Dissertations / Theses on the topic 'NF-kB activity'
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Lippolis, Davide Giosuè. "Stochastic modeling of fluctuations in the NF-kB activity of neoplastic cells." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2020. http://amslaurea.unibo.it/20550/.
Full textGuo, Canhui. "Mechanism of Anti-Cancer Activity of 9-Aminoacridine Based Drugs." Case Western Reserve University School of Graduate Studies / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=case1216215825.
Full textLunazzi, Giulia 1981. "Analysis of NFAT5 expression and activity in response to toll-like receptors." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/666120.
Full textEn las células del sistema inmunitario innato, la estimulación de los receptores de tipo Toll (TLR) activa la expresión de un programa génico pro-inflamatorio y antimicrobiano que está controlado por una red de reguladores transcripcionales. Hemos demostrado que el NFAT5, perteneciente a la familia de factores de transcripción Rel y previamente caracterizado como un factor de respuesta a estrés osmótico, es importante para la expresión de un grupo de genes de respuesta a TLRs, entre ellos Nos2, Il6 y Tnf. El reclutamiento del NFAT5 a sus genes diana requiere la actividad de IKKβ, la síntesis de novo de proteínas y es sensible a la acción de las deacetilasas de histonas. Resulta interesante el hecho de que el NFAT5 es esencial para responder a bajas dosis de ligando de los TLRs, y que regula grupos de genes específicos dependiendo de la intensidad del estímulo. También mostramos que NFAT5 facilita la accesibilidad de la cromatina en macrófagos, permitiendo el reclutamiento de reguladores transcripcionales como p65/NF-kB, c-Fos y p300 a sus regiones diana. Utilizando Nos2 como un gen cuya inducción es más dependiente de NFAT5 a bajas dosis de LPS, demostramos que el NFAT5 controla el reclutamiento de p65 gracias a que facilita la actividad de las demetilasas de H3K27, pero sin influir en la unión del complejo Polycomb 2 ni JMJD3. En conclusión, esta tesis caracteriza al NFAT5 como un nuevo regulador del sistema inmunitario implicado en el control de la accesibilidad local de la cromatina en respuesta a baja carga de patógenos.
FORLONI, MATTEO. "Immunogenicity of neuroblastoma tumors is controlled by impaired activity of NF-kB and IRF1 transcription factors." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2010. http://hdl.handle.net/2108/1424.
Full textLow expression of major histocompatibility complex class I (MHC I) molecules on the cell surface allows tumors to evade the host T cell-based immune response. These abnormalities are often related to either genetic defects of MHC I genes or aberrant expression of antigen processing machinery (APM) components. Neuroblastoma (NB), the most common solid extracranial cancer of childhood, is not an exception. MHC I surface expression is virtually undetectable in the most NB cell lines and primary tumors, and upregulated by gamma-interferon (IFN-γ). This phenotype is compatible with defects in the regulation of antigen processing and presentation components. In this study, the molecular mechanism underlying low immunogenicity in neuroblastoma was investigated. Amplification of the MYCN oncogene characterizes the most aggressive forms of NB and is believe to downregulate expression of MHC class I molecules. Although an inverse correlation between MYCN and MHC I has been reported in human NB cell lines, a direct demonstration of the MYCN-mediated down-regulation of MHC I expression has been questioned. Herein, we demonstrate that MYCN is not responsible for low MHC I, ERAP1 and ERAP2 protein levels in human NB cell lines, since their expression is not affected by neither transfection-mediated overexpression nor siRNA suppression of MYCN. Instead, we identified NF-kB and IRF1 as the main factors involved in the transcriptional regulation of MHC I and ERAPs proteins. By chromatin immunoprecipitation assay, we show a recruitment of p65 NF-kB to the MHC I, ERAP1 and ERAP2 promoters that is proportional with the expression of these genes. Moreover, low nuclear activity of both NF-kB and IRF1 factors correlated with the MHC I, ERAP1 and ERAP2-low phenotype of the most aggressive NB cell lines. Overexpression of either the transcription factors alone rescued the MHC I, ERAP1 and ERAP2-low phenotype, but only partially and in a cell-type depending manner. Important, the co-transfection of both NF-kB and IRF1 cooperated to strongly enhance the transactivation of MHC I, ERAP1 and ERAP2 in any cell lines. Notheworthy, NF-kB and IRF1 acted in a synergistic manner. We found an intriguing parallel in primary NB tumors, in fact, nuclear p65 was detected in the maturing neuroblastic cells (i.e. ganglionic cells) which express higher levels of MHC I molecules in human NB specimens. These findings provide molecular insight into defective MHC I expression in NB tumors and indicate that activating NF-kB and IRF1 in MHC I-low, aggressive NB cells could be instrumental for successful application of T cell-based immunotherapy.
