subject:(Receptor activator of NF KB RANK )

1. Papoutselis, Menelaos. Ο ρόλος των αδιαφοροποίητων φυσικών κυτταροκτόνων Τ (iNKT) λεμφοκυττάρων στην ομοιοστασία των οστών και την οστική νόσο του πολλαπλού μυελώματος.

Degree: 2017, Democritus University of Thrace (DUTH); Δημοκρίτειο Πανεπιστήμιο Θράκης (ΔΠΘ)

URL: http://hdl.handle.net/10442/hedi/40696

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Increased expression of RANKL on osteoblasts and T cells is central for osteoclast activation and development of bone disease in multiple myeloma. We tested the… (more)

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Increased expression of RANKL on osteoblasts and T cells is central for osteoclast activation and development of bone disease in multiple myeloma. We tested the hypothesis that iNKT cells, a CD1d-restricted, glycolipid-specific subset of potent immunoregulatory T cells, are also an important source of RANKL in the myeloma microenvironment. First we established that iNKT cells ex vivo isolated from normal individuals express mRNA and membrane-bound RANKL at a significantly higher level than conventional T cells. Notably, iNKT cells upregulate surface RANKL more efficiently than T cells under activating conditions and their supernatants generate osteoclasts more efficiently under limiting conditions. Similarly, blood and bone marrow iNKT cells from myeloma patients express higher surface RANKL than conventional T cells and at a higher level compared to iNKT cells from age-matched controls. Interestingly, compared to PB, iNKT cells are enriched in the bone marrow of patients with myeloma and they upregulate surface RANKL, thus showing a tissue-specific effect. Finally, in MM patients but not in normal controls, iNKT RANKL expression correlates with β-C-terminal telopeptide, a sensitive and specific marker of bone resorption. We propose that increased RANKL expression defines an acquired, myeloma-specific dysfunctional iNKT cell phenotype that may contribute to osteoclast activation and myeloma bone disease.

Η αυξημένη έκφραση της κυτταροκίνης RANKL στους οστεοβλάστες και τα Τ λεμφοκύτταρα είναι ουσιώδης για την ενεργοποίηση των οστεοκλαστών και την ανάπτυξη της οστικής νόσου του πολλαπλού μυελώματος. Στην παρούσα εργασία, ερευνήσαμε το ρόλο των iNKT λεμφοκυττάρων, μιας υποομάδας ισχυρών ανοσορρυθμιστικών, CD1d-εξαρτώμενων και ειδικών για λιπιδικά αντιγόνα Τ λεμφοκυττάρων, στην παραγωγή RANKL στο μικροπεριβάλλον του πολλαπλού μυελώματος. Αρχικά, αποδείξαμε ότι ex vivo τα iNKT λεμφοκύτταρα φυσιολογικών ατόμων εκφράζουν περισσότερο RANKL, τόσο σε επίπεδο mRNA όσο και σε πρωτεϊνικό επίπεδο, απ’ότι τα συμβατικά Τ λεμφοκύτταρα. Επιπρόσθετα, τα iNKT λεμφοκύτταρα αυξάνουν την παραγωγή RANKL μετά από ανοσοδιέγερση σε μεγαλύτερο βαθμό από τα Τ λεμφοκύτταρα ενώ έχουν την δυνατότητα να προάγουν το σχηματισμό οστεοκλαστών πιο αποτελεσματικά κάτω από περιοριστικές συνθήκες καλλιέργειας. Ομοίως, τα iNKT λεμφοκύτταρα από το περιφερικό αίμα και το μυελό των οστών ασθενών με πολλαπλούν μυέλωμα εκφράζουν επιφανειακό RANKL σε υψηλότερο ποσοστό απ΄ ότι τα Τ λεμφοκύτταρα αλλά και από iNKT λεμφοκύτταρα υγιών δοτών παρόμοιας ηλικίας. Αξιοσημείωτη είναι η παρατήρηση ότι, σε σχέση με το περιφερικό αίμα, τα iNKT λεμφοκύτταρα βρίσκονται σε αυξημένες συγκεντρώσεις στο μυελό των οστών όπου συμβάλλουν αποτελεσματικότερα στην παραγωγή RANKL, καταδεικνύοντας ένα ειδικό για το μυελό των οστών φαινόμενο. Τέλος, σε ασθενείς με πολλαπλούν μυέλωμα αλλά όχι σε υγιείς δότες, η έκφραση του RANKL στα iNKT λεμφοκύτταρα σχετίζεται στατιστικά με τα επίπεδα βCTx του ορού, έναν ειδικό και ευαίσθητο δείκτη οστικής απορρόφησης. Τα παραπάνω ευρήματα υποδεικνύουν ότι…

Subjects/Keywords: Αδιαφοροποίητα φυσικά κυτταροκτόνα Τ λεμφοκύτταρα; Πολλαπλούν μυέλωμα; Κυτταροκίνη RANKL; Invariant natural killer T lymphocytes; Multiple myeloma; Receptor activator of NF-KB ligand (RANKL)

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

APA (6^th Edition):

Papoutselis, M. (2017). Ο ρόλος των αδιαφοροποίητων φυσικών κυτταροκτόνων Τ (iNKT) λεμφοκυττάρων στην ομοιοστασία των οστών και την οστική νόσο του πολλαπλού μυελώματος. (Thesis). Democritus University of Thrace (DUTH); Δημοκρίτειο Πανεπιστήμιο Θράκης (ΔΠΘ). Retrieved from http://hdl.handle.net/10442/hedi/40696

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):

Papoutselis, Menelaos. “Ο ρόλος των αδιαφοροποίητων φυσικών κυτταροκτόνων Τ (iNKT) λεμφοκυττάρων στην ομοιοστασία των οστών και την οστική νόσο του πολλαπλού μυελώματος.” 2017. Thesis, Democritus University of Thrace (DUTH); Δημοκρίτειο Πανεπιστήμιο Θράκης (ΔΠΘ). Accessed April 17, 2021. http://hdl.handle.net/10442/hedi/40696.

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

MLA Handbook (7^th Edition):

Papoutselis, Menelaos. “Ο ρόλος των αδιαφοροποίητων φυσικών κυτταροκτόνων Τ (iNKT) λεμφοκυττάρων στην ομοιοστασία των οστών και την οστική νόσο του πολλαπλού μυελώματος.” 2017. Web. 17 Apr 2021.

Vancouver:

Papoutselis M. Ο ρόλος των αδιαφοροποίητων φυσικών κυτταροκτόνων Τ (iNKT) λεμφοκυττάρων στην ομοιοστασία των οστών και την οστική νόσο του πολλαπλού μυελώματος. [Internet] [Thesis]. Democritus University of Thrace (DUTH); Δημοκρίτειο Πανεπιστήμιο Θράκης (ΔΠΘ); 2017. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10442/hedi/40696.

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

Council of Science Editors:

Papoutselis M. Ο ρόλος των αδιαφοροποίητων φυσικών κυτταροκτόνων Τ (iNKT) λεμφοκυττάρων στην ομοιοστασία των οστών και την οστική νόσο του πολλαπλού μυελώματος. [Thesis]. Democritus University of Thrace (DUTH); Δημοκρίτειο Πανεπιστήμιο Θράκης (ΔΠΘ); 2017. Available from: http://hdl.handle.net/10442/hedi/40696

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

2. Τυροβολά, Ιωάννα. Συσχέτιση επιπέδων SRANKLκαι OPG στον ορό του αίματος και στο υγρό της ουλοδοντικής σχισμής και βαθμού ριζικής απορρόφησης κατά την ορθοδοντική θεραπεία.

