

Zhou, Alicia. “Elucidating the Regulation and Effectors of the Breast Cancer Oncogene, IKKepsilon.” 2012. Doctoral Dissertation, Harvard University. Accessed March 03, 2021. http://nrs.harvard.edu/urn-3:HUL.InstRepos:10086028.

MLA Handbook (7^th Edition):

Zhou, Alicia. “Elucidating the Regulation and Effectors of the Breast Cancer Oncogene, IKKepsilon.” 2012. Web. 03 Mar 2021.

Vancouver:

Zhou A. Elucidating the Regulation and Effectors of the Breast Cancer Oncogene, IKKepsilon. [Internet] [Doctoral dissertation]. Harvard University; 2012. [cited 2021 Mar 03]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:10086028.

Council of Science Editors:

Zhou A. Elucidating the Regulation and Effectors of the Breast Cancer Oncogene, IKKepsilon. [Doctoral Dissertation]. Harvard University; 2012. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:10086028

University of Illinois – Chicago

4. Barazia, Andrew. Role of DREAM in Neutrophil Function and Platelet-Neutrophil Interactions in Thrombo-Inflammatory Disease.

Degree: 2016, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/20945

► The interaction between neutrophils and activated endothelial cells (ECs) is critical for the pathogenesis of vascular inflammation. However, it remains poorly understood how neutrophil-EC interactions… (more)

▼ The interaction between neutrophils and activated endothelial cells (ECs) is critical for the pathogenesis of vascular inflammation. However, it remains poorly understood how neutrophil-EC interactions are regulated. Using intravital microscopy with mice lacking downstream regulatory element antagonist modulator (DREAM), a transcriptional repressor, we demonstrated that intravascular cell DREAM was important for neutrophil adhesion to TNF-α-activated ECs during vascular inflammation. Studies with bone marrow chimeras revealed that both hematopoietic and EC DREAM were required for neutrophil-EC interactions. DREAM-null neutrophils showed reduced membrane translocation and ligand-binding activity of αMβ2 integrin and β2-talin1 binding following stimulation with TNF-α, but not fMLF. Deletion of neutrophil DREAM resulted in upregulated expression of A20, a negative regulator of NF-κB signaling and downregulated expression of p65, a critical subunit of the NF-κB complex. Further, we found that neutrophil DREAM was required for gene transcription of TNFα, IL-1β, and IL-6, and phosphorylation of IκB kinase (IKK) following TNF- stimulation. Inhibition of IKK activity reduced the membrane translocation of αMβ2 integrin and degranulation in TNF-α-stimulated WT, but not DREAM-null, neutrophils. Thus, our results suggest that neutrophil DREAM plays an important role in both NF-κB-dependent gene transcription of pro-inflammatory cytokines and NF-κB-independent IKK activation during vascular inflammation. Since αMβ2 integrin and neutrophil-derived cytokines are important for the interaction of neutrophils with platelets, we further determined whether DREAM regulates platelet-neutrophil interaction during vascular inflammation. Our fluorescence intravital microscopy demonstrated that both hematopoietic and EC DREAM are crucial for regulating the interaction of platelets with adherent neutrophils in TNFα-inflamed venules in live mice. Additionally, using an in vitro heterotypic cell-cell aggregation assay, we found that both neutrophil and platelet DREAM are important in regulation neutrophil-platelet interactions under stirring conditions mimicking venous shear. Compared with WT platelets, DREAM KO platelets exhibited a significant reduction in P-selectin exposure on activated platelets which is required for platelet-neutrophil interaction. Taken together, these results provide important evidence that intravascular cell DREAM could be a novel therapeutic target for treatment of inflammatory diseases. Advisors/Committee Members: Cho, Jaehyung (advisor), Skidgel, Randal (committee member), Le Breton, Guy (committee member), Tiruppathi, Chinnaswamy (committee member), Dull, Randal (committee member).

Subjects/Keywords: Neutrophil; Platelet; Inflammation; NF-kappaB; DREAM

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APA (6^th Edition):

Barazia, A. (2016). Role of DREAM in Neutrophil Function and Platelet-Neutrophil Interactions in Thrombo-Inflammatory Disease. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/20945

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Barazia, Andrew. “Role of DREAM in Neutrophil Function and Platelet-Neutrophil Interactions in Thrombo-Inflammatory Disease.” 2016. Thesis, University of Illinois – Chicago. Accessed March 03, 2021. http://hdl.handle.net/10027/20945.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Barazia, Andrew. “Role of DREAM in Neutrophil Function and Platelet-Neutrophil Interactions in Thrombo-Inflammatory Disease.” 2016. Web. 03 Mar 2021.

Vancouver:

Barazia A. Role of DREAM in Neutrophil Function and Platelet-Neutrophil Interactions in Thrombo-Inflammatory Disease. [Internet] [Thesis]. University of Illinois – Chicago; 2016. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10027/20945.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Barazia A. Role of DREAM in Neutrophil Function and Platelet-Neutrophil Interactions in Thrombo-Inflammatory Disease. [Thesis]. University of Illinois – Chicago; 2016. Available from: http://hdl.handle.net/10027/20945

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Virginia Tech

5. Awwad, Yousef Ahmad. The Effect of Interleukin-1 (IL-1) Concentration on Single Cell NF-kappaB Activation in a Gradient-Generating Microfluidic Device.

Degree: MS, Biomedical Engineering, 2011, Virginia Tech

URL: http://hdl.handle.net/10919/35315

► Interleukin-1 (IL-1) is a multifunctional cytokine produced primarily by activated monocytes/macrophages and by a variety of other cell types. IL-1 plays an integral role in… (more)

▼ Interleukin-1 (IL-1) is a multifunctional cytokine produced primarily by activated monocytes/macrophages and by a variety of other cell types. IL-1 plays an integral role in the immuno-inflammatory response of the body to a variety of stimuli including infection, trauma and other bodily injuries. Once IL-1 is released from the synthesizing cell, it acts as a hormone, initializing a variety of responses in different cells and tissues. These responses are believed to be crucial to survival and are termed acute-phase responses. NF-ÎºB is a family of dimeric transcription factors that control the expression of hundreds of genes which regulate cellular stress responses, cell division, apoptosis, and inflammation. NF-ÎºB dwells in the cytoplasm of the cell until activation in response to a wide range of extracellular stimuli including signaling molecules such as cytokines. NF-ÎºB regulates transcription and gene expression through nucleocytoplasmic transport. Most previous studies on NF-ÎºB activation have been performed using bulk assays to look at populations of cells. Determining cell variance at a single-cell level is crucial in understanding the full mechanisms of drug response. The goal of this study is to analyze the effects of variant concentrations of IL-1Î² on the activation of NF-ÎºB in individual cells through use of a microfluidic gradient generator. The gradient generator was adopted from Jeon et al and used principles of diffusive mixing and splitting of flows in order create a solute concentration gradient. A soft lithography procedure was used. Briefly, the design was printed on a transparency using a high resolution printer. A master of the design is then created using an SU-8 photoresist and UV light to imprint the design on a silicon wafer. The master is then used to create a Polydimethylsiloxane (PDMS) mold of the design which can be irreversibly attached to a glass slide through oxidation in order to close off the microfluidic channels. FITC-conjugated Î²-Casein (a protein with similar molecular weight to IL-1Î²) was used in order to verify the gradient generated by the design. The concentration gradient was analyzed by measuring fluorescent intensity of images taken under a UV light microscope and found to agree with microfluidic simulations run on COMSOL. A procedure for culturing cells in a microfluidic device was then adapted from Jeon that is explained in detail in Chapter 3. Two main trends were revealed; firstly, as IL-1Î² concentration decreased, the percent of cells activated also decreased. Secondly, as IL-1Î² concentration decreased, the activation time of the responding cells increased. Cells were observed to act in a single-cell manner; in which multiple cells subjected to the same concentration would not all respond in the same fashion. No major activation threshold was observed but two minor thresholds were; the first at 0.02 ng/mL IL-1Î² where activation levels drop from 20% to around 5%. The second around 1 ng/mL, in which all greater concentrations show nearly complete… Advisors/Committee Members: Lu, Chang-Tien (committeechair), Davalos, Rafael V. (committee member), Li, Liwu (committee member).

Subjects/Keywords: Microfluidics; Single-Cell; NF-kappaB; Gradient

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Awwad, Y. A. (2011). The Effect of Interleukin-1 (IL-1) Concentration on Single Cell NF-kappaB Activation in a Gradient-Generating Microfluidic Device. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/35315

Chicago Manual of Style (16^th Edition):

Awwad, Yousef Ahmad. “The Effect of Interleukin-1 (IL-1) Concentration on Single Cell NF-kappaB Activation in a Gradient-Generating Microfluidic Device.” 2011. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/35315.

MLA Handbook (7^th Edition):

Awwad, Yousef Ahmad. “The Effect of Interleukin-1 (IL-1) Concentration on Single Cell NF-kappaB Activation in a Gradient-Generating Microfluidic Device.” 2011. Web. 03 Mar 2021.

Vancouver:

Awwad YA. The Effect of Interleukin-1 (IL-1) Concentration on Single Cell NF-kappaB Activation in a Gradient-Generating Microfluidic Device. [Internet] [Masters thesis]. Virginia Tech; 2011. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/35315.

Council of Science Editors:

Awwad YA. The Effect of Interleukin-1 (IL-1) Concentration on Single Cell NF-kappaB Activation in a Gradient-Generating Microfluidic Device. [Masters Thesis]. Virginia Tech; 2011. Available from: http://hdl.handle.net/10919/35315

University of Texas – Austin

6. Gardella, Kacie Alicia Thomas. Regulation of the NF-kappaB and p53 pathways by the aryl hydrocarbon receptor nuclear translocator.

Degree: PhD, Cell and Molecular Biology, 2015, University of Texas – Austin

URL: http://hdl.handle.net/2152/63854

► Nuclear factor-[kappa]B (NF-[kappa]B) signaling is critical for the proper function of the immune system, and when deregulated, promotes the development of immune disorders and cancer.… (more)

▼ Nuclear factor-[kappa]B (NF-[kappa]B) signaling is critical for the proper function of the immune system, and when deregulated, promotes the development of immune disorders and cancer. It is important to understand the complex regulatory mechanisms that govern NF-[kappa]B activity so that we can improve therapies for cancer and immune diseases. Notably, the aryl hydrocarbon receptor nuclear translocator (ARNT) has been shown to regulate the chromatin binding activity of the NF-[kappa]B subunit RelB, in turn promoting RelB-p50 DNA binding, a process that inhibits canonical NF-[kappa]B signaling. However, ARNT is expressed as two alternatively spliced isoforms, isoforms 1 and 3. Whether each isoform has a specific role in NF-κB signaling is unclear. In the first project, ARNT isoforms 1 and 3 are shown to contribute in distinctive ways to lymphoid cancer cell growth through regulating RelB and p53. Importantly, suppression of isoform 1 in lymphoid cancer cell lines triggered S-phase cell cycle arrest, spontaneous apoptosis, and sensitized cells to doxorubicin treatment. Furthermore, co-suppression of RelB or p53 with ARNT isoform 1 prevented cell cycle arrest and blocked doxorubicin-induced cell death. Together these findings reveal that certain hematological malignancies rely on ARNT isoform 1 to potentiate proliferation by antagonizing RelB and p53-dependent cell cycle arrest and apoptosis. In Chapter 4, the individual functions of ARNT isoforms 1 and 3 in NF-[kappa]B signaling were investigated. The results from this study point to ARNT as a regulator of RelB-p52/p100 nuclear import in a cell-type specific manner. Furthermore, while both ARNT isoform 1 and 3 were necessary for regulating RelB-p52/p100 nuclear import in Karpas 299 cells, isoform 3 was found to be a negative regulator of NF-[kappa]B target gene expression, whereas ARNT isoform 1 neither promoted nor inhibited NF-[kappa]B signaling. While in HEK 293T cells, the presence of both ARNT isoform 1 and 3 promoted p100 nuclear translocation and co-localization with RelB. Together, these data indicate that ARNT isoform 1 and 3 form a complex with RelB and p52/p100 to fine-tune NF-[kappa]B nuclear translocation and activity. Significantly, our results give insight into a novel regulatory mechanism of NF-[kappa]B activity and identify ARNT as a potential target for anticancer therapies. Advisors/Committee Members: Wright, Casey Wyatt (advisor), Tucker, Haley (committee member), Mills, Edward (committee member), Bratton, Shawn (committee member), Ehrlich, Lauren (committee member).