Gadd, Samantha. "Acetaminophen-induced proliferation of estrogen-responsive breast cancer cells is associated with increased c-mcy RNA expression and NF-kB activity." Morgantown, W. Va. : [West Virginia University Libraries], 2001. http://etd.wvu.edu/templates/showETD.cfm?recnum=2016.
Full textTitle from document title page. Document formatted into pages; contains xi, 147 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 128-143).
Tong, Lingying. "The Role of Nitric Oxide Synthase and Carnosol in UVB-induced NF-κB Activity and Skin Damage." Ohio University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1412768175.
Full textBrittain, George C. IV. "A Novel Role for the TRAFs as Co-Activators and Co-Repressors of Transcriptional Activity." Scholarly Repository, 2009. http://scholarlyrepository.miami.edu/oa_dissertations/451.
Full textQin, Zhihua. "SAMHD1 Negatively Regulates the Innate Immune Responses to Inflammatory Stimuli and Viral Infection." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1587587968104986.
Full textMOL, MARCO HENDRIKUS ADRIANUS. "Analytical Strategies for the Identification and Characterization of RAGE Binders of Proinflammatory mediators. AGEs and ALES." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/675044.
Full textTadlaoui, Hbibi Ali. "Détection de facteurs de transcription actifs dans le cancer colorectal et inhibition spécifique de leur activité par des oligonucléotides leurres : applications à STAT3 et NF-kB." Paris 13, 2008. http://www.theses.fr/2008PA132023.
Full textThe important role of transcription factors such as STAT3 and Nf-kB in biological processes, and their involvement in oncogenesis, justifies the numerous studies on these factors. To inhibit and control their activities appears to be promising therapeutic approach. Firstly, we have shown that STAT3 is constitutively activated in colon cancer and is associated with histopronostics features. In secondly, we inhibited the transcription factors STAT3 and NF-kB in cancer cell lines, we using decoy oligonucleotide containing the consensus target ssequences of these two factors. The decoy oligonucleotides induce the death of a cell line of colon cancer (SW480), however, the decoy ODN of STAT3 was found to interact with STAT1 and prevent IFNy action. Thus, it's of interest to inhibit transcription factors in tumor cells but specific issues are not resolved
Kuan-Dar, Huang, and 黃冠達. "The effects of glutathionylation of p65 in NF-kB activity." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/37148309814550317888.
Full text國立嘉義大學
生物醫藥科學研究所
98
The recent research found that NF-kB, a transcription factor, can transcribe about 150 categories of proteins which regulate many cellular physiological responses, such as cellular inflammation, growth and apoptosis. Therefore, NF-kB is an important transcription factor. Previous studies indicated glutathionylation of protein can inhibit protein activities. Recently, our study found cinnamaldehyde can increase GSH in ECs, which inhibits TNF-a-induced NF-kB activity in ECs. Therefore, this research will investigate GSSG and H2O2/GSH in TNF-a-induced ECs and discuss protein glutathionylation on NF-kB-p65. We found GSSG、H2O2/GSH and NAC can increase total glutathionylated protein and NF-kB-p65 glutathionylation. Moreover, GSSG and H2O2/GSH inhibit TNF-a-induced ICAM-1 expression in transcriptional level by decrease NF-kB-p65 translocation. In addition, GSSG and H2O2/GSH inhibit NF-kB-p65 translocation independent with IkB-a degradation. Taken together, these data suggest GSSG and H2O2/GSH decrease NF-kB-p65 translocation by increasing NF-kB-p65 glutathionylation. Therefore, We also transfected with GFP-p65 wild-type and GFP-p65 mutation c38s、c120s、c160s、c216s and then treat with GSSG to analyze NF-kB promoter activity. The result show NF-kB-p65 cystein 38、160、216 mutation will change GSSG inhibits TNF-a-induced NF-kB-p65 activation. To summarize, this research verifies that glutathionylation of NF-B-p65 in cystein 38、160、216 will affect the NF-kB-p65 protein activity.