Degree: 2009, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/27799

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The aim of the present study was the determination in a rat model of the levels of OPG and sRANKL in blood and in gingival… (more)

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The aim of the present study was the determination in a rat model of the levels of OPG and sRANKL in blood and in gingival crevicular fluid (GCF) in relation to the degree of root resorption during orthodontic tooth movement using healthy experimental animals and a carefully planned and organized experimental design. For this purpose fourteen 6 month old male Wistar rats 350-500 gr weight were used. At a first stage blood samples from the area of the eyes were taken and gingival crevicular fluid (GCF) was collected with the use of paperstrips (penopaper Harco Tustin, CA, USA) from the gingival crevicular area of each upper incisor. Blood samples were also collected after the orthodontic treatment had been completed. A 25gr sentalloy closed orthodontic coil spring(GAC, Ctr Iship, NY, USA) was inserted between the upper right first molar and the upper incisors in all animals. After 21 days of loading a mesial tipping of the right molars was obtained. All night first molars that were moved orthodontically and their cognate left molars (control teeth) were extracted and studied under microcomputed tomography scanning. After studying the extracted teeth the following results were obtained: a) there is a positive linear correlation between the initial concentration of RANKL in blood and the degree of root resorption (r=0.833, p<0.01), b) the ratio of the initial concentrations of OPG/RANKL in blood proved to be an independent prognostic factor of the degree of root resorption after orthodontic therapy (R²=0.87, Adj R²=0.73, Beta=0.872, p<0.01), c) the initial concentration of RANKL in GCF showed a negative correlation to the initial concentration of RANKL in blood serum (r=-0.7, p<0.05), d) it seems that for a concrete group of initial concentrations of OPG/RANKL in GCF, the dental root is protected against extreme external root resorption (R=0.81, p<0.05 for x² η R=0.83, p<0.05 for x³) and finally, e) the concentration of OPG in blood serum decreased significantly in cases of severe root resorption (r=-0.823, p=0.001).

Σκοπός της παρούσας ερευνητικής εργασίας ήταν η διερεύνηση της σχέσεως των επιπέδων της OPG και του s RANKL στο αίμα και στο υγρό της ουλοδοντικής σχισμής σε σχέση με το βαθμό της ριζικής απορρόφησης κατά την ορθοδοντική μετακίνηση των δοντιών. Στην ερευνητική μας εργασία χρησιμοποιήθηκαν 14 υγιείς επίμυες τύπου Wistar 350-500 γρ. περίπου ηλικίας 6 μηνών και όλοι αρσενικού φύλου. Σε κάθε ζώο λήφθηκε δείγμα αίματος πριν και μετά την ορθοδοντική παρέμβαση καθώς επίσης και διπλό (σε ορισμένες περιπτώσεις όπου οι περιοδοντικοί ιστοί δεν ερεθίστηκαν πολύ) δείγμα υγρού από την ουλοδοντική σχισμή του τομέα πριν την ορθοδοντική παρέμβαση. Μετά εφαρμόσθηκε μηχανισμός για την ορθοδοντική μετακίνηση κάθε δεξιού άνω πρώτου γομφίου προς τα εγγύς. Στην αντίθετη πλευρά δηλαδή στην περιοχή του πρώτου άνω γομφίου αριστερά δεν εφαρμόσθηκαν καθόλου ορθοδοντικές δυνάμεις (δόντι έλεγχου). Η ορθοδοντική θεραπεία είχε διάρκεια τριών εβδομάδων. Ακολούθησε αξονική τομογραφία τόσο των δοντιών παρέμβασης όσο και των δοντιών…

Subjects/Keywords: Οστεοπροτεγερίνη; Ριζική απορρόφηση; Ορθοδοντική θεραπεία; Υγρό ουλοδοντικής σχισμής; Ορός αίματος; Οστική αναδιαμόρφωση; Απόπτωση νεογιλού; Πρωτεΐνες; Osteoprotegerin (OPG); Receptor activator of NF-KB ligand (RANKL); Receptor activator of NF-KB (RANK); Root resorption; Orthodontic treatment; Blood serum; Gingival crevicular fluid (GCF); Proteins

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

APA (6^th Edition):

Τυροβολά, . �. (2009). Συσχέτιση επιπέδων SRANKLκαι OPG στον ορό του αίματος και στο υγρό της ουλοδοντικής σχισμής και βαθμού ριζικής απορρόφησης κατά την ορθοδοντική θεραπεία. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/27799

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):

Τυροβολά, Ιωάννα. “Συσχέτιση επιπέδων SRANKLκαι OPG στον ορό του αίματος και στο υγρό της ουλοδοντικής σχισμής και βαθμού ριζικής απορρόφησης κατά την ορθοδοντική θεραπεία.” 2009. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed April 17, 2021. http://hdl.handle.net/10442/hedi/27799.

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

MLA Handbook (7^th Edition):

Τυροβολά, Ιωάννα. “Συσχέτιση επιπέδων SRANKLκαι OPG στον ορό του αίματος και στο υγρό της ουλοδοντικής σχισμής και βαθμού ριζικής απορρόφησης κατά την ορθοδοντική θεραπεία.” 2009. Web. 17 Apr 2021.

Vancouver:

Τυροβολά �. Συσχέτιση επιπέδων SRANKLκαι OPG στον ορό του αίματος και στο υγρό της ουλοδοντικής σχισμής και βαθμού ριζικής απορρόφησης κατά την ορθοδοντική θεραπεία. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2009. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10442/hedi/27799.

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

Council of Science Editors:

Τυροβολά �. Συσχέτιση επιπέδων SRANKLκαι OPG στον ορό του αίματος και στο υγρό της ουλοδοντικής σχισμής και βαθμού ριζικής απορρόφησης κατά την ορθοδοντική θεραπεία. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2009. Available from: http://hdl.handle.net/10442/hedi/27799

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

University of Adelaide

3. Mohan, Geetha. Mechanisms of osteoarthritis : interrelationships between bone and cartilage.

Degree: 2012, University of Adelaide

URL: http://hdl.handle.net/2440/84538

► Osteoarthritis (OA) is a progressive joint disease and a common cause of disability. OA is characterised by loss of articular cartilage, subchondral bone sclerosis, cysts,… (more)

▼ Osteoarthritis (OA) is a progressive joint disease and a common cause of disability. OA is characterised by loss of articular cartilage, subchondral bone sclerosis, cysts, and osteophyte formation. Increased subchondral bone remodelling plays an important role in the pathophysiology of OA and is associated with disease progression. It is known that Osteoprotegerin (OPG), receptor activator of nuclear factor kappa b (RANK) and its ligand RANKL tightly control bone remodelling. In addition, RANK, RANKL and OPG gene expression has been shown to be dysregulated in human OA subchondral bone. Commonly OA is diagnosed at advanced stages, which makes it difficult to study the initiating events in the human disease. Animal models of OA are of considerable importance to study the progressive changes in OA, and to evaluate suitable OA drugs. Alendronate (ALN) is a potent bone resorption inhibitor and clinical trials using bisphosphonates to treat OA have yielded mixed results. This suggests that the effects of bisphosphonates may or may not be beneficial depending on the stage of OA progression. The first aim of this thesis was to characterise the temporal structural changes of tibial articular cartilage and subchondral bone in a low-dose MIA-induced OA rat model. The results from micro-CT analysis showed that the tibiae of the MIA-injected knees had significant bone loss at 2 weeks (early OA), followed by increased bone volume, trabecular thickness and separation at 6 weeks (intermediate OA) and 10 weeks (advanced OA). Micro-CT images revealed subchondral bone sclerosis, cysts, and osteophyte formation at 6 and 10 weeks. Histology revealed progressive cartilage degradation characteristic of the human disease. The second aim of this thesis was to study the effect of ALN treatment initiated at day 0 (pre-emptive), week 2 (early treatment), and week 6 (delayed treatment) in a low-dose MIA rat model. To address the second aim the efficacy of ALN was tested on cartilage degradation, subchondral bone remodelling, and joint discomfort observed in this animal model. The study demonstrated that pre-emptive ALN treatment preserved subchondral trabecular bone microarchitecture, decreased bone turnover, prevented joint discomfort, and offered moderate chondroprotection. Early and delayed ALN treatment prevented loss of trabeculae and decreased bone turnover but did not have any identified effect on cartilage. Finally, the RANK, RANKL, OPG gene expression in OA was characterised in a lowdose MIA rat model. The effect of ALN treatment on subchondral bone RANK, RANKL, and OPG gene expression at 2, 6, and 10 weeks after OA induction was assessed. This study showed that the RANKL and OPG gene expression was dysregulated in this animal model. In addition, the efficacy of ALN on early subchondral bone changes appears to occur through the modulation of RANKL and OPG gene expression. Collectively, these findings demonstrate that the low-dose MIA rat model closely mimics the pathological features of progressive human OA disease. Moreover, this… Advisors/Committee Members: Fazzalari, Nick (advisor), Kuliwaba, Julia Suzanne (advisor), Parkinson, Ian Henry (advisor), School of Medical Sciences (school).