Subjects/Keywords: ARNT; NF-kappaB; AHR; Lymphoid malignancies

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APA (6^th Edition):

Gardella, K. A. T. (2015). Regulation of the NF-kappaB and p53 pathways by the aryl hydrocarbon receptor nuclear translocator. (Doctoral Dissertation). University of Texas – Austin. Retrieved from http://hdl.handle.net/2152/63854

Chicago Manual of Style (16^th Edition):

Gardella, Kacie Alicia Thomas. “Regulation of the NF-kappaB and p53 pathways by the aryl hydrocarbon receptor nuclear translocator.” 2015. Doctoral Dissertation, University of Texas – Austin. Accessed March 03, 2021. http://hdl.handle.net/2152/63854.

MLA Handbook (7^th Edition):

Gardella, Kacie Alicia Thomas. “Regulation of the NF-kappaB and p53 pathways by the aryl hydrocarbon receptor nuclear translocator.” 2015. Web. 03 Mar 2021.

Vancouver:

Gardella KAT. Regulation of the NF-kappaB and p53 pathways by the aryl hydrocarbon receptor nuclear translocator. [Internet] [Doctoral dissertation]. University of Texas – Austin; 2015. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2152/63854.

Council of Science Editors:

Gardella KAT. Regulation of the NF-kappaB and p53 pathways by the aryl hydrocarbon receptor nuclear translocator. [Doctoral Dissertation]. University of Texas – Austin; 2015. Available from: http://hdl.handle.net/2152/63854

Johannes Gutenberg Universität Mainz

7. Reißig, Sonja. Misregulation of the tumour suppressor gene CYLD drives hyperactivation of T cells leading to intestinal pathology.

Degree: 2011, Johannes Gutenberg Universität Mainz

URL: http://ubm.opus.hbz-nrw.de/volltexte/2011/2918/

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The tumour suppressor gene cyld is mutated in familial cylindromatosis, an autosomal-dominant condition that predisposes to multiple skin tumours. The deubiquitinase CYLD acts as a… (more)

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The tumour suppressor gene cyld is mutated in familial cylindromatosis, an autosomal-dominant condition that predisposes to multiple skin tumours. The deubiquitinase CYLD acts as a negative regulator of NF-κB signaling. To analyse the function of CYLD in vivo we used the CYLDex7/8 mice, which are characterized by loss of the full-length transcript and overexpression of a short splice variant of CYLD (sCYLD). In CYLDex7/8 mice the overexpression of sCYLD results in splenomegaly and lymphadenopathy. Additionally, the B cell population in spleen and lymph nodes is increased at the expense of T cells. Analysis of CYLDex7/8 T cells showed a significant reduction of CD4 single positive (SP) and CD8 SP T cells in the thymus and in the periphery. By investigating the impact of sCYLD in TCR signaling in thymocytes, we could demonstrate that sCYLD partially inhibited the activation of Zap70 and thereby negatively regulated TCR signaling. In vitro as well as in vivo we could show that CD4+ T cells displayed a hyperactive phenotype, proliferated to a better extent than WT cells and expressed high amounts of inflammatory cytokines such as IL-6 and IL-17A. Western Blots of steady state thymocytes and peripheral CD4+ T cells were performed, showing that the noncanonical pathway was highly upregulated visualized by the expression levels of RelB and p100 leading to a hyperactive phenotype of CD4+ T cells. In order to investigate the contribution of sCYLD in positive and negative selection in the thymus in vivo, the HY-TCR transgene (HYtg) was crossed to CYLDex7/8 mice. The analysis of CYLDex7/8 HYtg males revealed an increase in CD4+CD8+ DP as well as in CD8+ SP thymocytes, suggesting a less pronounced negative selection in CYLD mutant mice compared to HYtg control mice. Interestingly, the impaired negative selection in the thymus was accompanied by a strong colitis phenotype at early ages (4 weeks). Since medullary TECs (mTECs) play an important role in the late stage of T cell development by negatively selecting autoreactive thymocytes, the levels of mTECs in the medullary compartment was investigated. Of note, low numbers of mTECs were observed, combined with decreased expression levels of the mTEC markers UEA-1, keratin-5, claudin-3 and claudin-4. The reduction of mTECs in the medullary compartment could explain the inflammatory phenotype of CD4+ T cells in CYLDex7/8 mice leading to the severe intestinal pathology observed in these mice. Taken together, these results show an important role of sCYLD in T cell development and function as well as in NF-кB signaling of T cells.

Das Tumorsuppressor Gen cyld ist mutiert in Patienten mit familiärer Zylindromatose, was zu einer autosomal-dominant vererbten Prädisposition für multiple Tumore der Haut führt. Die Deubiquitinase CYLD ist ein negativer Regulator des NF-κB Signalweges und hemmt die Aktivierung des Transkriptionsfaktors NF-κB, welcher an Entzündungsreaktion, Immunantwort, Apoptose und Onkogenese beteiligt ist. Um die in vivo Funktion von CYLD zu untersuchen, wurde der…

Subjects/Keywords: CYLD, T Zellen, NF-kappaB, Inflammatory Bowel Disease; CYLD, T cells, NF-kappaB, chronische Darmentzündung; Life sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Reißig, S. (2011). Misregulation of the tumour suppressor gene CYLD drives hyperactivation of T cells leading to intestinal pathology. (Doctoral Dissertation). Johannes Gutenberg Universität Mainz. Retrieved from http://ubm.opus.hbz-nrw.de/volltexte/2011/2918/

Chicago Manual of Style (16^th Edition):

Reißig, Sonja. “Misregulation of the tumour suppressor gene CYLD drives hyperactivation of T cells leading to intestinal pathology.” 2011. Doctoral Dissertation, Johannes Gutenberg Universität Mainz. Accessed March 03, 2021. http://ubm.opus.hbz-nrw.de/volltexte/2011/2918/.

MLA Handbook (7^th Edition):

Reißig, Sonja. “Misregulation of the tumour suppressor gene CYLD drives hyperactivation of T cells leading to intestinal pathology.” 2011. Web. 03 Mar 2021.

Vancouver:

Reißig S. Misregulation of the tumour suppressor gene CYLD drives hyperactivation of T cells leading to intestinal pathology. [Internet] [Doctoral dissertation]. Johannes Gutenberg Universität Mainz; 2011. [cited 2021 Mar 03]. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2011/2918/.

Council of Science Editors:

Reißig S. Misregulation of the tumour suppressor gene CYLD drives hyperactivation of T cells leading to intestinal pathology. [Doctoral Dissertation]. Johannes Gutenberg Universität Mainz; 2011. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2011/2918/

8. Rocca, Jeremy. Caractérisation d’un agent anti-inflammatoire et approches pharmacologiques pour contrôler l’inflammation pulmonaire dans le contexte de la mucoviscidose : Characterization of an anti-inflammatory agent and pharmacological approaches to control the pulmonary inflammation in cystic fibrosis context.

Degree: Docteur es, Biologie cellulaire et moléculaire, 2015, Université Paris-Est

URL: http://www.theses.fr/2015PESC0012

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La mucoviscidose (Cystic Fibrosis, CF) est caractérisée par une symptomatologie variée, dominée par la gravité de l'atteinte pulmonaire et une réponse inflammatoire inadaptée. Elle est… (more)

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La mucoviscidose (Cystic Fibrosis, CF) est caractérisée par une symptomatologie variée, dominée par la gravité de l'atteinte pulmonaire et une réponse inflammatoire inadaptée. Elle est due à des mutations du gène CFTR codant un canal chlorure AMPc-dépendant à la surface des cellules épithéliales. L'inflammation des voies aériennes de type neutrophilique est caractérisée au niveau cellulaire par une surproduction de cytokines pro-inflammatoires telles que l'interleukine-8 (IL-8) et une activation anormale des facteurs de transcription impliqués dans les voies de signalisation de l'inflammation comme NF-κB, AP-1 et PPARγ.Notre projet est d'identifier des agents à effet anti-inflammatoire dans le contexte de la mucoviscidose et d'en décrypter les mécanismes d'action. Nous avons pour cela étudié l'effet de molécules anti-inflammatoires avec une autorisation de mise sur le marché mais jamais testées pour la mucoviscidose et l'effet de COMMD1 une protéine pléïotropique impliquée dans l'inhibition de l'inflammation et identifiée au laboratoire pour interagir avec CFTR.Dans un premier temps nous avons montré l'activité anti-inflammatoire de COMMD1 dans le contexte de la mucoviscidose via son action anti-NF-κB. Dans un second temps nous avons montré que le sulindac et l'amlexanox permettent de moduler des facteurs dérégulés dans des cellules CF. Ces molécules inhibent l'activité de NF-κB et activent PPARγ. Le sulindac permet de diminuer la sécrétion d'IL-8 in vitro sur des cellules épithéliales bronchiques et in vivo sur modèles d'inflammation pulmonaire murin. De plus nous avons montré que le sulindac augmente le transport des ions chlorures via CFTR sur des cellules épithéliales nasales humaines non CF suggérant que le sulindac a un double effet anti-inflammatoire et potentiateur.Ce projet de recherche nous a permis de proposer de nouveaux candidats pour les thérapies anti-inflammatoires dans la mucoviscidose et d'initier l'étude de leur mécanisme d'action.

Cystic fibrosis (CF) is characterized by a varied symptomatology dominated by the lung injury severity and inappropriate inflammatory response. It is caused by mutations in the CFTR gene that encodes a cAMP-dependent chloride channel on the surface of epithelial cells. Airway inflammation with neutrphilic profil is characterised by increased Interleukine-8 (IL-8) secretion with dysregulation of transcription factors implicated in the inflammatory pathway such as NF-κB, AP-1 and PPARγ.Our aim is to evaluate agents with anti-inflammatory effect in CF context and to decrypt their mechanisms of action. We have study the effect of anti-inflammatory FDA approved drugs having a yet undefined effect in CF airway epithelial cells and the effect of COMMD1 a pleiotropic protein involved in the inhibition of inflammation and identified in the laboratory to interact with CFTR.In a first time we have shown the anti-inflammatory activity of COMMD1 mediated by its anti-NF-kB activity in the CF context. In a second time we have shown that sulindac and amlexanox can modulate factors…

Advisors/Committee Members: Fanen, Pascale (thesis director).

Subjects/Keywords: Mucoviscidose; Inflammation; NF-Kappab; Sulindac; Commd1; Amlexanox; Cystic fibrosis; Inflammation; NF-Kappab; Sulindac; Commd1; Amlexanox; 570

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Rocca, J. (2015). Caractérisation d’un agent anti-inflammatoire et approches pharmacologiques pour contrôler l’inflammation pulmonaire dans le contexte de la mucoviscidose : Characterization of an anti-inflammatory agent and pharmacological approaches to control the pulmonary inflammation in cystic fibrosis context. (Doctoral Dissertation). Université Paris-Est. Retrieved from http://www.theses.fr/2015PESC0012

Chicago Manual of Style (16^th Edition):

Rocca, Jeremy. “Caractérisation d’un agent anti-inflammatoire et approches pharmacologiques pour contrôler l’inflammation pulmonaire dans le contexte de la mucoviscidose : Characterization of an anti-inflammatory agent and pharmacological approaches to control the pulmonary inflammation in cystic fibrosis context.” 2015. Doctoral Dissertation, Université Paris-Est. Accessed March 03, 2021. http://www.theses.fr/2015PESC0012.

MLA Handbook (7^th Edition):

Rocca, Jeremy. “Caractérisation d’un agent anti-inflammatoire et approches pharmacologiques pour contrôler l’inflammation pulmonaire dans le contexte de la mucoviscidose : Characterization of an anti-inflammatory agent and pharmacological approaches to control the pulmonary inflammation in cystic fibrosis context.” 2015. Web. 03 Mar 2021.

Vancouver:

Rocca J. Caractérisation d’un agent anti-inflammatoire et approches pharmacologiques pour contrôler l’inflammation pulmonaire dans le contexte de la mucoviscidose : Characterization of an anti-inflammatory agent and pharmacological approaches to control the pulmonary inflammation in cystic fibrosis context. [Internet] [Doctoral dissertation]. Université Paris-Est; 2015. [cited 2021 Mar 03]. Available from: http://www.theses.fr/2015PESC0012.