梁凱程. "Dual mechanisms of inhibiting NF-kB activity by Carnosol-treated endothelial cells." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/s3dpxf.
Full text國立嘉義大學
微生物與免疫學系研究所
97
During early atherogenesis, the endothelial cells excess produces adhesion molecules, which promote adhesion of monocytes to endothelial cells. It is causing formation of atheromatous plaque. Thus these adhesion molecules play an important role in the development of this disease. Previous studies have indicated that carnosol is a major ingredient of extracts from rosemary which exhibit anti-carcinogen and anti-inflammatory properties, but the underlying mechanisms are largely undefined. In this study, we examine the effects of carnosol and rosemary essential oil on TNF-α-induced adhesion molecules expression in endothelial cells. We found that rosemary essential oil and carnosol inhibit the expression of TNF-alpha-induced ICAM-1. Moreover, the carnosol was found to abrogate the adhesion of TNF-α-induced monocytes to endothelial cells. TNF-α-induced ICAM-1 expression is via NF-�羠 singling pathways. Our study showed that Carnosol inhibits TNF-α-induced p65 translocation by blocking the degradation of the IkappaB-�� in short-term pretreatments, but not in long-term pretreatments. Our findings showed that carnosol inhibits TNF-α-induced IKK phosphorylation in 3 hours pretreatments. Moreover, carnosol inhibits p65 translocation in 12 hours pretreatments, that blocked by Nrf2 siRNA, these results indicated that the long-term anti-inflammatory of carnosol was associated with the Nrf2-related genes. Carnosol induced the Nrf2-related gene expression, including heme-oxygenase (HO-1), over long-term pretreatments. Treating endothelial cells with HO-1 siRNA, blocks the anti-inflammatory effects of carnosol, these results showed that treatment of carnosol induces HO-1 expresssion is involved in the long-term anti-inflammatory. Moreover, we found treating of endothelial cells with carnosol significantly induces translocation of Nrf2 into the nucleus, increases expression of glutamate-cysteine ligase (GCL), and cellular glutathione (GSH) level in long-term pretreatments. Treating endothelial cells with buthionine sulfoximine (BSO), a specific inhibitor of glutamate-cysteine ligase, blocks the anti-inflammatory effects of carnosol and carnosol induced p65 glutathionylation. These results indicated that carnosol suppresses TNF-α-induced ICAM-1 expression through blocking the phosphorylation of IKK in short-term pretreatments, whereas it does so via the induction of HO-1 and GSH in long-term pretreatments.
Zeng, Ju-yi, and 曾如意. "Interleukin-6 Increases Promoter Binding Activity of Intestine-specific homeobox via NF-kB Signaling." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/07673351834125079885.
Full text高雄醫學大學
醫學研究所
100
Chronic inflammation is often evolved into the multiple malignancies. Many literatures mentioned that interleukin-6 (IL-6) and NF-κB participate in the inflammatory and cancer processes. Intestine-specific homeobox (ISX)is a newly identified homeobox transcription factor, its expression has been linked to liver tumorigenesis. In this study, we investigated whether NF-κB can respond to IL-6 and regulate ISX gene transcription. A luciferase reporter assay should that the -260/-230 is an IL-6 responsive region. Next, we performed a nucleus/cytosol fraction analysis to examine the shuttle of IKKα and NF-κB subunits(p65, p50, p52, Rel-B, c-Rel). It showed that only p65 shuttle can respond to IL-6 treatment. In addition, it is known that the location of activated ISX is in nucleus. We further identified potent phosphorylated site on ISX that affects the location of ISX in nucleus by immunofluoresence assay.
Wang, Wei-Hsun, and 王偉勛. "Simultaneous Imaging of Temporal Changes of NF-kB Activity and Viable Tumor Cells During Sorafenib Treatments in Huh7/NF-kB-tk-luc2/rfp Tumor-bearing Mice with Multimodalities of Molecular Imaging." Thesis, 2013. http://ndltd.ncl.edu.tw/handle/53076741718009553539.