Subjects/Keywords: Osteoarthritis; subchondral bone; cartilage; micro-computed tomography; OA animal model; Alendronate; Monosodium iodoacetate; osteoprotegerin; receptor activator of nuclear factor KB ligand

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

APA (6^th Edition):

Mohan, G. (2012). Mechanisms of osteoarthritis : interrelationships between bone and cartilage. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/84538

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):

Mohan, Geetha. “Mechanisms of osteoarthritis : interrelationships between bone and cartilage.” 2012. Thesis, University of Adelaide. Accessed April 17, 2021. http://hdl.handle.net/2440/84538.

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

MLA Handbook (7^th Edition):

Mohan, Geetha. “Mechanisms of osteoarthritis : interrelationships between bone and cartilage.” 2012. Web. 17 Apr 2021.

Vancouver:

Mohan G. Mechanisms of osteoarthritis : interrelationships between bone and cartilage. [Internet] [Thesis]. University of Adelaide; 2012. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/2440/84538.

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

Council of Science Editors:

Mohan G. Mechanisms of osteoarthritis : interrelationships between bone and cartilage. [Thesis]. University of Adelaide; 2012. Available from: http://hdl.handle.net/2440/84538

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

4. 菊田,純. Jagged1-Notch2 signaling induces root resorption via RANKL and IL-6 : Jagged1-Notch2シグナルはRANKLとIL-6を介して歯根吸収を惹起する.

Degree: 博士（歯学）, 2015, Nihon University / 日本大学

URL: http://repository.nihon-u.ac.jp/xmlui/handle/11263/573 ; http://dx.doi.org/10.15006/32665A4967

Subjects/Keywords: Notchシグナル; Notch signaling; Receptor activator of NF-kB ligand; RANKL; Interleukin-6; IL-6; 矯正力; Orthodontic force; 歯根吸収; Root resorption

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

APA (6^th Edition):

菊田,純. (2015). Jagged1-Notch2 signaling induces root resorption via RANKL and IL-6 : Jagged1-Notch2シグナルはRANKLとIL-6を介して歯根吸収を惹起する. (Thesis). Nihon University / 日本大学. Retrieved from http://repository.nihon-u.ac.jp/xmlui/handle/11263/573 ; http://dx.doi.org/10.15006/32665A4967

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

Chicago Manual of Style (16^th Edition):

菊田,純. “Jagged1-Notch2 signaling induces root resorption via RANKL and IL-6 : Jagged1-Notch2シグナルはRANKLとIL-6を介して歯根吸収を惹起する.” 2015. Thesis, Nihon University / 日本大学. Accessed April 17, 2021. http://repository.nihon-u.ac.jp/xmlui/handle/11263/573 ; http://dx.doi.org/10.15006/32665A4967.

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

MLA Handbook (7^th Edition):

菊田,純. “Jagged1-Notch2 signaling induces root resorption via RANKL and IL-6 : Jagged1-Notch2シグナルはRANKLとIL-6を介して歯根吸収を惹起する.” 2015. Web. 17 Apr 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

菊田,純. Jagged1-Notch2 signaling induces root resorption via RANKL and IL-6 : Jagged1-Notch2シグナルはRANKLとIL-6を介して歯根吸収を惹起する. [Internet] [Thesis]. Nihon University / 日本大学; 2015. [cited 2021 Apr 17]. Available from: http://repository.nihon-u.ac.jp/xmlui/handle/11263/573 ; http://dx.doi.org/10.15006/32665A4967.

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

Council of Science Editors:

菊田,純. Jagged1-Notch2 signaling induces root resorption via RANKL and IL-6 : Jagged1-Notch2シグナルはRANKLとIL-6を介して歯根吸収を惹起する. [Thesis]. Nihon University / 日本大学; 2015. Available from: http://repository.nihon-u.ac.jp/xmlui/handle/11263/573 ; http://dx.doi.org/10.15006/32665A4967

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

5. Dolci, Gabriel Schmidt. Efeitos da atorvastatina sobre a ossificação endocondral de fêmures, remodelação óssea e movimentação dentária induzida, estudo em ratos.

Degree: 2016, Brazil

URL: http://hdl.handle.net/10183/142126

► As estatinas são medicamentos comumente prescritos para a prevenção da hiper-lipidemia. Além da redução do colesterol, tais medicamentos parecem estimular a osteogênese e suprimir a… (more)

▼ As estatinas são medicamentos comumente prescritos para a prevenção da hiper-lipidemia. Além da redução do colesterol, tais medicamentos parecem estimular a osteogênese e suprimir a reabsorção óssea, o que poderia afetar a movimentação dentária induzida (MDI) e a recidiva ortodôntica. Assim, o objetivo deste estudo foi determinar se a atorvastatina (ATV) pode afetar a MDI, a recidiva e a osteoclastogênese, por meio da modulação da expressão das moléculas: - ligante do receptor ativador de NFκB (RANKL) e osteoprotegerina (OPG). Ainda foram analisados os potenciais efeitos adversos da ATV sobre a ossificação endocondral e sobre o turnover de ossos longos. No primeiro experimento, 36 ratos foram sujeitos a MDI durante 21 dias, quando o aparelho foi removido. Aos animais, foram administrados, diariamente, ATV ou solução salina (SAL), via gavagem. Após 7, 14 e 21 dias de administração de ATV / SAL, a recidiva dentária foi mensurada, e foram obtidos os cortes histológicos da maxila e fêmur, os quais foram submetidos às seguintes colorações: - H&E – para análise histomorfométrica; - fosfatase acida tartrato resistente (TRAP) – para contagem de osteoclastos e; - imunohistoquímica para RANKL e OPG. A atorvastatina resultou numa inibição da recidiva ortodôntica (p < 0,05), e numa transiente redução do número de osteoclastos (p < 0,05); havendo uma correlação positiva e significativa (p < 0,01) entre o estes dois fatores (número de osteoclastos e a taxa de recidiva). A administração de estatinas também aumentou significativamente a expressão de OPG (p < 0,01), mas não a de RANKL. Além disso, após 21 dias de administração de ATV, a espessura da cartilagem da placa de crescimento e da zona hipertrófica condrocítica foi significativamente aumentada. Já no segundo experimento, 24 ratos começaram a receber diariamente ATV ou solução salina (SAL), via gavagem. Duas semanas mais tarde, a MDI foi iniciada. O deslocamento do dente foi medido após 7, 14 e 21 dias, enquanto que os cortes histológicos da maxila e do fêmur foram obtidos após 14 e 21 dias de MDI; sendo então submetidos às colorações de H&E e TRAP, para avaliação histomorfométrica e contagem de osteoclastos. A administração de atorvastatina gerou um menor movimento dentário (p <0,05) e uma redução transitória do número de osteoclastos (p <0,05). No grupo SAL, após 14 dias de MDI, ocorreu um aumento no número de osteoclastos, assim reduzindo a taxa de volume ósseo, quando comparado com as maxilas controle (sem movimento dentário), deste mesmo grupo. Contudo, tal comportamento não foi observado no grupo ATV. Interessantemente, depois de 35 dias, a atorvastatina não afetou a remodelação óssea nas maxilas controle, nem a ossificação endocondral em fêmures. Logo, guardando as devidas limitações deste estudo pré-clínico, nossos resultados sugerem que a administração sistêmica de atorvastatina é capaz de minimizar a MDI e recidiva ortodôntica. No entanto, os seus efeitos celulares sobre a ossificação endocondral e remodelação óssea durante a MDI e recidiva, parecem ser limitados a… Advisors/Committee Members: Fossati, Anna Christina Medeiros, Souza, Diogo Onofre Gomes de.

Subjects/Keywords: Atorvastatina; Ligante RANK; Ortodontia; Tooth movement; Osteoprotegerin; Receptor activator of nuclear factor-kappa B ligand; Atorvastatin

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

APA (6^th Edition):

Dolci, G. S. (2016). Efeitos da atorvastatina sobre a ossificação endocondral de fêmures, remodelação óssea e movimentação dentária induzida, estudo em ratos. (Doctoral Dissertation). Brazil. Retrieved from http://hdl.handle.net/10183/142126

Chicago Manual of Style (16^th Edition):

Dolci, Gabriel Schmidt. “Efeitos da atorvastatina sobre a ossificação endocondral de fêmures, remodelação óssea e movimentação dentária induzida, estudo em ratos.” 2016. Doctoral Dissertation, Brazil. Accessed April 17, 2021. http://hdl.handle.net/10183/142126.