Council of Science Editors:

Rocca J. Caractérisation d’un agent anti-inflammatoire et approches pharmacologiques pour contrôler l’inflammation pulmonaire dans le contexte de la mucoviscidose : Characterization of an anti-inflammatory agent and pharmacological approaches to control the pulmonary inflammation in cystic fibrosis context. [Doctoral Dissertation]. Université Paris-Est; 2015. Available from: http://www.theses.fr/2015PESC0012

Université Paris-Sud – Paris XI

9. Dubois, Sonia. Caractérisation de nouveaux régulateurs de l'activation lymphocytaire et de la lymphomagenèse : Identification of New Regulators of Lymphocytes Activation and Lymphomagenesis.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2015, Université Paris-Sud – Paris XI

URL: http://www.theses.fr/2015PA11T033

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Le lymphome diffus à grandes cellules B (DLBCL, Diffuse Large B-Cell Lymphoma) constitue le lymphome non Hodgkinien le plus fréquemment diagnostiqué. Les DLBCL sont composés… (more)

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Le lymphome diffus à grandes cellules B (DLBCL, Diffuse Large B-Cell Lymphoma) constitue le lymphome non Hodgkinien le plus fréquemment diagnostiqué. Les DLBCL sont composés principalement de deux sous groupes : l’entité nommée ABC (Activated B Cell-like) qui est la plus agressive, avec un taux de survie de 30% après traitement, et l’entité GCB (Germinal-Center B Cell). Contrairement aux GCB DLBCL, les ABC DLBCL se caractérisent par une signature génique similaire aux lymphocytes B activés par leur récepteur antigénique (BCR, B Cell Receptor) à cause de l'accumulation de mutations génétiques. Ceci a pour conséquence une activation constitutive du facteur de transcription NF-κB pour laquelle les lymphomes ABC DLBCL ont développé une profonde addiction. Toutefois, la nature pléiotrope de NF-κB rend son ciblage thérapeutique inenvisageable. Mon projet de thèse visait à caractériser de nouveaux régulateurs de la voie d’activation du facteur NF-κB par les récepteurs antigéniques en condition physiologique et pathologique. Dans un premier temps, grâce à un crible protéomique par spectrométrie de masse, nous avons identifié un complexe ternaire nommé LUBAC (Linear Ubiquitin Chain Assembly Complex) comme un acteur majeur de l’activation de NF-κB par le TCR et le BCR, et de la survie des lymphomes ABC DLBCL. Dans un second temps, le crible d’une librairie de mille deux cents molécules chimiques nous a permis d’isoler un composé sélectivement toxique in vitro pour les lymphomes ABC DLBCL. Nous montrons que ce composé entraine la mort apoptotique des ABC DLBCL sans toutefois affecter la signalisation NF-κB. Un tel composé pourrait, dans le futur, être utilisé comme une nouvelle molécule thérapeutique pour le traitement du lymphome ABC DLBCL.

The diffuse large B cell lymphoma (DLBCL) is the most common non Hodgkinien lymphoma. Two main different entities composed the DLBCL : the Activated B Cell-like subtype (ABC DLBCL) witch is the most aggressive and associated with a poor survival prognostic, and the Germinal-Center B Cell subtype (GCB DLBCL). Unlike the GCB DLBCL, ABC DLBCL are characterized by a genetic signature similar to activated B lymphocytes stimulated by their antigen receptor (BCR, B cell receptor) which results from mutations accumulation. As a consequence, ABC DLBCL survival and proliferation requires the constitutive activation of NF-κB transcription factors. Because NF-κB has pleiotropic effect on different tissues, strategies aiming at targeting NF-κB heterodimers might have deleterious consequences on an organism.My project focuses on identifying new modulators involved in antigen receptor mediated NF-κB activation in physiological and pathological condition.We first performed a mass spectrometry analysis and identified the LUBAC (Linear Ubiquitin Chain Assembly Complex) as a new regulator of antigen receptor mediated a NF-κB ctivation and ABC DLBCL survival. Then, we screened a library of one thousand two hundred chemical compounds on DLBCL viability and identified one compound selectively toxic in vitro…

Advisors/Committee Members: Bidère, Nicolas (thesis director).

Subjects/Keywords: NF-kappaB; LUBAC; Lymphome; ABC DLBCL; Récepteurs antigéniques; NF-kappaB; LUBAC; Lymphoma; ABC DLBCL; Antigen receptors

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dubois, S. (2015). Caractérisation de nouveaux régulateurs de l'activation lymphocytaire et de la lymphomagenèse : Identification of New Regulators of Lymphocytes Activation and Lymphomagenesis. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2015PA11T033

Chicago Manual of Style (16^th Edition):

Dubois, Sonia. “Caractérisation de nouveaux régulateurs de l'activation lymphocytaire et de la lymphomagenèse : Identification of New Regulators of Lymphocytes Activation and Lymphomagenesis.” 2015. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed March 03, 2021. http://www.theses.fr/2015PA11T033.

MLA Handbook (7^th Edition):

Dubois, Sonia. “Caractérisation de nouveaux régulateurs de l'activation lymphocytaire et de la lymphomagenèse : Identification of New Regulators of Lymphocytes Activation and Lymphomagenesis.” 2015. Web. 03 Mar 2021.

Vancouver:

Dubois S. Caractérisation de nouveaux régulateurs de l'activation lymphocytaire et de la lymphomagenèse : Identification of New Regulators of Lymphocytes Activation and Lymphomagenesis. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2015. [cited 2021 Mar 03]. Available from: http://www.theses.fr/2015PA11T033.

Council of Science Editors:

Dubois S. Caractérisation de nouveaux régulateurs de l'activation lymphocytaire et de la lymphomagenèse : Identification of New Regulators of Lymphocytes Activation and Lymphomagenesis. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2015. Available from: http://www.theses.fr/2015PA11T033

Université de Grenoble

10. Jacomin, Anne-Claire. Fonctions des déubiquitinases dans l'inflammation et l'autophagie. Régulation de la voie du TNF-R1 des mammifères par USP36 et crible génétique pour l'identification des déubiquitinases impliquées dans l'autophagie chez la drosophile : Functions of deubiquitinating enzymes in inflammation and autophagy : Regulation of the mammalian TNF-R1 pathway by USP36 and genetic screening to identify deubiquitinating enzymes involved in autophagy in Drosophila.

Degree: Docteur es, Sciences de la vie, 2014, Université de Grenoble

URL: http://www.theses.fr/2014GRENV067

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La survie des êtres vivants repose sur leur capacité d'adaptation à leur environnement et au maintien de l'homéostasie cellulaire. Au cours de mon doctorat, je… (more)

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La survie des êtres vivants repose sur leur capacité d'adaptation à leur environnement et au maintien de l'homéostasie cellulaire. Au cours de mon doctorat, je me suis intéressée à deux de ces aspects : d'abord à la réponse immunitaire innée et inflammatoire par l'étude des voies associées aux facteurs de transcription NF-kB et ensuite à l'autophagie, qui consiste en la capacité d'une cellule à dégrader certains composants cellulaires ou des pathogènes intracellulaires. La rapidité d'activation/inactivation de ces processus cellulaires est permise par des modifications post-traductionnelles de certains acteurs parmi lesquelles l'ubiquitination des protéines, qui consiste en la liaison covalente de mono- ou polymères d'ubiquitines sur des protéines, et qui apparaît désormais comme un mécanisme majeur. Dans ce contexte, mes travaux ont consisté d'une part, en la mise en évidence de la fonction de la déubiquitinase USP36 dans la régulation de la voie immunitaire NF-B associée au récepteur 1 au TNFa (TNF-R1) en cellules humaines en culture. J'ai montré par des approches de biologie cellulaire et de biochimie qu'USP36 est un régulateur négatif spécifique de cette voie et est constitutivement associée au récepteur, contribuant ainsi à la régulation de l'ubiquitination de RIP1, un composant essentiel de la voie du TNF-R1. De cette étude, nous avons conclu qu'USP36 est un acteur clé de la voie du TNF-R1 permettant la répression de la voie en absence d'activation et favorisant un retour à l'état stationnaire en réponse à une stimulation au TNFa. D'autre part, mes travaux ont consisté en la réalisation d'un crible génétique in vivo chez la Drosophile pour l'identification de déubiquitinases impliquées dans la régulation de l'autophagie. J'ai identifié UBPY et USP12 dont la perte de fonction affecte à la fois la progression de l'autophagie et de l'endocytose. A partir de l'étude de ces enzymes, nous avons pu établir qu'une voie endocytaire intacte est requise pour le bon fonctionnement de l'autophagie.

The survival of living organisms is based on their ability to adapt to their environment and to maintain their cellular integrity. During my PhD, I was interested in two of these aspects: first, the innate immunity and inflammatory response through the study of the NF-kB-associated pathways, and then in autophagy, consisting in the ability of a cell to degrade some cellular components or intracellular pathogens. The rapid activation/inactivation of these cellular processes is permitted by the post-translational modifications of some components. Among these changes, protein ubiquitination, consisting in the covalent binding of ubiquitin mono- or polymers on target proteins, appears to be an essential mechanism. In this context, my work consisted on one hand, in showing the function of the deubiquitinating enzyme USP36 in the regulation of the immune pathway depending on the TNFa-associated receptor 1 (TNF -R1) pathway in cultured human cells. Using cellular and biochemical approaches, I showed that USP36 is a specific negative…

Advisors/Committee Members: Fauvarque, Marie-Odile (thesis director), Taillebourg, Emmanuel (thesis director).

Subjects/Keywords: Ubiquitination; NF-kappaB; Transduction du signal; Autophagie; Endocytose; Drosophile; Ubiquitination; NF-kappaB; Signal transduction; Autophagy; Endocytosis; Drosophila; 570

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Jacomin, A. (2014). Fonctions des déubiquitinases dans l'inflammation et l'autophagie. Régulation de la voie du TNF-R1 des mammifères par USP36 et crible génétique pour l'identification des déubiquitinases impliquées dans l'autophagie chez la drosophile : Functions of deubiquitinating enzymes in inflammation and autophagy : Regulation of the mammalian TNF-R1 pathway by USP36 and genetic screening to identify deubiquitinating enzymes involved in autophagy in Drosophila. (Doctoral Dissertation). Université de Grenoble. Retrieved from http://www.theses.fr/2014GRENV067

Chicago Manual of Style (16^th Edition):

Jacomin, Anne-Claire. “Fonctions des déubiquitinases dans l'inflammation et l'autophagie. Régulation de la voie du TNF-R1 des mammifères par USP36 et crible génétique pour l'identification des déubiquitinases impliquées dans l'autophagie chez la drosophile : Functions of deubiquitinating enzymes in inflammation and autophagy : Regulation of the mammalian TNF-R1 pathway by USP36 and genetic screening to identify deubiquitinating enzymes involved in autophagy in Drosophila.” 2014. Doctoral Dissertation, Université de Grenoble. Accessed March 03, 2021. http://www.theses.fr/2014GRENV067.

MLA Handbook (7^th Edition):

Jacomin, Anne-Claire. “Fonctions des déubiquitinases dans l'inflammation et l'autophagie. Régulation de la voie du TNF-R1 des mammifères par USP36 et crible génétique pour l'identification des déubiquitinases impliquées dans l'autophagie chez la drosophile : Functions of deubiquitinating enzymes in inflammation and autophagy : Regulation of the mammalian TNF-R1 pathway by USP36 and genetic screening to identify deubiquitinating enzymes involved in autophagy in Drosophila.” 2014. Web. 03 Mar 2021.

Vancouver:

Jacomin A. Fonctions des déubiquitinases dans l'inflammation et l'autophagie. Régulation de la voie du TNF-R1 des mammifères par USP36 et crible génétique pour l'identification des déubiquitinases impliquées dans l'autophagie chez la drosophile : Functions of deubiquitinating enzymes in inflammation and autophagy : Regulation of the mammalian TNF-R1 pathway by USP36 and genetic screening to identify deubiquitinating enzymes involved in autophagy in Drosophila. [Internet] [Doctoral dissertation]. Université de Grenoble; 2014. [cited 2021 Mar 03]. Available from: http://www.theses.fr/2014GRENV067.

Council of Science Editors:

Jacomin A. Fonctions des déubiquitinases dans l'inflammation et l'autophagie. Régulation de la voie du TNF-R1 des mammifères par USP36 et crible génétique pour l'identification des déubiquitinases impliquées dans l'autophagie chez la drosophile : Functions of deubiquitinating enzymes in inflammation and autophagy : Regulation of the mammalian TNF-R1 pathway by USP36 and genetic screening to identify deubiquitinating enzymes involved in autophagy in Drosophila. [Doctoral Dissertation]. Université de Grenoble; 2014. Available from: http://www.theses.fr/2014GRENV067

University of California – San Diego

11. Ramsey, Kristen Michelle. The Role of Protein Structure and Dynamics in the Inhibition of NF-kappaB by IkappaB Proteins.