Full text國立陽明大學
生物醫學影像暨放射科學系
101
Here a human hepatocellular carcinoma Huh7/NF-kB-tk-luc2/rfp cell clone was established using NF-kB responsive element as a promoter to drive herpes simplex virus thymidine kinase (tk) and firefly luciferase (luc2) dual reporter genes for monitoring NF-kB activity, and co-transfected with red fluorescent protein gene (rfp) for identifying the viable tumor cells. With this Huh7/NF-kB-tk-luc2/rfp tumor-bearing animal model combined with multimodalities of molecular imaging, simultaneous imaging of temporal changes of NF-kB activity and viable tumor cells during sorafenib treatments could be performed. Sorafenib is a multikinase inhibitor approved by FDA for the treatment of renal carcinoma via Ras-Raf-MAPK-MEK-ERK pathway, and was found to be beneficial for other types of cancers as well, especially hepatoma. NF-kB responsive element with tk-luc2 dual reporter genes were used to combined with multimodalities of molecular imaging, such as bioluminescent imaging (BLI) for tracking the real-time NF-kB activity, and rfp gene for the imaging (RFPI) assay of viable tumor cells during sorafenib treatment. The NF-kB activity has been reported to be associated with chemo- and radioresistance during cancer treatments. The results showed that sorafenib could suppress the NF-κB/DNA binding activity, and the expression of downstream effector proteins to enhance tumor cell killing through inhibition of anti-apoptotic pathway, tumor cell proliferation, and invasion, while increase apoptosis of tumor cells. In addition, the relative photon fluxes obtained from RFPI and BLI, each represented the viable tumor cells and cells with NF-κB activation, respectively, decreased after sorafenib treatment by 50 to 65%, and 87.5 to >90%, suggesting that the percentage of suppression of NF-κB activation was much higher than that of HCC tumor cell killing in the tumor mass at anytime during sorafenib treatments. In conclusion, simultaneous molecular imaging of the temporal change of NF-κB activity and the viable tumor cells in the same Huh7/NF-κB-tk-luc2/rfp tumors of the animal may reflect the real status of NF-κB activity and the viable tumor cells at the time of imaging. This system may be applied for screening the potential chemotherapeutic drugs, and for the therapeutic efficacy evaluation of new preclinical trials, which using NF-κB as a major target.
wang, Chorngder, and 王崇德. "A composite element for NF-kB and RBPJk mediates the promoter activity of the rat pregnancy specific glycoprotein gene,rnCGM3." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/90075302351796225164.
Full text國立臺灣大學
生化科學研究所
88
Pregnancy-specific glycoproteins (PSGs) are primarily expressed in the placenta and become the major glycoproteins at term. To understand the function and regulation of PSG regulation in pregnancy, the promoter elements and cDNA sequences of a rodent PSG gene have been characterized. The cDNA of the rat pregnancy gene, rnCGM3, is 2761bp in length and contains an open reading frame that encodes a 475 amino acid polypeptide. The transcription initiation site of rnCGM3 is located at nucleotide —197 upstream of the translation start site. Three nuclear protein binding sites: FPⅠ, FPⅡ and FPⅢ in 5’-flanking region of rnCGM3 gene have been characterized. The FPⅡ binding factor was shown to be C/EBPβ. RBPJκ was found to be the factor binds to both FPⅠ and FPⅢ. We also found another important transcription factor, the p65 subunit of NF-κB, which binds to the FPⅢ element in the yeast one-hybrid system. In this study, we showed that both p50 and p65 subunits of NF-κB bind to the FPⅢ element in the electrophoretic mobility shift assay (EMSA). A core sequence, 5'-GGGAAA-3', on the FPⅢ element for NF-κB was defined by mutagenesis analysis. Based on EMSA with NF-κB-enriched nuclear extracts from 293 cells transfected with different subunits of NF-κB, we found that both mono- and heterodimer of NF-κB bind to FPⅢ. We further studied the effect of two different transcription factors, NF-κB and RBPJκ, on the regulation of rnCGM3 gene expression. By transient expression analyses, we found the expression of CAT reporter gene could be activated by p65 and this stimulatory effect of p65 could be repressed by RBPJκ. Our results suggest that rnCGM3 gene expression may be mediated by the NF-κB and the Notch signaling pathway via RBPJκ.