MLA Handbook (7^th Edition):

Dolci, Gabriel Schmidt. “Efeitos da atorvastatina sobre a ossificação endocondral de fêmures, remodelação óssea e movimentação dentária induzida, estudo em ratos.” 2016. Web. 17 Apr 2021.

Vancouver:

Dolci GS. Efeitos da atorvastatina sobre a ossificação endocondral de fêmures, remodelação óssea e movimentação dentária induzida, estudo em ratos. [Internet] [Doctoral dissertation]. Brazil; 2016. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10183/142126.

Council of Science Editors:

Dolci GS. Efeitos da atorvastatina sobre a ossificação endocondral de fêmures, remodelação óssea e movimentação dentária induzida, estudo em ratos. [Doctoral Dissertation]. Brazil; 2016. Available from: http://hdl.handle.net/10183/142126

IUPUI

6. Cogill, Steven B. PURIFICATION OF SIMPL ANTIBODY AND IMMUNOFLUORESCENCE OF SIMPL SUB-CELLULAR LOCALIZATION IN RESPONSE TO TNFα- AND IL-1.

Degree: 2011, IUPUI

URL: http://hdl.handle.net/1805/2493

►

Indiana University-Purdue University Indianapolis (IUPUI)

SIMPL is a transcriptional co-activator that alters the activity of transcription factor, NF-κB. In response to pathogens, cytokines such as… (more)

Subjects/Keywords: SIMPL; Transcriptional Co-Activator; NF-kB; NF-kappa B (DNA-binding protein); Transcription factors; Cytokines; Immunoglobulins; Immunofluorescence

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

APA (6^th Edition):

Cogill, S. B. (2011). PURIFICATION OF SIMPL ANTIBODY AND IMMUNOFLUORESCENCE OF SIMPL SUB-CELLULAR LOCALIZATION IN RESPONSE TO TNFα- AND IL-1. (Thesis). IUPUI. Retrieved from http://hdl.handle.net/1805/2493

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):

Cogill, Steven B. “PURIFICATION OF SIMPL ANTIBODY AND IMMUNOFLUORESCENCE OF SIMPL SUB-CELLULAR LOCALIZATION IN RESPONSE TO TNFα- AND IL-1.” 2011. Thesis, IUPUI. Accessed April 17, 2021. http://hdl.handle.net/1805/2493.

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

MLA Handbook (7^th Edition):

Cogill, Steven B. “PURIFICATION OF SIMPL ANTIBODY AND IMMUNOFLUORESCENCE OF SIMPL SUB-CELLULAR LOCALIZATION IN RESPONSE TO TNFα- AND IL-1.” 2011. Web. 17 Apr 2021.

Vancouver:

Cogill SB. PURIFICATION OF SIMPL ANTIBODY AND IMMUNOFLUORESCENCE OF SIMPL SUB-CELLULAR LOCALIZATION IN RESPONSE TO TNFα- AND IL-1. [Internet] [Thesis]. IUPUI; 2011. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/1805/2493.

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

Council of Science Editors:

Cogill SB. PURIFICATION OF SIMPL ANTIBODY AND IMMUNOFLUORESCENCE OF SIMPL SUB-CELLULAR LOCALIZATION IN RESPONSE TO TNFα- AND IL-1. [Thesis]. IUPUI; 2011. Available from: http://hdl.handle.net/1805/2493

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

University of Melbourne

7. PEARSON, JACLYN. Type III effectors of enteropathogenic Escherichia coli.

Degree: 2013, University of Melbourne

URL: http://hdl.handle.net/11343/38586

► Enteropathogenic Escherichia coli (EPEC) is an extracellular gastrointestinal pathogen that colonises and adheres intimately to the small intestinal mucosa via the formation of attaching and… (more)

▼ Enteropathogenic Escherichia coli (EPEC) is an extracellular gastrointestinal pathogen that colonises and adheres intimately to the small intestinal mucosa via the formation of attaching and effacing (A/E) lesions. The genes required to form A/E lesions are encoded on a 35 kb genomic pathogenicity island (PAI) called the locus of enterocyte effacement (LEE). The LEE PAI encodes a number of genes that are essential for EPEC pathogenesis, including a type III secretion system (T3SS), translocated effector proteins, an outer membrane adhesion along with its cognate receptor and chaperones. EPEC utilises the T3SS to translocate a diverse repertoire of effector proteins directly into host cells to subvert normal cellular processes, including cytoskeletal organisation, phagocytosis, inflammatory and apoptotic signaling pathways, which ultimately promote disease progression and dissemination. The genes that encode the translocated EPEC effector proteins are located on a number of distinct genomic pathogenicity islands and due to multiple acquisitions during evolution there is a degree of redundancy among them. A common theme among type III translocated effectors is targeting of host innate immune signaling pathways. Infection by wild-type EPEC potently inhibits the production of the proinflammatory cytokine, IL-8 in the early stages of infection. Here we discovered that NleE and NleC act synergistically to dampen IL-8 during EPEC infection by inhibiting canonical NF-κB activation. NleE and its close homologue from Shigella, OspZ, inhibited IκB degradation and p65 nuclear translocation and their activity was dependent on a C-terminal six amino acid motif (IDSYM/IK). NleC contains a zinc metalloprotease consensus motif and specifically targeted NF-κB Rel proteins for degradation. NleC directly cleaved NF-κB p65 (RelA) and enhanced the inhibition of IL-8 during EPEC infection. Another innate immune mechanism targeted by microbial pathogens is apoptosis. Activation of caspases via extrinsic or intrinsic stimuli leads to rapid cell death and some bacterial pathogens have evolved mechanisms to inhibit these processes in order to survive longer in the host. Here we showed that the translocated EPEC effector, NleB1, bound to death domain proteins and inhibited Fas and TNF-induced caspase-8 activation and subsequent cell death during infection. Furthermore, we showed that Fas-deficient mice were more susceptible to infection with the EPEC-like mouse pathogen C. rodentium. Previous studies have indicated that NleB is important in transmission of C. rodentium amongst co-housed littermates and is associated epidemiologically with EPEC, enterohemorrhagic E. coli (EHEC) O157:H7 and non-O157 outbreak strains. Therefore, we have proposed that Fas signaling is an important host defence factor against A/E pathogens and that NleB assists in promoting the longevity of infected cells at the intestinal epithelial surface by inhibiting Fas and TNF-induced…

Subjects/Keywords: inflammation; apoptosis; death receptor signaling; NF-KB; gastrointestinal pathogens

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

APA (6^th Edition):

PEARSON, J. (2013). Type III effectors of enteropathogenic Escherichia coli. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/38586

Chicago Manual of Style (16^th Edition):

PEARSON, JACLYN. “Type III effectors of enteropathogenic Escherichia coli.” 2013. Doctoral Dissertation, University of Melbourne. Accessed April 17, 2021. http://hdl.handle.net/11343/38586.

MLA Handbook (7^th Edition):

PEARSON, JACLYN. “Type III effectors of enteropathogenic Escherichia coli.” 2013. Web. 17 Apr 2021.

Vancouver:

PEARSON J. Type III effectors of enteropathogenic Escherichia coli. [Internet] [Doctoral dissertation]. University of Melbourne; 2013. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/11343/38586.

Council of Science Editors:

PEARSON J. Type III effectors of enteropathogenic Escherichia coli. [Doctoral Dissertation]. University of Melbourne; 2013. Available from: http://hdl.handle.net/11343/38586

8. 吉野,智一. TNF-α induces orthodontic root resorption via the expression of RANKL : TNF-αはRANKL存在下で歯科矯正治療中の歯根吸収を増悪させる.

Degree: 博士（歯学）, 2014, Nihon University / 日本大学

URL: http://repository.nihon-u.ac.jp/xmlui/handle/11263/246 ; http://dx.doi.org/10.15006/32665A4828

Subjects/Keywords: Tumor necrosis factor-α; TNF-α; Receptor activator of NF-kB ligand; RANKL; 歯根吸収; Root resorption; 矯正学的歯牙移動; Orthodontic tooth movement

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

APA (6^th Edition):

吉野,智一. (2014). TNF-α induces orthodontic root resorption via the expression of RANKL : TNF-αはRANKL存在下で歯科矯正治療中の歯根吸収を増悪させる. (Thesis). Nihon University / 日本大学. Retrieved from http://repository.nihon-u.ac.jp/xmlui/handle/11263/246 ; http://dx.doi.org/10.15006/32665A4828

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

Chicago Manual of Style (16^th Edition):

吉野,智一. “TNF-α induces orthodontic root resorption via the expression of RANKL : TNF-αはRANKL存在下で歯科矯正治療中の歯根吸収を増悪させる.” 2014. Thesis, Nihon University / 日本大学. Accessed April 17, 2021. http://repository.nihon-u.ac.jp/xmlui/handle/11263/246 ; http://dx.doi.org/10.15006/32665A4828.