Degree: Chemistry and Biochemistry, 2018, University of California – San Diego

URL: http://www.escholarship.org/uc/item/6j05k57m

► The NFκB signaling pathway is a central regulator of inflammatory and immune responses in virtually all human cell and tissue types, and aberrant signaling by… (more)

▼ The NFκB signaling pathway is a central regulator of inflammatory and immune responses in virtually all human cell and tissue types, and aberrant signaling by NFκB has been implicated in a wide array of disease states including cancer, autoimmune diseases, and Alzheimer’s disease among others. Inhibition of NFκB by binding of IκB proteins represents the most robust regulatory mechanism for controlling the initiation and duration of the NFκB signaling event. NFκB and IκB both denote families of dimeric transcription factors and their inhibitor proteins, respectively. NFκB transcription factors self associate to form functionally active dimers which then bind in a specific manner to different IκB family members.Here I present an extensive review of transcription factors and the NFκB pathway (Chapter I) to provide context for my work. I then describe a detailed analysis using hydrogen-deuterium exchange mass spectrometry (HDXMS) to probe the impact of IκBα binding on the internal dynamics of the p50/RelA NFκB heterodimer and demonstrate that long-range conformational changes induced by IκBα binding are of central importance to the inhibitory nature of the IκBα binding event (Chapter II).Chapter III describes the first detailed biophysical analysis of the most recently discovered IκB protein, IκBε. I combined homology modeling and HDXMS to establish the presence of a seventh ankyrin repeat (AR) in IκBε and further provide a framework for utilizing HDXMS as a tool to complement homology modeling of proteins with no known structures. After identifying the seventh AR in IκBε, I performed the first comprehensive examination of IκBε’s ability to bind all NFκB dimers and the biophysical consequences on IκBε’s internal dynamics upon binding to its preferred NFκB dimers (Chapter IV). Finally, to further probe the interaction of IκBε with its preferred NFκB binding partners, I describe the impact of IκBε binding on the dynamics of the cRel heterodimers which are the NFκB proteins which bind IκBε with the highest affinity and discover the importance of entropic forces in driving these high affinity interactions (Chapter V).

Subjects/Keywords: Biophysics; Biochemistry; biophysics; ikappab; nf-kappab; protein biochemistry

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ramsey, K. M. (2018). The Role of Protein Structure and Dynamics in the Inhibition of NF-kappaB by IkappaB Proteins. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/6j05k57m

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ramsey, Kristen Michelle. “The Role of Protein Structure and Dynamics in the Inhibition of NF-kappaB by IkappaB Proteins.” 2018. Thesis, University of California – San Diego. Accessed March 03, 2021. http://www.escholarship.org/uc/item/6j05k57m.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ramsey, Kristen Michelle. “The Role of Protein Structure and Dynamics in the Inhibition of NF-kappaB by IkappaB Proteins.” 2018. Web. 03 Mar 2021.

Vancouver:

Ramsey KM. The Role of Protein Structure and Dynamics in the Inhibition of NF-kappaB by IkappaB Proteins. [Internet] [Thesis]. University of California – San Diego; 2018. [cited 2021 Mar 03]. Available from: http://www.escholarship.org/uc/item/6j05k57m.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ramsey KM. The Role of Protein Structure and Dynamics in the Inhibition of NF-kappaB by IkappaB Proteins. [Thesis]. University of California – San Diego; 2018. Available from: http://www.escholarship.org/uc/item/6j05k57m

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Rochester

12. Perez-Nazario, Nelissa. Alveolar Epithelial Cell Activation of IKK2 during Pneumocystis Infection Regulates Immunity and Organism Clearance.

Degree: PhD, 2013, University of Rochester

URL: http://hdl.handle.net/1802/27241

► Pneumocystis (Pc) is an atypical fungal pathogen which causes severe, often fatal, pneumonia (PcP) in immunocompromised patients and remains a hallmark opportunistic infection in AIDS… (more)

Subjects/Keywords: Alveolar Epithelial Cells; IKK2; NF-KappaB; Pneumocystis; Th17

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Perez-Nazario, N. (2013). Alveolar Epithelial Cell Activation of IKK2 during Pneumocystis Infection Regulates Immunity and Organism Clearance. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/27241

Chicago Manual of Style (16^th Edition):

Perez-Nazario, Nelissa. “Alveolar Epithelial Cell Activation of IKK2 during Pneumocystis Infection Regulates Immunity and Organism Clearance.” 2013. Doctoral Dissertation, University of Rochester. Accessed March 03, 2021. http://hdl.handle.net/1802/27241.

MLA Handbook (7^th Edition):

Perez-Nazario, Nelissa. “Alveolar Epithelial Cell Activation of IKK2 during Pneumocystis Infection Regulates Immunity and Organism Clearance.” 2013. Web. 03 Mar 2021.

Vancouver:

Perez-Nazario N. Alveolar Epithelial Cell Activation of IKK2 during Pneumocystis Infection Regulates Immunity and Organism Clearance. [Internet] [Doctoral dissertation]. University of Rochester; 2013. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1802/27241.

Council of Science Editors:

Perez-Nazario N. Alveolar Epithelial Cell Activation of IKK2 during Pneumocystis Infection Regulates Immunity and Organism Clearance. [Doctoral Dissertation]. University of Rochester; 2013. Available from: http://hdl.handle.net/1802/27241

University of Alberta

13. van Buuren, Nicholas J. Ectromelia Virus Encodes A Novel Family Of Ankyrin/F-box Proteins That Manipulate The SCF Ubiquitin Ligase And NF-κB Activation.

Degree: PhD, Department of Medical Microbiology and Immunology, 2012, University of Alberta

URL: https://era.library.ualberta.ca/files/kd17ct24x

► Ectromelia virus (ECTV) is the causative agent of lethal mousepox, and is highly related to the human pathogen, variola virus, the causative agent of smallpox.… (more)

▼ Ectromelia virus (ECTV) is the causative agent of lethal mousepox, and is highly related to the human pathogen, variola virus, the causative agent of smallpox. Poxviruses contain large dsDNA genomes that encode numerous open reading frames that manipulate cellular signalling pathways. We used bioinformatics to identify a family of four genes encoded by ECTV that contain N-terminal ankyrin repeats in conjunction with a C-terminal F-box domain. The ECTV encoded ankyrin/F-box proteins: EVM002, EVM005, EVM154 and EVM165, all interact with the cellular SCF (Skp1/Cul-1/F-box) ubiquitin ligase complex through an interaction mediated by their C-terminal F-box domain. These four proteins bind to the SCF complex in a similar manner to cellular F-box-containing substrate adaptor proteins. We hypothesize that each of the ECTV encoded ankyrin/F-box proteins recruits a unique family of target proteins to the SCF complex for ubiquitylation. The NF-κB signalling cascade is an important mediator of innate immunity, and is tightly regulated by ubiquitylation. A critical step in the activation of NF-κB is the ubiquitylation and degradation of the inhibitor of kappaB (IκBα), by the cellular SCFβ-TRCP ubiquitin ligase. Upon stimulation with TNFα or IL-1β, orthopoxvirus-infected cells display an accumulation of phosphorylated IκBα, indicating that NF-κB activation is inhibited during poxvirus infection at the point of IκBα degradation. Since degradation of IκBα is catalyzed by the SCFβ-TRCP ubiquitin ligase complex we investigated the role of the ECTV encoded ankyrin/F-box proteins in the regulation of NF-κB activation. Expression of Flag-EVM005 inhibited both IκBα degradation and p65 nuclear translocation in response to TNFα or IL-1β. Regulation of the NF-κB pathway by EVM005 was dependent on the F-box domain, and interaction with the SCF complex. Additionally, we created ECTV knockout viruses devoid of each of the four ankyrin/F-box genes using a novel “Selectable and Excisable Marker” system. The EVM005 deletion virus was shown to inhibit NF-κB activation despite lacking the EVM005 open reading frame; however, this virus was attenuated in two mouse strains. The contribution of EVM005 to virulence is therefore independent from its ability to inhibit NF-κB activation, and is potentially linked to unique target proteins ubiquitylated through the SCF complex during infection.

Subjects/Keywords: NF-kappaB; Poxvirus; Ubiquitin; F-box; SCF ubiqutin ligase

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APA (6^th Edition):

van Buuren, N. J. (2012). Ectromelia Virus Encodes A Novel Family Of Ankyrin/F-box Proteins That Manipulate The SCF Ubiquitin Ligase And NF-κB Activation. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/kd17ct24x

Chicago Manual of Style (16^th Edition):

van Buuren, Nicholas J. “Ectromelia Virus Encodes A Novel Family Of Ankyrin/F-box Proteins That Manipulate The SCF Ubiquitin Ligase And NF-κB Activation.” 2012. Doctoral Dissertation, University of Alberta. Accessed March 03, 2021. https://era.library.ualberta.ca/files/kd17ct24x.

MLA Handbook (7^th Edition):

van Buuren, Nicholas J. “Ectromelia Virus Encodes A Novel Family Of Ankyrin/F-box Proteins That Manipulate The SCF Ubiquitin Ligase And NF-κB Activation.” 2012. Web. 03 Mar 2021.

Vancouver:

van Buuren NJ. Ectromelia Virus Encodes A Novel Family Of Ankyrin/F-box Proteins That Manipulate The SCF Ubiquitin Ligase And NF-κB Activation. [Internet] [Doctoral dissertation]. University of Alberta; 2012. [cited 2021 Mar 03]. Available from: https://era.library.ualberta.ca/files/kd17ct24x.

Council of Science Editors:

van Buuren NJ. Ectromelia Virus Encodes A Novel Family Of Ankyrin/F-box Proteins That Manipulate The SCF Ubiquitin Ligase And NF-κB Activation. [Doctoral Dissertation]. University of Alberta; 2012. Available from: https://era.library.ualberta.ca/files/kd17ct24x

Temple University

14. Happel, Christine. Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression.

Degree: PhD, 2009, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,28438

►

Molecular Biology and Genetics

Opioid receptor modulation of pro-inflammatory cytokine production is vital for host defense and the inflammatory response. Previous results have shown the… (more)

Subjects/Keywords: Biology, Microbiology; Chemokines; NF-kappaB; Opioid; Opioid receptor; PKC

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APA (6^th Edition):

Happel, C. (2009). Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,28438

Chicago Manual of Style (16^th Edition):

Happel, Christine. “Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression.” 2009. Doctoral Dissertation, Temple University. Accessed March 03, 2021. http://digital.library.temple.edu/u?/p245801coll10,28438.

MLA Handbook (7^th Edition):

Happel, Christine. “Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression.” 2009. Web. 03 Mar 2021.

Vancouver:

Happel C. Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression. [Internet] [Doctoral dissertation]. Temple University; 2009. [cited 2021 Mar 03]. Available from: http://digital.library.temple.edu/u?/p245801coll10,28438.

Council of Science Editors:

Happel C. Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression. [Doctoral Dissertation]. Temple University; 2009. Available from: http://digital.library.temple.edu/u?/p245801coll10,28438

Vanderbilt University

15. Hill-McAlester, Andrea Alyssa. Activation of NF-κB drives the enhanced survival of adipose tissue macrophages in an obesogenic environment.

Degree: PhD, Molecular Physiology and Biophysics, 2015, Vanderbilt University

URL: http://hdl.handle.net/1803/14070

► Objective: Obesity has become a major worldwide health issue over the past few years and often leads to insulin resistance (IR) and type 2 diabetes… (more)

▼ Objective: Obesity has become a major worldwide health issue over the past few years and often leads to insulin resistance (IR) and type 2 diabetes (T2D). Macrophage accumulation in adipose tissue (AT) during obesity contributes to inflammation and IR. In the decade since macrophages were shown to accumulate in AT, the majority of studies have focused on recruitment-dependent mechanisms for their accrual. However, recent evidence suggests that recruitment-independent mechanisms, including increased proliferation and decreased egress, may also regulate pro-inflammatory AT macrophage (ATM) numbers. Interestingly the regulation of longevity in ATM accrual in obesity had not been explored. The work in my dissertation shows that increased ATM survival during obesity is a recruitment-independent mechanism that contributes to ATM accumulation. Results: My studies demonstrated that cleaved caspase 3 activation is significantly reduced in the ATMs of diet-induced and genetically obese mice. This data suggests that activation of apoptotic pathways is significantly reduced in ATMs from diet-induced and genetically obese mice. Concurrently, pro-survival Bcl-2 family member protein levels and localization to the mitochondria was elevated in ATMs from obese mice. Conversely, the activities of pro-apoptotic proteins Bax and Bak were decreased in ATMs from obese compared to lean mice. Interestingly, this increased pro-survival signaling in obese ATMs was associated with elevated activation of the p65 subunit of the transcription factor, NF-κB. Furthermore, NF-κB was more nuclear localized in ATMs of obese mice, resulting in increased expression of NF-κB pro-survival target genes, XIAP and cIAP. Finally, an obesogenic milieu increased ATM viability only when NF-κB signaling pathways were functional. Conclusions: Our data demonstrate that obesity promotes survival of inflammatory ATMs, possibly through an NF-κB-regulated mechanism. Advisors/Committee Members: Fiona Yull (committee member), Bryan Venters (committee member), Linda Sealy (committee member), Owen McGuinness (Committee Chair).