Tai, Dar-In, and 戴達英. "The significance of Tumor Necrosis Factor Signal Transduction Pathway and NF-kB Transactivation Activity in Chronic Hepatitis and Hepatocellular Carcinoma." Thesis, 2000. http://ndltd.ncl.edu.tw/handle/74085578194130048803.
Full text長庚大學
臨床醫學研究所
89
Tumor necrosis factor (TNF) is a multifunction cytokine that plays important roles in the program cell death, inflammatory response and viral clearance. On the othre hand, TNF may promote cell regeneration by activate Nuclear factor kappB (NF-kB) transactivation pathway. The cytotoxicity induced by TNF plays an important role in the pathogenesis of chronic hepatitis B and C. The activation of NF-kB may inhibit apoptosis that may faccilitate viral persistent and hepatocarcinogenesis. For better understanding the differences of persistent infection and pathogenesis between chronic hepatitis B and C, we studied 38 patients with chronic hepatitis B, 40 with chronic hepatitis C, 9 with dual hepatitis B and C for cytokine levels and compared with 12 healthy controls. Plasma levels of TNFa, soluble TNF receptor-I (TNFR-I), soluble TNF receptor-II (TNFR-II) and related cytokines were quantified by ELISA and correlated with histology activity index. Expressions of TNFR-I and II in liver tissues were also examined in 33 with HBV and 15 with HCV by semi-quantitative reverse transcription- polymerase chain reaction (RT-PCR). The results showed that sTNFR-I levels correlated with liver inflammation in the whole study patients. Type 1 helper T cells (Th1) cytokines levels were higher in the groups with higher inflammatory activities. Most importantly, sTNFR-I levels correlated with liver inflammation in HBV, whereas sTNFR-II levels correlated with liver inflammation in HCV. The expressions of TNFR-I and -II messanger RNA (mRNA) in liver tissues were similar and comparable between hepatitis B virus (HBV) and hepatitis C virus (HCV). These findings suggest that TNFR signal transduction pathway is differentially modulated between HBV and HCV infection, and may be relevant to immunopathogenesis. The HCV core protein is also a multifunctional protein. It may bind to the death domain of TNFR-I, and to the cytoplasmic tail of lymphotoxin-b receptor, implying that it may be involved in the apoptosis and anti-apoptosis signaling pathways. To address this issue, electrophoretic mobility shift assay and immunohistochemical studies were used to demonstrate the activation of NF-kB in HCV-infected liver tissues and in HCV core-transfected cells. The activation of NF-kB was correlated with the apoptosis assays. The results showed that NF-kB activation could be demonstrated in HCV-infected livers and HCV core-transfected cells. The data of electromobility shift assay (EMSA) correlated with those of immunohistochemical studies which revealed a higher frequency of NF-kB nuclear staining in HCV-infected than in normal livers. NF-kB activation conferred resistance to TNFa-induced apoptosis in HCV core-transfected cells. Inhibition of NF-kB activation by pyrrolidine dithiocarbamate sensitized them to TNFa-induced apoptosis. These findings suggest that HCV infection may cause anti-apoptosis by activation of NF-kB and implicate a mechanism by which HCV may evade the host's immune surveillance leading to viral persistence and possibly to hepatocarcinogenesis. The NF-kB activation status in hepatocellular carcinoma (HCC) has not yet been explored, therefore. immunohistochemical stainings were done on formalin fixed liver tissues from 65 HCCs and 9 normal control subjects to search for active nuclear RelA and nuclear IkBa proteins. Nuclear extract from 37 pairs of fresh frozen tumor and non-tumor liver tissues and 7 normal controls were tested for NF-kB-DNA binding activity by electrophoretic motility shift assay. The RelA and IkBa protein expressions were studied by Western blotting. Nuclear NF-kB stainings were significantly more abundant in HBV or HCV infected tumor as well as non-tumor part of HCC than in normal controls. Nuclear NF-kB-DNA binding activity and nuclear RelA proteins expression were higher in tumor than in non-tumor tissues; whereas, cytosolic IkBa protein expression was generally higher in non-tumor than in tumor tissues. Constitutive activation of NF-kB was found more frequently in tumor than in non-tumor tissues. NF-kB overexpression accompanied by dysregulation of IkBa may play a role in hepatocarcinogenesis of HBV or HCV infection.