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

MLA Handbook (7^th Edition):

吉野,智一. “TNF-α induces orthodontic root resorption via the expression of RANKL : TNF-αはRANKL存在下で歯科矯正治療中の歯根吸収を増悪させる.” 2014. Web. 17 Apr 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

吉野,智一. TNF-α induces orthodontic root resorption via the expression of RANKL : TNF-αはRANKL存在下で歯科矯正治療中の歯根吸収を増悪させる. [Internet] [Thesis]. Nihon University / 日本大学; 2014. [cited 2021 Apr 17]. Available from: http://repository.nihon-u.ac.jp/xmlui/handle/11263/246 ; http://dx.doi.org/10.15006/32665A4828.

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

Council of Science Editors:

吉野,智一. TNF-α induces orthodontic root resorption via the expression of RANKL : TNF-αはRANKL存在下で歯科矯正治療中の歯根吸収を増悪させる. [Thesis]. Nihon University / 日本大学; 2014. Available from: http://repository.nihon-u.ac.jp/xmlui/handle/11263/246 ; http://dx.doi.org/10.15006/32665A4828

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

National University of Ireland – Galway

9. Masterson, Claire. Understanding the Mechanisms of Action of Hypercapnic Acidosis and the Therapeutic Potential of Human Mesenchymal Stromal Cells in Diminishing Inflammation and Enhancing Repair in Acute Respiratory Distress Syndrome.

Degree: 2013, National University of Ireland – Galway

URL: http://hdl.handle.net/10379/4407

► Acute respiratory distress syndrome (ARDS) is a term used to describe severe lung injury characterised by uncontrolled inflammatory response and resultant damage to endothelial and… (more)

▼ Acute respiratory distress syndrome (ARDS) is a term used to describe severe lung injury characterised by uncontrolled inflammatory response and resultant damage to endothelial and epithelial layers leading to eventual loss of pulmonary function. ARDS can be aggravated by the only therapy currently available to prolong survival - mechanical ventilation. To date many attempts have been made to alter ventilation protocols to reduce the over-distension and cycle of atelectasis and shear stresses associated with artificial gas delivery to the lung. Thus far the most effective therapeutic strategy overall has been to reduce the tidal volumes used which can lead to the build-up of CO2, this is termed "permissive hypercapnia". Experimental studies recommend avoiding buffering the resultant acidosis as there is no evidence of benefit. In fact, both the decrease in pH and the elevated CO2 may confer their own beneficial effects during lung inflammation and injury, but may also have adverse effects such as slowing repair and inhibiting the host response to infection. The anti-inflammatory effects of hypercapnic acidosis (HCA), appears to be mediated, at least in part, by the suppression of NF-kB, a key transcription factor in inflammation, injury and repair. however the exact mechanisms by which HCA suppresses activation of the NF-kB pathway remain to be elucidated. A greater understanding of these mechanisms may provide opportunities to develop strategies to harness the benefits of hypercapnia while minimising any potential for harm. The investigation of the therapeutic potential of mesenchymal stem/stromal cells (MSCs) is a rapidly escalating, including recent application to the area of lung disease and injury. The safety, and in some cases, efficacy of hMSCs has been established in disease states such as skeletal muscle injury, myocardial infarction, stroke, and graft versus host disease. In fact, an initial phase 1 dose escalation efficacy and safety study of MSCs has recently commenced in patients with ARDS. However, much remains to be understood in regard to the efficacy and mechanisms of action of MSCs before we can move forward to definitive clinical testing. Therefore these studies, in a continuation of previous studies from our laboratory are aimed at determining the precise mechanism of action of HCA on the pulmonary NF-kB pathway and following this, to provide critical pre-clinical data that will enable the safe and effective use of human MSCs in ARDS. Methods: In vitro models of lung injury were used to determine the effects of HCA on the NF-kB pathway. Pulmonary cell lines were transfected or transduced with an NF-kB luciferase reporter and subjected to TNF-a, IL-1b or endotoxin injury. Therapeutic HC was administered by increasing CO2 levels in cell culture environments for 24 hours. NF-kB activation was assessed based on luciferase production in cell lysates and IL-8 concentration in cell culture media. Effects of HCA on intracellular proteins were analysed in cellular fractions which were prepared using… Advisors/Committee Members: Laffey, John (advisor).

Subjects/Keywords: ARDS; NF-kB; Hypercapnia; MSCs; Department of Anaesthesia; School of Medicine

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APA (6^th Edition):

Masterson, C. (2013). Understanding the Mechanisms of Action of Hypercapnic Acidosis and the Therapeutic Potential of Human Mesenchymal Stromal Cells in Diminishing Inflammation and Enhancing Repair in Acute Respiratory Distress Syndrome. (Thesis). National University of Ireland – Galway. Retrieved from http://hdl.handle.net/10379/4407

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):

Masterson, Claire. “Understanding the Mechanisms of Action of Hypercapnic Acidosis and the Therapeutic Potential of Human Mesenchymal Stromal Cells in Diminishing Inflammation and Enhancing Repair in Acute Respiratory Distress Syndrome. ” 2013. Thesis, National University of Ireland – Galway. Accessed April 17, 2021. http://hdl.handle.net/10379/4407.

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

MLA Handbook (7^th Edition):

Masterson, Claire. “Understanding the Mechanisms of Action of Hypercapnic Acidosis and the Therapeutic Potential of Human Mesenchymal Stromal Cells in Diminishing Inflammation and Enhancing Repair in Acute Respiratory Distress Syndrome. ” 2013. Web. 17 Apr 2021.

Vancouver:

Masterson C. Understanding the Mechanisms of Action of Hypercapnic Acidosis and the Therapeutic Potential of Human Mesenchymal Stromal Cells in Diminishing Inflammation and Enhancing Repair in Acute Respiratory Distress Syndrome. [Internet] [Thesis]. National University of Ireland – Galway; 2013. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10379/4407.

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

Council of Science Editors:

Masterson C. Understanding the Mechanisms of Action of Hypercapnic Acidosis and the Therapeutic Potential of Human Mesenchymal Stromal Cells in Diminishing Inflammation and Enhancing Repair in Acute Respiratory Distress Syndrome. [Thesis]. National University of Ireland – Galway; 2013. Available from: http://hdl.handle.net/10379/4407

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

10. Jules, Joel. In vitro elucidation of the role and mechanism of RANKL in TNF- and IL-1-mediated osteoclast formation and function.

Degree: PhD, 2010, University of Alabama – Birmingham

URL: http://contentdm.mhsl.uab.edu/u?/etd,917

►

The receptor activator of NF-қB (RANK) ligand (RANKL) and its receptor RANK play a critical role in osteoclast biology. RANK has three tumor necrosis factor… (more)

▼

The receptor activator of NF-қB (RANK) ligand (RANKL) and its receptor RANK play a critical role in osteoclast biology. RANK has three tumor necrosis factor receptor associated factor (TRAF)-binding motifs [PFQEP369-373 (Motif 1), PVQEET559- 564 (Motif 2), and PVQEQG604-609 (Motif 3)] that regulate osteoclast formation and function. RANK also contains a TRAF-independent motif (IVVY535-538) that commits bone marrow macrophages (BMMs), which are osteoclast precursors, to the osteoclast lineage for osteoclastogenesis. Notably, tumor necrosis factor-α (TNF) and interleukin-1 (IL-1) utilize TRAFs to initiate most of the signaling pathways known to be activated by RANKL but fail to form osteoclasts unless attended by permissive levels of RANKL, suggesting that TNF- and IL-1-mediated osteoclastogenesis may require priming of BMMs by RANKL. Moreover, unlike RANK, TNF and IL-1 receptors lack the IVVY motif, which may explain the inability of TNF or IL-1 alone to stimulate osteoclastogenesis. Herein, I sought to determine the molecular mechanism underlying the RANKL requirement for TNF- and IL-1-mediated osteoclast formation and function by using a chimeric-receptor approach. In the first and second parts of my thesis, I addressed the role of the RANK IVVY motif in TNF- and IL-1-mediated osteoclastogenesis, respectively. I then determined the role of Motif 1/Motif 2/Motif 3 of RANK in TNF- and IL-1-mediated osteoclast formation and function. The results indicate that TNF- and IL-1-mediated osteoclastogenesis require RANK signaling from IVVY motif, Motif 2 and Motif 3. Significantly, my thesis work has established that the RANK IVVY535-538, PVQEET559-564, and PVQEQG604-609 motifs may serve as attractive therapeutic targets for bone loss accompanying many bone disorders.