Subjects/Keywords: Adipose Tissue Macrophages; Survival; NF-kappaB; Inflammation; Obesity

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APA (6^th Edition):

Hill-McAlester, A. A. (2015). Activation of NF-κB drives the enhanced survival of adipose tissue macrophages in an obesogenic environment. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14070

Chicago Manual of Style (16^th Edition):

Hill-McAlester, Andrea Alyssa. “Activation of NF-κB drives the enhanced survival of adipose tissue macrophages in an obesogenic environment.” 2015. Doctoral Dissertation, Vanderbilt University. Accessed March 03, 2021. http://hdl.handle.net/1803/14070.

MLA Handbook (7^th Edition):

Hill-McAlester, Andrea Alyssa. “Activation of NF-κB drives the enhanced survival of adipose tissue macrophages in an obesogenic environment.” 2015. Web. 03 Mar 2021.

Vancouver:

Hill-McAlester AA. Activation of NF-κB drives the enhanced survival of adipose tissue macrophages in an obesogenic environment. [Internet] [Doctoral dissertation]. Vanderbilt University; 2015. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1803/14070.

Council of Science Editors:

Hill-McAlester AA. Activation of NF-κB drives the enhanced survival of adipose tissue macrophages in an obesogenic environment. [Doctoral Dissertation]. Vanderbilt University; 2015. Available from: http://hdl.handle.net/1803/14070

Vanderbilt University

16. Carver, Billy Joe. NF-κB interacts with SP3 to limit SP1-mediated FGF-10 expression in the developing fetal lung.

Degree: PhD, Cell and Developmental Biology, 2013, Vanderbilt University

URL: http://hdl.handle.net/1803/13944

► Arrested lung development in preterm infants leads to bronchopulmonary dysplasia (BPD). Inflammation and NF-κB activation in the fetal lung inhibit airway morphogenesis and contribute to… (more)

Subjects/Keywords: inflammation; developmental biology; branching morphogenesis; NF-kappaB; mesenchymal cells; lung development

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APA (6^th Edition):

Carver, B. J. (2013). NF-κB interacts with SP3 to limit SP1-mediated FGF-10 expression in the developing fetal lung. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/13944

Chicago Manual of Style (16^th Edition):

Carver, Billy Joe. “NF-κB interacts with SP3 to limit SP1-mediated FGF-10 expression in the developing fetal lung.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed March 03, 2021. http://hdl.handle.net/1803/13944.

MLA Handbook (7^th Edition):

Carver, Billy Joe. “NF-κB interacts with SP3 to limit SP1-mediated FGF-10 expression in the developing fetal lung.” 2013. Web. 03 Mar 2021.

Vancouver:

Carver BJ. NF-κB interacts with SP3 to limit SP1-mediated FGF-10 expression in the developing fetal lung. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1803/13944.

Council of Science Editors:

Carver BJ. NF-κB interacts with SP3 to limit SP1-mediated FGF-10 expression in the developing fetal lung. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://hdl.handle.net/1803/13944

McMaster University

17. Lai, Frances W. The Human Coronavirus Nucleocapsid Protein and Its Effects on the Innate Immune Response.

Degree: PhD, 2013, McMaster University

URL: http://hdl.handle.net/11375/15288

►

Coronaviruses are the largest known RNA viruses and infect a wide range of hosts. Human coronaviruses traditionally have been known to be the cause… (more)

Subjects/Keywords: interferon; NF-kappaB; microRNA; immune evasion; Virology; Virology

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APA (6^th Edition):

Lai, F. W. (2013). The Human Coronavirus Nucleocapsid Protein and Its Effects on the Innate Immune Response. (Doctoral Dissertation). McMaster University. Retrieved from http://hdl.handle.net/11375/15288

Chicago Manual of Style (16^th Edition):

Lai, Frances W. “The Human Coronavirus Nucleocapsid Protein and Its Effects on the Innate Immune Response.” 2013. Doctoral Dissertation, McMaster University. Accessed March 03, 2021. http://hdl.handle.net/11375/15288.

MLA Handbook (7^th Edition):

Lai, Frances W. “The Human Coronavirus Nucleocapsid Protein and Its Effects on the Innate Immune Response.” 2013. Web. 03 Mar 2021.

Vancouver:

Lai FW. The Human Coronavirus Nucleocapsid Protein and Its Effects on the Innate Immune Response. [Internet] [Doctoral dissertation]. McMaster University; 2013. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/11375/15288.

Council of Science Editors:

Lai FW. The Human Coronavirus Nucleocapsid Protein and Its Effects on the Innate Immune Response. [Doctoral Dissertation]. McMaster University; 2013. Available from: http://hdl.handle.net/11375/15288

Penn State University

18. Yang, Chen. Epigenetic analysis Of immune associated signaling molecules during mouse retina development .

Degree: 2013, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/17636

► The retina is an immune-privileged organ. Many autoimmune diseases, such as age-related macular degeneration, glaucoma, and diabetic retinopathy, are caused by excessive inflammatory responses targeting… (more)

Subjects/Keywords: histone modification; retina; mouse; immunity; NF-kappaB; epigenetics; development

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APA (6^th Edition):

Yang, C. (2013). Epigenetic analysis Of immune associated signaling molecules during mouse retina development . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/17636

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Yang, Chen. “Epigenetic analysis Of immune associated signaling molecules during mouse retina development .” 2013. Thesis, Penn State University. Accessed March 03, 2021. https://submit-etda.libraries.psu.edu/catalog/17636.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Yang, Chen. “Epigenetic analysis Of immune associated signaling molecules during mouse retina development .” 2013. Web. 03 Mar 2021.

Vancouver:

Yang C. Epigenetic analysis Of immune associated signaling molecules during mouse retina development . [Internet] [Thesis]. Penn State University; 2013. [cited 2021 Mar 03]. Available from: https://submit-etda.libraries.psu.edu/catalog/17636.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Yang C. Epigenetic analysis Of immune associated signaling molecules during mouse retina development . [Thesis]. Penn State University; 2013. Available from: https://submit-etda.libraries.psu.edu/catalog/17636

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Boston University

19. Brennan, Joseph. Role of a sea anemone (Nematostella vectensis) toll-like receptor in pathogen detection, development, and activation of NF-kappaB signaling.

Degree: PhD, Biology, 2018, Boston University

URL: http://hdl.handle.net/2144/33241

► In organisms from insects to vertebrates, Toll-like receptors (TLRs) are primary pathogen detectors that activate downstream pathways, specifically those that direct expression of innate immune… (more)

Subjects/Keywords: Biology; Development; Evolution; Immunity; NF-kappaB; Pathogen; TLR

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APA (6^th Edition):

Brennan, J. (2018). Role of a sea anemone (Nematostella vectensis) toll-like receptor in pathogen detection, development, and activation of NF-kappaB signaling. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/33241

Chicago Manual of Style (16^th Edition):

Brennan, Joseph. “Role of a sea anemone (Nematostella vectensis) toll-like receptor in pathogen detection, development, and activation of NF-kappaB signaling.” 2018. Doctoral Dissertation, Boston University. Accessed March 03, 2021. http://hdl.handle.net/2144/33241.

MLA Handbook (7^th Edition):

Brennan, Joseph. “Role of a sea anemone (Nematostella vectensis) toll-like receptor in pathogen detection, development, and activation of NF-kappaB signaling.” 2018. Web. 03 Mar 2021.

Vancouver:

Brennan J. Role of a sea anemone (Nematostella vectensis) toll-like receptor in pathogen detection, development, and activation of NF-kappaB signaling. [Internet] [Doctoral dissertation]. Boston University; 2018. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2144/33241.

Council of Science Editors:

Brennan J. Role of a sea anemone (Nematostella vectensis) toll-like receptor in pathogen detection, development, and activation of NF-kappaB signaling. [Doctoral Dissertation]. Boston University; 2018. Available from: http://hdl.handle.net/2144/33241

National University of Ireland – Galway

20. Sessler, Tamas. Regulators of TRAIL resistance in normal and transformed cells .

Degree: 2015, National University of Ireland – Galway

URL: http://hdl.handle.net/10379/5061

► TRAIL is a member of the Tumor Necrosis Factor superfamily which was shown to be able to induce apoptotic cell death in a wide variety… (more)

▼ TRAIL is a member of the Tumor Necrosis Factor superfamily which was shown to be able to induce apoptotic cell death in a wide variety of transformed cells, leaving normal, healthy cells unharmed. However, approximately 50-60% of the cancer cells were shown to be resistant to the cytotoxic effect of TRAIL, a large number of chemotherapeutics are being studied to broaden the efficacy of TRAIL. However the effect of these co-treatments on non-transformed cells is unpredictable as at present we do not have a proper understanding on the regulation behind the resistance of normal cells to TRAIL. Preliminary works in our lab showed that in primary non-transformed cells TRAIL resistance is maintained by multiple anti-apoptotic proteins. In order to overcome the resistance toward TRAIL-induced apoptosis, the pathway has to be inhibited at two different stages by removal of anti-apoptotic proteins (cFLIP, Mcl-1, Bcl-2, Bcl-XL or XIAP). Using different transcription site searches we have identified the transcription factor Sp1 as a candidate for maintaining the expression levels of these anti-apoptotic proteins, which in turn is regulated by the activity of GSK3 and CDK1. In contrast to the observed redundancy in resistance mechanism to TRAIL seen in non-transformed cell lines, the majority of the cancer cell lines tend to rely on a single mechanism of resistance against TRAIL. This redundancy in TRAIL resistance in non-transformed cells indicate that there is a safe therapeutic window using TRAIL-based combination therapies, which targets a single, dominating resistance pathway. However knowledge of the mechanism of resistance should aid the choice of therapy. TRAIL also activates non-apoptotic/inflammatory signaling, such as the NF-kappaB pathway which in certain cases may drive the resistance to TRAIL. In order to examine the involvement of this non-apoptotic pathway in TRAIL signaling, a reliable inhibitor would be needed that is able to uncouple the death ligand-mediated canonical NF-kappaB activation from apoptosis signaling. Using computer-aided drug design we have performed several virtual screening methods to identify lead molecules that would be able to break up the interaction between TRADD and TRAF2 and thus selectively block death receptor induced NF-kappaB activation. Advisors/Committee Members: Szegezdi, Eva (advisor).

Subjects/Keywords: TRAIL; Apoptosis; NF-kappaB; Virtual screening; Apoptosis Centre; Biochemistry; Natural Sciences

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APA (6^th Edition):

Sessler, T. (2015). Regulators of TRAIL resistance in normal and transformed cells . (Thesis). National University of Ireland – Galway. Retrieved from http://hdl.handle.net/10379/5061

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sessler, Tamas. “Regulators of TRAIL resistance in normal and transformed cells .” 2015. Thesis, National University of Ireland – Galway. Accessed March 03, 2021. http://hdl.handle.net/10379/5061.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sessler, Tamas. “Regulators of TRAIL resistance in normal and transformed cells .” 2015. Web. 03 Mar 2021.

Vancouver:

Sessler T. Regulators of TRAIL resistance in normal and transformed cells . [Internet] [Thesis]. National University of Ireland – Galway; 2015. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10379/5061.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sessler T. Regulators of TRAIL resistance in normal and transformed cells . [Thesis]. National University of Ireland – Galway; 2015. Available from: http://hdl.handle.net/10379/5061

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Boston University

21. Cote, Shaun. Characterization of the structure and function of NF-KappaB essential modulator and its interaction with inhibitor of KappaB Kinase Beta and development of a screening protocol to discover and validate inhibitors of the interaction.

Degree: PhD, Chemistry, 2014, Boston University

URL: http://hdl.handle.net/2144/14292

► Protein-protein interactions (PPI) mediate numerous biological processes, but inhibiting these interactions with small molecules has been difficult to achieve in drug discovery. A small number… (more)

Subjects/Keywords: Biochemistry; Macrocycles; NEMO; NF-kappaB; Protein-protein interactions

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APA (6^th Edition):

Cote, S. (2014). Characterization of the structure and function of NF-KappaB essential modulator and its interaction with inhibitor of KappaB Kinase Beta and development of a screening protocol to discover and validate inhibitors of the interaction. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/14292

Chicago Manual of Style (16^th Edition):

Cote, Shaun. “Characterization of the structure and function of NF-KappaB essential modulator and its interaction with inhibitor of KappaB Kinase Beta and development of a screening protocol to discover and validate inhibitors of the interaction.” 2014. Doctoral Dissertation, Boston University. Accessed March 03, 2021. http://hdl.handle.net/2144/14292.