Chang-Jer, Wu, and 吳彰哲. "Studies on the induction of NF-kB activity by the latent membrane protein 1 of Epstein-Barr virus and its therapeutic application." Thesis, 1998. http://ndltd.ncl.edu.tw/handle/59328348418692749113.
Full text國防醫學院
生命科學研究所
86
Epstein-Barr virus (EBV) is associated with many malignant tumors including nasopharyngeal carcinoma (NPC). Previous stuides have indicated that EBV-encoded oncoprotein, latent membrane protein 1 (LMP 1), is expressed in many NPC tissues. LMP 1 has been shown to stimulate HIV LTR through the two NF-kB binding sites within this promoter. In this thesis, I tested the feasibility of using this property of LMP 1 as a therapeutic strategy for treatment of NPC. In appendix of this thesis, I took advantage of the retroviral trapping sysytem to screen for new cellular factors that could be activated or inhibited by LMP 1 of EBV. The therapeutic strategy combines preferential killing of the LMP 1-expressing cells by gene transfer of NF-kB-mediated herpes simplex virus thymidine kinase (HSV-tk) and ganciclovir(GCV) treatment. The 800-bp HIV-LTR, which contains two NF-kB binding sites, was used to drive the HSV-tk gene. C33A and NPC076 cell clones stably expressing the LMP 1 and the HSV-tk genes were subjected to the GCV sensitivity test. Results showed that cells expressing both the LMP 1 and the HSV-tk genes were highly sensitive to GCV treatment. These cells were introduced into nude mice subcutaneously and tumors became plapable within 2 weeks. GCV was then introduced intraperitoneally to these mice and the sizes of the tumors were measured daily.Results showed that the tumors regressed in the group of mice carrying cells that stably expressed both the LMP 1 and the HSV-tk genes, but not in mice carrying cells containing LMP 1 or HSV-TK alone. Date indicate that the HSVtk gene expressed from a NF-kB-binding motif-containing promter that is regulated by LMP 1 may be used as an in vivo gene therapeutic strategy for EBV LMP 1-expressing cancers such as NPC.
Schmidt-Ullrich, R., Desmond J. Tobin, D. Lenhard, P. Schneider, R. Paus, and C. Scheidereit. "NF-kappaB transmits Eda A1/EdaR signalling to activate Shh and cyclin D1 expression, and controls post-initiation hair placode down growth." 2000. http://hdl.handle.net/10454/3870.
Full textA novel function of NF-KB in the development of most ectodermal appendages, including two types of murine pelage hair follicles, was detected in a mouse model with suppressed NF-KB activity (CI¿B¿¿N). However, the developmental processes regulated by NF-¿B in hair follicles has remained unknown. Furthermore, the similarity between the phenotypes of CI¿BA¿N mice and mice deficient in Eda A1 (tabby) or its receptor EdaR (downless) raised the issue of whether in vivo NF-KB regulates or is regulated by these novel TNF family members. We now demonstrate that epidermal NF-KB activity is first observed in placodes of primary guard hair follicles at day E14.5, and that in vivo NF-KB signalling is activated downstream of Eda A1 and EdaR. Importantly, ectopic signals which activate NF-KB can also stimulate guard hair placode formation, suggesting a crucial role for NF-KB in placode development. In downless and CI¿B¿¿N mice, placodes start to develop, but rapidly abort in the absence of EdaR/NF-KB signalling. We show that NF-KB activation is essential for induction of Shh and cyclin D1 expression and subsequent placode down growth. However, cyclin D1 induction appears to be indirectly regulated by NF-KB, probably via Shh and Wnt. The strongly decreased number of hair follicles observed in CI¿B¿¿N mice compared with tabby mice, indicates that additional signals, such as TROY, must regulate NF-KB activity in specific hair follicle subtypes.
Khalfi, Soumia. "Rôles de TRIM5 et Atg5 dans la réponse immune innée de cellules infectées par le VIH-1." Thèse, 2020. http://depot-e.uqtr.ca/id/eprint/9688/1/eprint9688.pdf.
Full text