1 online resource (xii, 144 p. : ill., digital, PDF file)

Pathology;

Joint Health Sciences;

RANKL RANK TNF IL-1 osteoclast IVVY motif

UNRESTRICTED

Advisors/Committee Members: Feng, Xu, Ballinger, Scott W.<br>, Javed, Amjad<br>, McDonald, Jay M.<br>, Mountz, John D..

Subjects/Keywords: Amino Acid Motifs<; br>; Cell Differentiation<; br>; Cytoplasm – metabolism<; br>; Osteoclasts – cytology<; br>; RANK Ligand – metabolism<; br>; Receptor Activator of Nuclear Factor-kappa B – chemistry<; br>; Receptor Activator of Nuclear Factor-kappa B – metabolism<; br>; Tumor Necrosis Factor-alpha – metabolism

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

APA (6^th Edition):

Jules, J. (2010). In vitro elucidation of the role and mechanism of RANKL in TNF- and IL-1-mediated osteoclast formation and function. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,917

Chicago Manual of Style (16^th Edition):

Jules, Joel. “In vitro elucidation of the role and mechanism of RANKL in TNF- and IL-1-mediated osteoclast formation and function.” 2010. Doctoral Dissertation, University of Alabama – Birmingham. Accessed April 17, 2021. http://contentdm.mhsl.uab.edu/u?/etd,917.

MLA Handbook (7^th Edition):

Jules, Joel. “In vitro elucidation of the role and mechanism of RANKL in TNF- and IL-1-mediated osteoclast formation and function.” 2010. Web. 17 Apr 2021.

Vancouver:

Jules J. In vitro elucidation of the role and mechanism of RANKL in TNF- and IL-1-mediated osteoclast formation and function. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2010. [cited 2021 Apr 17]. Available from: http://contentdm.mhsl.uab.edu/u?/etd,917.

Council of Science Editors:

Jules J. In vitro elucidation of the role and mechanism of RANKL in TNF- and IL-1-mediated osteoclast formation and function. [Doctoral Dissertation]. University of Alabama – Birmingham; 2010. Available from: http://contentdm.mhsl.uab.edu/u?/etd,917

University of Alberta

11. Fagan-Garcia, Katharine. A large deletion virus reveals the presence of previously uncharacterized vaccinia virus inhibitors of NF-kB signaling.

Degree: MS, Department of Medical Microbiology and Immunology, 2010, University of Alberta

URL: https://era.library.ualberta.ca/files/jq085k72q

► The classical Nuclear Factor kappa B (NF-κB) signaling pathway is an important regulator of inflammation and innate immune responses. Poxviruses, including vaccinia virus, encode multiple… (more)

Subjects/Keywords: vaccinia; virus; NF-kB; inhibitors

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

APA (6^th Edition):

Fagan-Garcia, K. (2010). A large deletion virus reveals the presence of previously uncharacterized vaccinia virus inhibitors of NF-kB signaling. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/jq085k72q

Chicago Manual of Style (16^th Edition):

Fagan-Garcia, Katharine. “A large deletion virus reveals the presence of previously uncharacterized vaccinia virus inhibitors of NF-kB signaling.” 2010. Masters Thesis, University of Alberta. Accessed April 17, 2021. https://era.library.ualberta.ca/files/jq085k72q.

MLA Handbook (7^th Edition):

Fagan-Garcia, Katharine. “A large deletion virus reveals the presence of previously uncharacterized vaccinia virus inhibitors of NF-kB signaling.” 2010. Web. 17 Apr 2021.

Vancouver:

Fagan-Garcia K. A large deletion virus reveals the presence of previously uncharacterized vaccinia virus inhibitors of NF-kB signaling. [Internet] [Masters thesis]. University of Alberta; 2010. [cited 2021 Apr 17]. Available from: https://era.library.ualberta.ca/files/jq085k72q.

Council of Science Editors:

Fagan-Garcia K. A large deletion virus reveals the presence of previously uncharacterized vaccinia virus inhibitors of NF-kB signaling. [Masters Thesis]. University of Alberta; 2010. Available from: https://era.library.ualberta.ca/files/jq085k72q

12. Πηλιχού, Αναστασία. Συσχέτιση μεταξύ επιπέδων οστεοπρωτεγερίνης σε άτομα με προχωρημένη οστεοαρθρίτιδα γόνατος και κλινικής βαρύτητας της νόσου.

Degree: 2008, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/18463

► Η αναγνώριση και ο χαρακτηρισμός των τριών νέων μορίων (RANKL, RANK, OPG) που ανήκουν στην οικογένεια των παραγόντων νέκρωσης του όγκου (TNF) έχει ανοίξει νέα… (more)

▼ Η αναγνώριση και ο χαρακτηρισμός των τριών νέων μορίων (RANKL, RANK, OPG) που ανήκουν στην οικογένεια των παραγόντων νέκρωσης του όγκου (TNF) έχει ανοίξει νέα μονοπάτια στην μελέτη της παθοφυσιολογίας της οστεοκλαστογένεσης και επομένως και στην μελέτη της παθοφυσιολογίας πολλών νοσημάτων των οστών. Το RANKL εκφράζεται από ενεργοποιημένα Τ κύτταρα, από στρωματικά κύτταρα του μυελού των οστών και από οστεοβλάστες και στη συνέχεια συνδέεται με τον υποδοχέα του, δηλαδή το RANK, το οποίο με τη σειρά του έχει παραχθεί από πρόδρομα κύτταρα των οστεοκλαστών, χονδροκύτταρα και ώριμους οστεοκλάστες. Η διασύνδεση των δυο αυτών μορίων προάγει την ωρίμανση και ενεργοποίηση των οστεοκλαστών (154). H OPG είναι ο κρυφός υποδοχέας του RANKL, ο οποίος παρεμποδίζει τη διασύνδεση RANK-RANKL, με αποτέλεσμα να παρεμποδίζεται η διαφοροποίηση και η λειτουργία των οστεοκλαστών (199). Επομένως, από τα παραπάνω γίνεται σαφές ότι η ισορροπία μεταξύ της έκφρασης RANKL και OPG είναι αυτή που καθορίζει τον βαθμό της οστεοκλαστικής δραστηριότητας και τον βαθμό της οστικής απορρόφησης. Τα επίπεδα του λόγου RANKL/OPG έχει δειχθεί να παίζουν σημαντικό ρόλο στην παθογένεια της οστικής απώλειας σε περιπτώσεις κακοήθειας με οστικές μεταστάσεις (244, 245). Επιπλέον, στην ρευματοειδή αρθρίτιδα ο λόγος RANKL/OPG, τόσο όσον αφορά το mRna όσο και τα επίπεδα των μορίων στο αρθρικό υγρό και στον ορό είναι αυξημένος, γεγονός που οδηγεί στην οστική αποδόμηση που παρατηρείται στη νόσο (210, 243, 246). Παρά το γεγονός ότι υπάρχουν πολλές δημοσιεύσεις και πολλά στοιχεία για το ρόλο του λόγου RANKL/OPG στις κακοήθειες και στις φλεγμονώδεις καταστάσεις, πολύ λίγα έχουν αναφερθεί στην βιβλιογραφία για τον ρόλο των μορίων αυτών στην παθογένεια της οστεοαρθρίτιδας και ιδιαίτερα της πρωτοπαθούς οστεοαρθρίτιδας του γόνατος. Στόχος λοιπόν της παρούσας μελέτης είναι η αξιολόγηση των επιπέδων RANKL και OPG τόσο στο αρθρικό υγρό όσο και στον ορό των ασθενών με πρωτοπαθή οστεοαρθρίτιδα του γόνατος και η συσχέτιση των αποτελεσμάτων με κλινικές και ακτινολογικές παραμέτρους σε μια προσπάθεια διερεύνησης της παθοφυσιολογίας της νόσου. Με βάση τα αποτελέσματά μας υποθέτουμε ότι το αρθρικό υγρό των ατόμων με οστεοαρθρίτιδα προάγει την τοπική παραγωγή του RANKL (υψηλή θετική συσχέτιση των επιπέδων RANKL ορού και αρθρικού υγρού στους ασθενείς μας) και σε ανταπόδοση τοπικοί κυτταρικοί παράγοντες παράγουν μεγάλες ποσότητες OPG προκειμένου να προστατεύσουν την άρθρωση, χωρίς όμως αποτέλεσμα. Ωστόσο, η υπόθεση αυτή δεν μπορεί να εξηγήσει τα υψηλά επίπεδα RANKL του ορού που παρατηρήθηκαν στην μελέτη μας. Οι μόνες μέχρι σήμερα δημοσιευμένες πληροφορίες σχετικά με την οστεοαρθρίτιδα του ισχίου προτείνουν μια ανισορροπία στην γονιδιακή έκφραση των μορίων RANKL και OPG υπέρ της OPG, ενώ αντίθετα στην οστεοπόρωση του αυχένα του μηριαίου η ανισορροπία αυτή είναι υπέρ του RANKL (247). Φαίνεται λοιπόν πως η ισορροπία του συστήματος RANKL/OPG είναι κριτικής σημασίας στην ανάπτυξη της οστεοαρθίτιδας και της οστεοπόρωσης. Όμως, ο ρόλος του ανοσοποιητικού συστήματος στην διατήρηση της…