MLA Handbook (7^th Edition):

Cote, Shaun. “Characterization of the structure and function of NF-KappaB essential modulator and its interaction with inhibitor of KappaB Kinase Beta and development of a screening protocol to discover and validate inhibitors of the interaction.” 2014. Web. 03 Mar 2021.

Vancouver:

Cote S. Characterization of the structure and function of NF-KappaB essential modulator and its interaction with inhibitor of KappaB Kinase Beta and development of a screening protocol to discover and validate inhibitors of the interaction. [Internet] [Doctoral dissertation]. Boston University; 2014. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2144/14292.

Council of Science Editors:

Cote S. Characterization of the structure and function of NF-KappaB essential modulator and its interaction with inhibitor of KappaB Kinase Beta and development of a screening protocol to discover and validate inhibitors of the interaction. [Doctoral Dissertation]. Boston University; 2014. Available from: http://hdl.handle.net/2144/14292

Oklahoma State University

22. Saffarian Tousi, Neda. Neuromelanin and Alpha-synuclein Modulation of Inflammatory Signaling in Human Astroglial Cells.

Degree: Department of Biochemistry and Molecular Biology, 2011, Oklahoma State University

URL: http://hdl.handle.net/11244/6674

► The findings from the current study concluded a cytokine-dependent regulation of astroglial CXCL10 and iNOS expression by alpha-synuclein and neuromelanin. Alpha-synuclein induced the expression of… (more)

Subjects/Keywords: alpha-synuclein; cxcl10; inos; neuromelanin; nf-kappab; parkinson's disease

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APA (6^th Edition):

Saffarian Tousi, N. (2011). Neuromelanin and Alpha-synuclein Modulation of Inflammatory Signaling in Human Astroglial Cells. (Thesis). Oklahoma State University. Retrieved from http://hdl.handle.net/11244/6674

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Saffarian Tousi, Neda. “Neuromelanin and Alpha-synuclein Modulation of Inflammatory Signaling in Human Astroglial Cells.” 2011. Thesis, Oklahoma State University. Accessed March 03, 2021. http://hdl.handle.net/11244/6674.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Saffarian Tousi, Neda. “Neuromelanin and Alpha-synuclein Modulation of Inflammatory Signaling in Human Astroglial Cells.” 2011. Web. 03 Mar 2021.

Vancouver:

Saffarian Tousi N. Neuromelanin and Alpha-synuclein Modulation of Inflammatory Signaling in Human Astroglial Cells. [Internet] [Thesis]. Oklahoma State University; 2011. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/11244/6674.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Saffarian Tousi N. Neuromelanin and Alpha-synuclein Modulation of Inflammatory Signaling in Human Astroglial Cells. [Thesis]. Oklahoma State University; 2011. Available from: http://hdl.handle.net/11244/6674

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Illinois – Urbana-Champaign

23. Willis, Kristen L. Characterization of the anti-viral effects inhibited by the vaccinia virus K1 protein.

Degree: PhD, 0322, 2011, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/18499

► Vaccinia virus (VV), a member of the poxvirus family of double-stranded DNA viruses, is well-known as a highly effective vaccine against variola virus, the causative… (more)

▼ Vaccinia virus (VV), a member of the poxvirus family of double-stranded DNA viruses, is well-known as a highly effective vaccine against variola virus, the causative agent of smallpox. Poxviruses encode many strategies to evade the host immune and anti-viral response. One such host anti-viral response, activation of the double-stranded RNA activated protein kinase (PKR) pathway, is important in sensing the presence of intracellular viral genomes and their products. PKR is activated by dsRNA, a by-product of many virus infections, and exhibits its anti-viral effects in part via inhibition of protein synthesis and activation of the pro-inflammatory transcription factor NF-κB. I have identified the vaccinia virus K1 protein as an inhibitor of PKR activation. I determined that the C-terminal portion of the 2nd ankyrin repeat, a motif important for protein-protein interactions, is important for this inhibitory function. Further, K1 mediated PKR inhibition also blocks activation of downstream NF-κB in VV infected cells. Previous characterization of the K1 protein identified it as a host-range protein required for a productive infection. When the K1L gene is absent, replication is aborted due to shut-down in viral protein synthesis. I queried whether PKR was responsible for this effect. I found that replication when K1 was lacking could not be rescued by depletion of PKR protein levels. Hence K1 inhibition of PKR is not related to the host-range function. I next identified that the trigger for PKR activation is viral dsRNAs derived from early or intermediate viral transcription. As early dsRNAs have never been reported during a poxvirus infection, this finding was novel. Further, I found that there were higher levels of dsRNA present during a VV infection when K1 was absent or mutated. Finally, ectopic expression of K1 was able to inhibit PKR activation induced by viral dsRNAs. Together these data identifies a new function for the K1 protein and elucidates a strategy viruses utilize to inhibit detrimental host cell responses. Advisors/Committee Members: Shisler, Joanna L. (advisor), Shisler, Joanna L. (Committee Chair), Cronan, John E. (committee member), Blanke, Steven R. (committee member), Metcalf, William W. (committee member).

Subjects/Keywords: vaccinia virus; protein kinase (PKR); NF-kappaB; K1 protein

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APA (6^th Edition):

Willis, K. L. (2011). Characterization of the anti-viral effects inhibited by the vaccinia virus K1 protein. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/18499

Chicago Manual of Style (16^th Edition):

Willis, Kristen L. “Characterization of the anti-viral effects inhibited by the vaccinia virus K1 protein.” 2011. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed March 03, 2021. http://hdl.handle.net/2142/18499.

MLA Handbook (7^th Edition):

Willis, Kristen L. “Characterization of the anti-viral effects inhibited by the vaccinia virus K1 protein.” 2011. Web. 03 Mar 2021.

Vancouver:

Willis KL. Characterization of the anti-viral effects inhibited by the vaccinia virus K1 protein. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2011. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2142/18499.

Council of Science Editors:

Willis KL. Characterization of the anti-viral effects inhibited by the vaccinia virus K1 protein. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2011. Available from: http://hdl.handle.net/2142/18499

University of Illinois – Urbana-Champaign

24. Martin, Stefani. Examination of the role of early viral protein expression in MVA-induced NF-??B activation.

Degree: PhD, 0322, 2012, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/29572

► NF-??B, a potent pro-inflammatory cellular transcription factor, is an inhibition target for many viruses, including the prototypic poxvirus member, vaccinia virus (VACV). However, infection of… (more)

▼ NF-??B, a potent pro-inflammatory cellular transcription factor, is an inhibition target for many viruses, including the prototypic poxvirus member, vaccinia virus (VACV). However, infection of HEK293T cells with the attenuated Modified Vaccinia Virus Ankara (MVA) no longer inhibits NF-??B activation, due to the absence of various host range and immunosuppressive genes in this strain. The work presented here focused on investigating the viral molecular mechanism responsible for the activation of NF-??B. To that end, we found that infection with MVA in the presence of AraC, a drug that inhibits viral DNA replication and intermediate and late gene expression, results in NF-??B nuclear translocation. However, under conditions where either viral entry is blocked, the virions are inactivated, or viral mRNA synthesis is prevented, NF-??B remains inactive in virus-infected cells. Thus, early viral gene transcription is responsible for MVA-triggered NF-??B activation. To identify the viral ORF(s) whose products activate NF-??B during MVA infection, we first tested a VACV plasmid library to identify which viral ORF could activate a NF-??B-controlled firefly luciferase gene. We then utilized chemically synthesized siRNAs, testing the effect of silencing each of the viral genes individually on MVA-induced NF-??B activation in these cells. Three viral genes (C11R, E7R, and A35R) have been identified whose silencing can prevent MVA-induced ERK1/2 activation, which occurs upstream of NF-??B activation. The product of C11R, a viral growth factor protein, is capable of inducing ERK1/2 and NF-??B activation in the host 293T cells when it is expressed ectopically. Furthermore, infection with a deletion mutant virus, MVA??C11R, resulted in reduced ERK2 phosphorylation and NF-??B activation compared to cells infected with the parental MVA strain. This reduction was observed in both 293T cells and in keratenocyte cell line, HaCaT, indicating the C11R protein product modulates viral-induced NF-??B activation in multiple cell types. Future work should focus on the molecular pathway utilized by C11 and the additional contributions the E7 and A35 proteins have in MVA-induced NF-??B activation. Advisors/Committee Members: Shisler, Joanna L. (advisor), Tapping, Richard I. (committee member), Wilson, Brenda A. (committee member), Kuzminov, Andrei (committee member).

Subjects/Keywords: Modified Vaccinia Virus Ankara (MVA); NF-kappaB; Vaccinia

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Martin, S. (2012). Examination of the role of early viral protein expression in MVA-induced NF-??B activation. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/29572

Chicago Manual of Style (16^th Edition):

Martin, Stefani. “Examination of the role of early viral protein expression in MVA-induced NF-??B activation.” 2012. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed March 03, 2021. http://hdl.handle.net/2142/29572.

MLA Handbook (7^th Edition):

Martin, Stefani. “Examination of the role of early viral protein expression in MVA-induced NF-??B activation.” 2012. Web. 03 Mar 2021.

Vancouver:

Martin S. Examination of the role of early viral protein expression in MVA-induced NF-??B activation. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2012. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2142/29572.

Council of Science Editors:

Martin S. Examination of the role of early viral protein expression in MVA-induced NF-??B activation. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2012. Available from: http://hdl.handle.net/2142/29572

25. Wang, Gaochan. Diarrheagenic Escherichia coli signaling and interactions with host innate immunity and intestinal microbiota.

Degree: PhD, Department of Diagnostic Medicine/Pathobiology, 2017, Kansas State University

URL: http://hdl.handle.net/2097/35735

► Diarrheagenic Escherichia coli (E. coli) strains are common etiological agents of diarrhea. Diarrheagenic E. coli are classified into enterotoxigenic E. coli (ETEC), Shiga toxin-producing E.… (more)

▼ Diarrheagenic Escherichia coli (E. coli) strains are common etiological agents of diarrhea. Diarrheagenic E. coli are classified into enterotoxigenic E. coli (ETEC), Shiga toxin-producing E. coli (STEC or enterohemorrhagic E. coli [EHEC]), enteropathogenic E. coli (EPEC), enteroinvasive E. coli (EIEC), enteroaggregative E. coli (EAEC), diffuse-adherent E. coli (DAEC), and adherent invasive E. coli (AIEC). In addition to encoding toxins that cause diarrhea, diarrheagenic E. coli have evolved numerous strategies to interfere with host defenses. In the first project, we identified an ETEC-secreted factor (ESF) that blocked TNF-induced NF-[kappa]B activation. One of the consequences of TNF-induced NF-[kappa]B activation is the production of pro-inflammatory cytokines that help to eliminate pathogens. Modulation of NF-[kappa]B signaling may promote ETEC colonization of the host small intestine. In this study, we fractionated ETEC supernatants and identified flagellin as necessary and sufficient for blocking the degradation of the NF-[kappa]B inhibitor I[kappa]B[alpha] in response to TNF[alpha]. In the second project, we attempted to identify an ETEC cAMP importer. ETEC diarrhea leads to cAMP release into the lumen of the small intestine. cAMP is a key secondary messenger that regulates ETEC adhesin expression. We hypothesized that a cAMP importer is present in ETEC, accounting for its hypersensitivity to extracellular cAMP. We used Tn5 transposome-mediated mutagenesis to construct a mutant library and screen for cAMP-hyporesponsive mutants. However, none of the 17,956 mutants we screened were cAMP-hyporesponsive. In the third project, we focused on gut microbiota and the T3SS effector NleH. We used the mouse-specific pathogen C. rodentium and transplanted performed microbiota between different mouse strains. We evaluated microbiota populations as a function of infection with WT and [Delta]nleH C. rodentium strains before and after microbiota transplantation. Microbiota transfer altered the resistance to WT C. rodentium infection in C57BL/10ScNJ mice and the NleH effector promoted host resistance to C. rodentium. Advisors/Committee Members: Philip R. Hardwidge.