Subjects/Keywords: Γόνατα, Οστεοαρθρίτιδα; Οστεοπρωτεγερίνη; Αρθρικό υγρό; Ορός αίματος; Knee osteoarthritis; Osteoprotegerin; Receptor activator of nuclear factor kb ligand; Synovial fluid; Serum

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

APA (6^th Edition):

Πηλιχού, . �. (2008). Συσχέτιση μεταξύ επιπέδων οστεοπρωτεγερίνης σε άτομα με προχωρημένη οστεοαρθρίτιδα γόνατος και κλινικής βαρύτητας της νόσου. (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/18463

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):

Πηλιχού, Αναστασία. “Συσχέτιση μεταξύ επιπέδων οστεοπρωτεγερίνης σε άτομα με προχωρημένη οστεοαρθρίτιδα γόνατος και κλινικής βαρύτητας της νόσου.” 2008. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed April 17, 2021. http://hdl.handle.net/10442/hedi/18463.

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

MLA Handbook (7^th Edition):

Πηλιχού, Αναστασία. “Συσχέτιση μεταξύ επιπέδων οστεοπρωτεγερίνης σε άτομα με προχωρημένη οστεοαρθρίτιδα γόνατος και κλινικής βαρύτητας της νόσου.” 2008. Web. 17 Apr 2021.

Vancouver:

Πηλιχού �. Συσχέτιση μεταξύ επιπέδων οστεοπρωτεγερίνης σε άτομα με προχωρημένη οστεοαρθρίτιδα γόνατος και κλινικής βαρύτητας της νόσου. [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2008. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10442/hedi/18463.

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

Council of Science Editors:

Πηλιχού �. Συσχέτιση μεταξύ επιπέδων οστεοπρωτεγερίνης σε άτομα με προχωρημένη οστεοαρθρίτιδα γόνατος και κλινικής βαρύτητας της νόσου. [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2008. Available from: http://hdl.handle.net/10442/hedi/18463

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

University of Guelph

13. Siracusa, Laura. Mechanisms of Glucocorticoid-Mediated Suppression of Tracheal Antimicrobial Peptide Expression in Bovine Tracheal Epithelial Cells.

Degree: MS, Department of Pathobiology, 2019, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/14742

► This research aimed to identify the mechanism by which glucocorticoid downregulates inducible innate immune responses in bovine tracheal epithelial cells (bTEC). It adds knowledge regarding… (more)

Subjects/Keywords: Pathobiology; Molecular Biology; tracheal antimicrobial peptide; dual luciferase; NF-kB; mRNA; IkB; Inflammation; stress; glucocorticoid; cloning; toll-like receptor; TLR 2

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

APA (6^th Edition):

Siracusa, L. (2019). Mechanisms of Glucocorticoid-Mediated Suppression of Tracheal Antimicrobial Peptide Expression in Bovine Tracheal Epithelial Cells. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/14742

Chicago Manual of Style (16^th Edition):

Siracusa, Laura. “Mechanisms of Glucocorticoid-Mediated Suppression of Tracheal Antimicrobial Peptide Expression in Bovine Tracheal Epithelial Cells.” 2019. Masters Thesis, University of Guelph. Accessed April 17, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/14742.

MLA Handbook (7^th Edition):

Siracusa, Laura. “Mechanisms of Glucocorticoid-Mediated Suppression of Tracheal Antimicrobial Peptide Expression in Bovine Tracheal Epithelial Cells.” 2019. Web. 17 Apr 2021.

Vancouver:

Siracusa L. Mechanisms of Glucocorticoid-Mediated Suppression of Tracheal Antimicrobial Peptide Expression in Bovine Tracheal Epithelial Cells. [Internet] [Masters thesis]. University of Guelph; 2019. [cited 2021 Apr 17]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/14742.

Council of Science Editors:

Siracusa L. Mechanisms of Glucocorticoid-Mediated Suppression of Tracheal Antimicrobial Peptide Expression in Bovine Tracheal Epithelial Cells. [Masters Thesis]. University of Guelph; 2019. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/14742

Vanderbilt University

14. Thu, Yee Mon. The role of NF-kB inducing kinase (NIK) in modulating melanoma tumorigenesis.

Degree: PhD, Cancer Biology, 2011, Vanderbilt University

URL: http://hdl.handle.net/1803/14261

► Nuclear factor-êB (NF-êB) inducing kinase (NIK) is a MAP3K that regulates activation of NF-êB. NIK is often over-expressed in tumor cells, including melanoma, but the… (more)

▼ Nuclear factor-êB (NF-êB) inducing kinase (NIK) is a MAP3K that regulates activation of NF-êB. NIK is often over-expressed in tumor cells, including melanoma, but the significance of this in melanoma progression remains unclear. Tissue microarray analysis of NIK expression reveals that dysplastic nevi (n=22), primary (n=15) and metastatic melanoma (n=13) lesions showed a statistically significant elevation in NIK expression when compared to benign nevi (n=30). Depletion of NIK using shRNA in melanoma cell lines decreased proliferation, increased apoptosis, delayed cell cycle progression, and reduced tumor growth in a mouse xenograft model. Consistent with the previous studies, NIK deficiency reduced activation of the non-canonical NF-êB pathway, while canonical NF-êB activation remained intact. NIK depletion also reduced expression of genes that contribute to tumor growth, including CXCR4, c-MYC and c-MET, as well as pro-survival factors BCL2 and survivin. These changes in gene expression are not fully explained by the attenuation of the non-canonical NF-êB pathway. Shown here for the first time is the demonstration that NIK depletion decreases â-catenin mediated transcription to down-regulate expression of survivin as well as other â-catenin regulated genes including c-MYC, c-MET and CCND2. These data indicate NIK mediates both â-catenin and NF-êB regulated transcription to modulate melanoma survival and growth. Thus, NIK may be a promising therapeutic target for melanoma. In addition, novel NIK-interacting proteins were identified by using mass spectrometry analysis. Some of these proteins include heat shock protein 90 (Hsp90), ribosomal protein S3 (RPS3) and DEAD box polypeptide 5 (DDX5). Inhibitor of IêB kinase â (IKKâ), another kinase of NF-êB pathway, also contributes to melanoma growth. Systemic inhibition of this kinase in a melanoma xenograft model was characterized using a pharmacological IKKâ inhibitor, BMS-345541. Results show that inhibition of IKKâ alters the host immune cell composition and the composition of leukocytes infiltrating tumor, suggesting that systemic NF-êB inhibition should be evaluated more carefully before going forward as a cancer therapy. In this research, I identified NIK as a new potential target for melanoma growth, revealed important new biological functions of NIK, and unraveled key effects of IKKâ inhibition on the tumor microenvironment. Advisors/Committee Members: Ann Richmond (committee member), Josiean Eid (Committee Chair).