Subjects/Keywords: Diarrheagenic E. coli; NF-kappaB; flagellin; Microbiota; cyclin AMP; T3SS effector

10 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Wang, G. (2017). Diarrheagenic Escherichia coli signaling and interactions with host innate immunity and intestinal microbiota. (Doctoral Dissertation). Kansas State University. Retrieved from http://hdl.handle.net/2097/35735

Chicago Manual of Style (16^th Edition):

Wang, Gaochan. “Diarrheagenic Escherichia coli signaling and interactions with host innate immunity and intestinal microbiota.” 2017. Doctoral Dissertation, Kansas State University. Accessed March 03, 2021. http://hdl.handle.net/2097/35735.

MLA Handbook (7^th Edition):

Wang, Gaochan. “Diarrheagenic Escherichia coli signaling and interactions with host innate immunity and intestinal microbiota.” 2017. Web. 03 Mar 2021.

Vancouver:

Wang G. Diarrheagenic Escherichia coli signaling and interactions with host innate immunity and intestinal microbiota. [Internet] [Doctoral dissertation]. Kansas State University; 2017. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/2097/35735.

Council of Science Editors:

Wang G. Diarrheagenic Escherichia coli signaling and interactions with host innate immunity and intestinal microbiota. [Doctoral Dissertation]. Kansas State University; 2017. Available from: http://hdl.handle.net/2097/35735

University of New South Wales

26. Tan, Meijun Bernice. BIRC proteins in the control of TNF signalling in pancreatic beta cells.

Degree: Clinical School - St Vincent's Hospital, 2012, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/52467 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11140/SOURCE01?view=true

► TNFα contributes to type 1 diabetes pathogenesis by impairing beta cell function and driving beta cell apoptosis. How TNFα directs these processes is not fully… (more)

▼ TNFα contributes to type 1 diabetes pathogenesis by impairing beta cell function and driving beta cell apoptosis. How TNFα directs these processes is not fully understood. Of note, baculoviral-IAP-repeat-containing (BIRC) proteins associate with the TNF complex to control down stream signaling but their function in beta cells is not known. Following TNF receptor ligation, Birc3 but not Birc1,2,4,5 or -6 was induced in mouse islets and MIN6 cells. Contact with TNFα triggers signaling cascades converging on the NF-κB, JNK, and p38 pathways that regulate inflammatory genes. The Birc3-promoter harboured three NF-κB and an AP-1 binding sites. Induction of endogenous Birc3 by TNFα was completely blocked by NF-κB inhibitors - thus NF-κB regulates Birc3 transcription. Further, BIRC3 gain-of-function induced activation of an NF-κB reporter and potentiated TNFα-induced NF-κB activation. Surprisingly, Birc3-/- islets showed delayed but functional NF-κB activation and exhibited dysregulated TNFα-induced Ccl2, Cxcl10 and Icam-1. Some data demonstrate BIRC2 can compensate for loss of BIRC3. Expectedly, Birc2-/-Birc3-/- islets showed markedly delayed IκBα degradation kinetics; suggesting that BIRC2/3 are crucial for NF-κB signaling. Remarkably, Birc2-/- and Birc3-/- islets showed unexpected phenotypes independent of NF-κB. Genetic analysis showed Birc2-/- islets exhibited increased basal Ccl2 and Cxcl10 expression. Cell signaling was further dysregulated by the addition of BIRC3 deficiency. Birc2-/-Birc3-/- islets exhibited increased basal A20, Icam-1, Ccl2 and Cxcl10, which were blocked by antagonizing JNK but not NF-κB or p38 pathway. Moreover, Birc2-/-Birc3-/- islets showed hyperphosphorylation of the JNK-target, c-Jun. BIRC proteins ubiquitinate substrates targeting them for proteosomal degradation. Proteosome inhibition in MIN6 cells mimicked the Birc2-/-Birc3-/- islet phenotype – increased basal Cxcl10, Ccl2 and Icam-1 expression with c-Jun-hyperphosphorylation. Birc2-/-Birc3-/- islets transplanted into diabetic-allogeneic recipients showed rapid loss of function indicative of dysregulated stress response. We propose that loss of BIRC2/3 uncoupled molecular control of inflammatory genes from TNF-signaling cascades. These present data demonstrate a novel, cell specific role for BIRC2 and BIRC3 as molecular rheostat that fine-tune NF-κB and JNK signaling to ensure transcriptional responses are appropriately matched to extra-cellular inputs. These pathways may be critical for beta cell stress responses. Advisors/Committee Members: Grey, Shane, Faculty of Medicine, UNSW.

Subjects/Keywords: Diabetes; Beta cell; BIRC; Gene; Inflammation; JNK; NF-kappaB; TNF

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APA (6^th Edition):

Tan, M. B. (2012). BIRC proteins in the control of TNF signalling in pancreatic beta cells. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/52467 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11140/SOURCE01?view=true

Chicago Manual of Style (16^th Edition):

Tan, Meijun Bernice. “BIRC proteins in the control of TNF signalling in pancreatic beta cells.” 2012. Doctoral Dissertation, University of New South Wales. Accessed March 03, 2021. http://handle.unsw.edu.au/1959.4/52467 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11140/SOURCE01?view=true.

MLA Handbook (7^th Edition):

Tan, Meijun Bernice. “BIRC proteins in the control of TNF signalling in pancreatic beta cells.” 2012. Web. 03 Mar 2021.

Vancouver:

Tan MB. BIRC proteins in the control of TNF signalling in pancreatic beta cells. [Internet] [Doctoral dissertation]. University of New South Wales; 2012. [cited 2021 Mar 03]. Available from: http://handle.unsw.edu.au/1959.4/52467 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11140/SOURCE01?view=true.

Council of Science Editors:

Tan MB. BIRC proteins in the control of TNF signalling in pancreatic beta cells. [Doctoral Dissertation]. University of New South Wales; 2012. Available from: http://handle.unsw.edu.au/1959.4/52467 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:11140/SOURCE01?view=true

University of New South Wales

27. Malle, Elisabeth Karin. The non-canonical NF-kappaB pathway as a novel player in beta cell dysfunction in diabetes.

Degree: Clinical School - St Vincent's Hospital, 2014, University of New South Wales

URL: http://handle.unsw.edu.au/1959.4/54132 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:13257/SOURCE02?view=true

► Loss of pancreatic β cell mass and function is a feature of both type-1 and type-2 diabetes. The non-canonical NF-κB pathway has recently garnered attention… (more)

▼ Loss of pancreatic β cell mass and function is a feature of both type-1 and type-2 diabetes. The non-canonical NF-κB pathway has recently garnered attention at being involved in the development of peripheral insulin resistance (liver, muscle) in diabetes. Whether pancreatic β cell non-canonical NF-κB signalling contributes to glucose homeostasis and diabetes is unknown. We found that the non-canonical NF-κB pathway was activated in islets from diet-induced obese (DIO) mice compared to chow controls, as evidenced by accumulation of NF-κB-inducing kinase (NIK), IKKα phosphorylation, p100 to p52 processing and RelB accumulation. To examine the effect of NIK accumulation in β cells, we generated a genetic β cell-specific mouse model of constitutive NIK activation. The TRAF2/TRAF3/BIRC2/3 E3 ubiquitin ligase complex tightly controls activation of NIK. Deletion of either component (βTRAF or βBIRC) promotes β cell-intrinsic NIK activation. βTRAF2 mice showed exacerbated glucose intolerance and impaired first-phase insulin secretion in a DIO model. β cell mass was increased in βTRAF2 mice, indicating severely impaired insulin secretory capacity. βTRAF2 islets exhibited dysregulated TNFα-stimulated canonical NF-κB and MAPK signalling. To dissect out whether NIK activation was promoting β cell dysfunction, we next utilized a β cell-specific deletion of TRAF3. βTRAF3 mice phenocopied βTRAF2 mice showing defective first-phase insulin secretion and increased β cell mass. βTRAF3 islets exhibited hyper-activation of NIK but normal TNFα-stimulated canonical NF-κB and MAPK signalling. Next, we set out to determine whether increased β cell expansion in NIK ON mice per se might trigger β cell dysfunction or whether acute NIK activation would also alter β cell function. Using a drug-based approach, we examined function in islets treated with a BIRC-inhibitor (MV1; Smac-mimetic). Ex vivo, MV1-treated mouse islets showed impaired GSIS. In vivo, MV1 disrupted glucose homeostasis as MV1-treated islets failed to provide normal metabolic control in syngeneic transplant recipients, and MV1-injected zebrafish larvae exhibited hyper-glycosuria. In summary, we have discovered that the diabetic milieu triggers β cell-intrinsic NIK activation. Constitutive as well as acute activation of NIK precipitates β cell secretory defects in mice and fish. Thus, NIK is a critical signalling node regulating glucose homeostasis in diabetes. Advisors/Committee Members: Grey, Shane, Garvan Institute of Medical Research, Faculty of Medicine, UNSW.

Subjects/Keywords: Islet; Beta cell dysfunction; NF-kappaB; Inflammation; Diabetes

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APA (6^th Edition):

Malle, E. K. (2014). The non-canonical NF-kappaB pathway as a novel player in beta cell dysfunction in diabetes. (Doctoral Dissertation). University of New South Wales. Retrieved from http://handle.unsw.edu.au/1959.4/54132 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:13257/SOURCE02?view=true

Chicago Manual of Style (16^th Edition):

Malle, Elisabeth Karin. “The non-canonical NF-kappaB pathway as a novel player in beta cell dysfunction in diabetes.” 2014. Doctoral Dissertation, University of New South Wales. Accessed March 03, 2021. http://handle.unsw.edu.au/1959.4/54132 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:13257/SOURCE02?view=true.

MLA Handbook (7^th Edition):

Malle, Elisabeth Karin. “The non-canonical NF-kappaB pathway as a novel player in beta cell dysfunction in diabetes.” 2014. Web. 03 Mar 2021.

Vancouver:

Malle EK. The non-canonical NF-kappaB pathway as a novel player in beta cell dysfunction in diabetes. [Internet] [Doctoral dissertation]. University of New South Wales; 2014. [cited 2021 Mar 03]. Available from: http://handle.unsw.edu.au/1959.4/54132 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:13257/SOURCE02?view=true.

Council of Science Editors:

Malle EK. The non-canonical NF-kappaB pathway as a novel player in beta cell dysfunction in diabetes. [Doctoral Dissertation]. University of New South Wales; 2014. Available from: http://handle.unsw.edu.au/1959.4/54132 ; https://unsworks.unsw.edu.au/fapi/datastream/unsworks:13257/SOURCE02?view=true

University of Cincinnati

28. Haar, Lauren. Acute High Fat Mediated Cardioprotection and the Underlying Mechanisms of Action.

Degree: PhD, Medicine: Systems Biology and Physiology, 2014, University of Cincinnati

URL: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406901036

► AbstractBackground and Significance: Evidence from large-scale clinical studies shows a paradoxical relationship between a high fat diet and myocardial pathophysiology. Termed the `obesity paradox’, data… (more)

▼ AbstractBackground and Significance: Evidence from large-scale clinical studies shows a paradoxical relationship between a high fat diet and myocardial pathophysiology. Termed the `obesity paradox’, data from these studies indicate that obesity and a high BMI have an inverse relationship with mortality after myocardial infarction (MI), even with increased risk for an initial coronary event. Chronically, high fat diets lead to dyslipidemia, obesity-induced inflammation, adipogenesis, glucose resistance, diabetes, and sustained elevation of serum cholesterol levels. This work will investigate the discovery that cardioprotection against ischemia/reperfusion (I/R) injury occurs after a very short duration of high fat feeding. This timeline suggests that this cardioprotection is independent from the chronic effects of high fat feeding. Rather, there must be an acute effect, the nature of which has not previously been studied. Objectives: These studies investigated the effects of the high fat diet on infarct size post-MI, on NF-?B activation in the heart, and the potential mechanistic relationship between NF-?B and high fat diet (HFD) induced cardioprotection. We hypothesize that NF-?B is activated acutely in the heart via high fat diet, and contributes to the regulation of a cardioprotective gene network. NF-?B is known to be activated in inflammatory states and also is activated by specific oxidized lipids in tissues. NF-?B has been shown to play a pro-cell death role in I/R as well as a protective role in ischemic preconditioning. Thus, it is a likely mediator of the effects of a high fat diet on cardiac myocyte signaling. Understanding this mechanism is essential to revealing new therapeutic targets (genes and their products) that can be manipulated to utilize cardioprotection in the clinical setting. Major Findings: The primary finding of this study shows that short-term high fat diet elicits a cardioprotective effect against I/R injury. This effect is attenuated with long term high fat feeding. Since short term feeding does not present complications commonly found in chronic high fat studies it presents a promising option for development into clinical therapy. High fat mediated protection is predicated on the activation of NF-?B gene programs that contribute to the upregulation of autophagy. This is commonly observed in cardioprotective preconditioning phenomena. The activation of these gene programs may be facilitated by neural-hormonal activation of cell receptors via adiponectin, influential changes in intestinal microflora and activation of serum-mediated events.Conclusions: Acute high fat feeding is cardioprotective against I/R injury. A regulatory checkpoint in this effect occurs at the level of NF-?B transcription. High fat feeding regulates activation of NF-?B profiles known to play a role in cardioprotection, including HSP70.3 and Beclin-1. The induction of autophagic programs without subsequent increase in apoptosis also contributes to this effect. This activation is hypothesized to be due, in part, to the… Advisors/Committee Members: Jones, Walter (Committee Chair).

Subjects/Keywords: Physiological Psychology; high fat diet; ischemia reperfusion injury; cardioprotection; NF kappaB

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APA (6^th Edition):

Haar, L. (2014). Acute High Fat Mediated Cardioprotection and the Underlying Mechanisms of Action. (Doctoral Dissertation). University of Cincinnati. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406901036

Chicago Manual of Style (16^th Edition):

Haar, Lauren. “Acute High Fat Mediated Cardioprotection and the Underlying Mechanisms of Action.” 2014. Doctoral Dissertation, University of Cincinnati. Accessed March 03, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406901036.

MLA Handbook (7^th Edition):

Haar, Lauren. “Acute High Fat Mediated Cardioprotection and the Underlying Mechanisms of Action.” 2014. Web. 03 Mar 2021.

Vancouver:

Haar L. Acute High Fat Mediated Cardioprotection and the Underlying Mechanisms of Action. [Internet] [Doctoral dissertation]. University of Cincinnati; 2014. [cited 2021 Mar 03]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406901036.

Council of Science Editors:

Haar L. Acute High Fat Mediated Cardioprotection and the Underlying Mechanisms of Action. [Doctoral Dissertation]. University of Cincinnati; 2014. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406901036

29. Souza, Ana Carolina Cavalcanti Pessôa de. Ação protetora da eritropoietina na injúria renal aguda em modelo experimental de sepse.

Degree: PhD, Nefrologia, 2010, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5148/tde-07052010-151836/ ;

►

A sepse envolve mecanismos complexos de respostas imunológicas e inflamatórias, e o papel do NF- B é essencial. A diminuição da NO sintase endotelial (eNOS)… (more)

▼

A sepse envolve mecanismos complexos de respostas imunológicas e inflamatórias, e o papel do NF- B é essencial. A diminuição da NO sintase endotelial (eNOS) durante a sepse contribui com a disfunção endotelial. A eritropoietina (EPO) é uma citocina protetora de diversos tecidos durante o estresse. Investigamos o papel da EPO na injúria renal aguda (IRA) induzida pela sepse usando o modelo de ligadura e punção do ceco (LPC). Ratos Wistar foram divididos em três grupos: controle; LPC e LPC+EPO (EPO, 4.000UI/kg, administrada 24h e 1h antes da cirurgia). Com a finalidade de estudar os efeitos precoces e tardios da EPO sobre a IRA induzida pela sepse realizamos três etapas de experimentos: Primeira etapa: 24 horas após LPC; Segunda etapa: 48 horas após LPC; Terceira etapa: análise de sobrevida. No estudo precoce o grupo LPC+EPO apresentou clearance de inulina significativamente maior que o grupo LPC. Recuperou os níveis de hematócrito na sepse, melhorou a pressão arterial e a acidose metabólica. No estudo tardio o grupo LPC+EPO apresentou clearance de creatinina significativamente maior que o grupo LPC. Nesta fase tardia a EPO recuperou os níveis de eNOS, suprimiu a infiltração de macrófagos no tecido renal e inibiu a ativação do NF- B. A EPO protege a função renal e aumenta a sobrevida neste modelo de sepse. A proteção da EPO na sepse é dependente, em parte, da inibição do NF- B e do aumento da expressão de eNOS

The pathophysiology of sepsis involves complex cytokine and inflammatory mediator networks, a mechanism to which nuclear factor-kappa B (NF- B ) activation is central. Downregulation of endothelial nitric oxide synthase (eNOS) contributes to sepsis-induced endothelial dysfunction. Erythropoietin (EPO) has emerged as a major tissue-protective cytokine in the setting of stress. We investigated the role of EPO in sepsis-related acute kidney injury (AKI) using a cecal ligation and puncture (CLP) model. Wistar rats were divided into three groups: control (sham-operated); CLP-only; and CLP+EPO. The EPO (4000 IU/kg BW, i.p.) was administered 24 h and 1 h before CLP. To study the early and late effects of EPO on sepsis-induced AKI, we performed experiments at 24 h and 48 h after CLP/sham operation, and we plotted the survival curves. At post-procedure hour 24, CLP+EPO rats presented significantly higher inulin clearance than did CLP-only rats; EPO treatment restored hematocrit levels, as well as mean arterial pressure and metabolic balance. At post-procedure hour 48, CLP+EPO rats presented significantly higher creatinine clearance than did CLP-only rats; EPO treatment restored eNOS levels, suppressed macrophage infiltration, and inhibited NF-B activation,thereby increasing survival. In conclusion, EPO protects renal function and increases survival in this model of sepsis-induced AKI. This protection is dependent on eNOS activation and is partly due to inhibition of the inflammatory response via downregulation of NF- B

Advisors/Committee Members: Andrade, Lucia da Conceição.

Subjects/Keywords: Eritropoetina; Erythropoietin; Insuficiência renal aguda; NF- kappaB; NF- kappaB; Nitric oxide synthase type III; Óxido nítrico sintase tipo III; Ratos Wistar; Renal insufficiency acute; Sepse; Sepsis; Wistar rats

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APA (6^th Edition):

Souza, A. C. C. P. d. (2010). Ação protetora da eritropoietina na injúria renal aguda em modelo experimental de sepse. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5148/tde-07052010-151836/ ;

Chicago Manual of Style (16^th Edition):

Souza, Ana Carolina Cavalcanti Pessôa de. “Ação protetora da eritropoietina na injúria renal aguda em modelo experimental de sepse.” 2010. Doctoral Dissertation, University of São Paulo. Accessed March 03, 2021. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-07052010-151836/ ;.

MLA Handbook (7^th Edition):

Souza, Ana Carolina Cavalcanti Pessôa de. “Ação protetora da eritropoietina na injúria renal aguda em modelo experimental de sepse.” 2010. Web. 03 Mar 2021.

Vancouver:

Souza ACCPd. Ação protetora da eritropoietina na injúria renal aguda em modelo experimental de sepse. [Internet] [Doctoral dissertation]. University of São Paulo; 2010. [cited 2021 Mar 03]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5148/tde-07052010-151836/ ;.

Council of Science Editors:

Souza ACCPd. Ação protetora da eritropoietina na injúria renal aguda em modelo experimental de sepse. [Doctoral Dissertation]. University of São Paulo; 2010. Available from: http://www.teses.usp.br/teses/disponiveis/5/5148/tde-07052010-151836/ ;

Tampere University

30. Kleino, Anni. The Imd pathway-mediated immune response in Drosophila .

Degree: Lääketieteellisen teknologian instituutti - Institute of Medical Technology, 2010, Tampere University

URL: https://trepo.tuni.fi/handle/10024/66627

► Kohtaamme elinympäristössämme päivittäin monenlaisia mikrobeja. Vaikka useimmat niistä ovat meille haitattomia tai jopa hyödyllisiä, osa voi kuitenkin aiheuttaa sairauksia. Nisäkkäillä, joihin ihminenkin kuuluu, kyky puolustautua… (more)

▼ Kohtaamme elinympäristössämme päivittäin monenlaisia mikrobeja. Vaikka useimmat niistä ovat meille haitattomia tai jopa hyödyllisiä, osa voi kuitenkin aiheuttaa sairauksia. Nisäkkäillä, joihin ihminenkin kuuluu, kyky puolustautua mikrobeja vastaan perustuu sekä synnynnäiseen että hankittuun immuniteettiin. Synnynnäinen immuniteetti on välttämätön niin infektioiden ehkäisyssä kuin hankitun immuunivasteen kehityksessä ja säätelyssä. Se perustuu perimän koodaamien proteiinien kykyyn tunnistaa erilaisia mikrobien pintarakenteita ja viestiä tästä soluille signalointireittien välityksellä. Eräs näistä signalointireiteistä, TNFR -signalointireitti, ja sen käynnistämä sytokiinieritys, ovat tarkkaan säädeltyjä ja välttämättömiä normaalille immuunivasteelle. Signaloinnin mekanismeja ja niiden säätelyä ei kuitenkaan vielä täysin tunneta. Synnynnäisen immuniteetin signalointireitit ovat säilyneet hyvin evoluutiossa hyönteisistä ihmisiin. Siksi niiden toimintaa ja säätelyä tutkittaessa voidaan käyttää mallina kodeissakin biojäteastian liepeillä usein tavattavaa banaanikärpästä (Drosophila melanogaster). Banaanikärpäsen Imd-signalointireitti muistuttaa nisäkkäiden TNFR-signalointireittiä. Tässä tutkimusprojektissa pyrimme RNA-häirintää (RNAi) ja muita molekyylibiologian menetelmiä hyödyntäen tunnistamaan Imd-signalointireittiin kuuluvia ja sen säätelyyn osallistuvia proteiineja. Tutkimuksessa löydettiin kolme uutta säätelijää, Tab2, Iap2 ja Pirk. Näiden proteiinien toimintaa ja merkitystä banaanikärpäsen immuunivasteelle selvitettiin tarkemmin. Osoitimme kärpässolumallia apuna käyttäen, että Tab2 ja Iap2 ovat välttämättömiä Imd-signaloinnille. Lisäksi havaitsimme, että banaanikärpäset, joilta Iap2 on poistettu, ovat herkkiä Gram-negatiivisten bakteerien aiheuttamille infektioille. Pirk puolestaan on aiemmin tuntematon proteiini, jonka osoitimme hillitsevän Imd signalointia sekä solumallissa että elävissä kärpäsissä. Pirkin vaikutus oli niin tehokas, että geenin yli-ilmentäminen kärpäsissä riitti herkistämään ne Gram-negatiivisten bakteerien aiheuttamille infektioille. Tehty tutkimus osoittaa, että Imd signalointi on tarkkaan säädeltyä ja aiempaa luultua monimutkaisempaa. Banaanikärpänen mallieläimenä tarjoaa mahdollisuuden tutkia tehokkaasti synnynnäisen immuniteetin säätelyä. Tab2:lla ja Iap2:lla on vastineensa myös nisäkkäissä, joten on mahdollista, että tutkimuksesta saadut tulokset tuovat uusia näkökulmia myös nisäkkäiden immuunisignaloinnin toiminnan selvittämiseen.; Innate immunity is the first line of defense against microbes and it is indispensable in preventing infections as well as in the development and regulation of the adaptive immune system. Innate immunity is based on the ability of genome-encoded proteins to recognize and bind microbial surface structures, which is followed by the activation of the innate immune response via various cell signaling pathways. Tumor necrosis factor receptor (TNFR) signaling and cytokine release are strictly regulated and essential for a normal immune response. However, in certain…

Subjects/Keywords: synnynnäinen immuniteetti ; NF-kappaB-signalointi ; banaanikärpänen ; innate immunity ; NF-kappaB signaling ; Drosophila

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APA (6^th Edition):

Kleino, A. (2010). The Imd pathway-mediated immune response in Drosophila . (Doctoral Dissertation). Tampere University. Retrieved from https://trepo.tuni.fi/handle/10024/66627

Chicago Manual of Style (16^th Edition):

Kleino, Anni. “The Imd pathway-mediated immune response in Drosophila .” 2010. Doctoral Dissertation, Tampere University. Accessed March 03, 2021. https://trepo.tuni.fi/handle/10024/66627.

MLA Handbook (7^th Edition):

Kleino, Anni. “The Imd pathway-mediated immune response in Drosophila .” 2010. Web. 03 Mar 2021.

Vancouver:

Kleino A. The Imd pathway-mediated immune response in Drosophila . [Internet] [Doctoral dissertation]. Tampere University; 2010. [cited 2021 Mar 03]. Available from: https://trepo.tuni.fi/handle/10024/66627.

Council of Science Editors:

Kleino A. The Imd pathway-mediated immune response in Drosophila . [Doctoral Dissertation]. Tampere University; 2010. Available from: https://trepo.tuni.fi/handle/10024/66627

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