Subjects/Keywords: melanoma; cancer; NF-kB inducing kinase; NF-kB

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

APA (6^th Edition):

Thu, Y. M. (2011). The role of NF-kB inducing kinase (NIK) in modulating melanoma tumorigenesis. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/14261

Chicago Manual of Style (16^th Edition):

Thu, Yee Mon. “The role of NF-kB inducing kinase (NIK) in modulating melanoma tumorigenesis.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed April 17, 2021. http://hdl.handle.net/1803/14261.

MLA Handbook (7^th Edition):

Thu, Yee Mon. “The role of NF-kB inducing kinase (NIK) in modulating melanoma tumorigenesis.” 2011. Web. 17 Apr 2021.

Vancouver:

Thu YM. The role of NF-kB inducing kinase (NIK) in modulating melanoma tumorigenesis. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/1803/14261.

Council of Science Editors:

Thu YM. The role of NF-kB inducing kinase (NIK) in modulating melanoma tumorigenesis. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://hdl.handle.net/1803/14261

15. Ribeiro Bravo, Isabel. Investigating the role of MyD88-NF-kB signalling in regulating the inflammatory response to the emerging pre-neoplastic cells.

Degree: PhD, 2019, University of Edinburgh

URL: http://hdl.handle.net/1842/36166

► Chronic inflammation has long been considered an enabling characteristic of the cancer microenvironment. The release of growth and survival factors, extracellular matrix-modifying enzymes and other… (more)

▼ Chronic inflammation has long been considered an enabling characteristic of the cancer microenvironment. The release of growth and survival factors, extracellular matrix-modifying enzymes and other bioactive molecules by inflammatory cells into the tumour microenvironment contributes to the acquisition of cancer hallmark capabilities. It is now known that oncogenes can activate signals that promote the formation of an inflammatory microenvironment, even in the absence of external stimuli, placing inflammation as an early phenomenon in the timeline of tumour development. The over-expression of an oncogene in pre-neoplastic cells has been shown to promote the release of cytokines and other pro-inflammatory markers and consequent recruitment of neutrophils and macrophages. The recruitment of neutrophils has been previously associated with increased proliferation of oncogene-transformed cells, however, the mechanisms by which neutrophils exercise this trophic role are yet poorly understood. Nuclear factor kappa B (NF-kB) transcription factors are crucial elements for the regulation of inflammation, immune response as well as cellular stress response. Activation of NF-kB signalling pathway leads to the expression of mitogenic and anti-apoptotic factors, thus having the potential to promote tumorigenesis. MyD88 is an adaptor protein that mediates TLR/IL-1-R activation of the NF-kB pathway. MyD88 has been shown to play both positive and negative roles in cancer development. It is unclear however, whether the MyD88-NF-kB signalling pathway plays a role during the earliest stages of preneoplastic development of tumour initiation. To better understand the role of MyD88-NF-kB in oncogene driven inflammation during preneoplastic cell development, I was involved in the development of a zebrafish (Danio rerio) tissue specific inducible model which allowed the temporal control of HRasG12V oncogene expression for generation of pre-neoplastic cells (PNCs) and the detection of the earliest signalling events that initiate the process of tumour development. Using reporter lines, generated elsewhere, I demonstrate the activation of MyD88-NF-kB signalling pathway in both PNCs and recruited neutrophils. I also evaluate the effect of its downregulation, through the expression of the murine dominant negative mutant of IkBa, on PNCs proliferation and modulation of recruited neutrophil behaviour. Alongside the study of NF-kB as an inducer of tumour initiation, I also provide evidence of heterogeneity within the neutrophil population recruited to the PNCs and the different behaviours they exhibit. This work demonstrates the potential of zebrafish for the study of tumour initiation highlighting the involvement of NF-kB signalling pathway in the establishment of an inflammatory milieu that allows the progression of this first stage of tumorigenesis.

Subjects/Keywords: inflammation; NF-kB; zebrafish; inflammatory response; tumour initiation; NF-kB activation

10 more images…

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

APA (6^th Edition):

Ribeiro Bravo, I. (2019). Investigating the role of MyD88-NF-kB signalling in regulating the inflammatory response to the emerging pre-neoplastic cells. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/36166

Chicago Manual of Style (16^th Edition):

Ribeiro Bravo, Isabel. “Investigating the role of MyD88-NF-kB signalling in regulating the inflammatory response to the emerging pre-neoplastic cells.” 2019. Doctoral Dissertation, University of Edinburgh. Accessed April 17, 2021. http://hdl.handle.net/1842/36166.

MLA Handbook (7^th Edition):

Ribeiro Bravo, Isabel. “Investigating the role of MyD88-NF-kB signalling in regulating the inflammatory response to the emerging pre-neoplastic cells.” 2019. Web. 17 Apr 2021.

Vancouver:

Ribeiro Bravo I. Investigating the role of MyD88-NF-kB signalling in regulating the inflammatory response to the emerging pre-neoplastic cells. [Internet] [Doctoral dissertation]. University of Edinburgh; 2019. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/1842/36166.

Council of Science Editors:

Ribeiro Bravo I. Investigating the role of MyD88-NF-kB signalling in regulating the inflammatory response to the emerging pre-neoplastic cells. [Doctoral Dissertation]. University of Edinburgh; 2019. Available from: http://hdl.handle.net/1842/36166

16. Andressa Duarte. Participação da via PI3K/AKT na produção de óxido nítrico por macrófagos peritoneais.

Degree: 2013, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/17/17147/tde-21102013-112320/

►

A imunidade inata é responsável pela resposta inicial aos microrganismos, uma vez que impede, controla ou elimina a infecção. Esse sistema consiste em barreiras epiteliais,… (more)

▼

A imunidade inata é responsável pela resposta inicial aos microrganismos, uma vez que impede, controla ou elimina a infecção. Esse sistema consiste em barreiras epiteliais, proteínas plasmáticas e células circulantes e teciduais. Dentre esses componentes, os macrófagos possuem grande importância, sendo capazes de controlar e eliminar agentes patogênicos através da fagocitose e produção de espécies reativas de oxigênio e nitrogênio. A ativação de PRRs por constituintes oriundos dos patógenos em macrófagos desencadeia eventos da resposta imune inata, ativados por diversas vias de sinalização intracelular. A via das PI3Ks é conhecida por regular várias funções nas células, como a regulação do ciclo celular, migração e produção de espécies reativas de oxigênio e nitrogênio. O NO é um mediador central na imunidade inata que, após estímulos inflamatórios, é produzido em altas quantidades através da iNOS. Macrófagos deficientes em PI3K produzem menos NO e apresentam prejudicado controle da infecção quando infectados por T. cruzi. O objetivo do presente trabalho foi investigar o papel da via PI3K na produção de NO por macrófagos peritoneais estimulados com LPS. Os macrófagos empregados no estudo, WT e PI3K-/-, possuem o mesmo fenótipo. Observamos que macrófagos PI3K-/- possuem uma menor produção de NO e expressam menos iNOS. A reduzida expressão de iNOS, após estímulo com LPS, é também observada quando macrófagos WT são tratados com inibidores seletivos da PI3K e AKT. Além disso, demonstramos que, concomitantemente à menor expressão da iNOS, ocorre deficiência na fosforilação da AKT e diminuição da ativação do fator de transcrição NF-kB, sugerindo que a PI3K participa da ativação do NF-kB. Foi observado ainda que o tratamento com PTX também diminui a expressão da iNOS. No entanto, macrófagos PAFR-/- expostos ao LPS presentam maior expressão da iNOS, enquanto os macrófagos CCR2-/- apresentam menor expressão dessa enzima nessas condições. Para investigar a implicação da via PI3K in vivo foi administrado LPS i.v., como modelo de choque endotoxemico, no qual observamos maior sobrevida em animais PI3K-/- comparado aos animais WT e menores níveis de nitrito no soro. Nossos dados sugerem que a enzima PI3K é crítica para expressão de iNOS e produção de NO pelos macrófagos, possivelmente através da ativação do receptor CCR2, estando envolvida na fisiopatologia do choque induzido por LPS.

Innate immunity is the initial response to microorganisms, since it prevents, controls and eliminates infection. This system consists in epithelial barriers, plasma proteins and circulating and tissue cells. Among these components, macrophages have great importance, being capable of control and eliminate pathogen agents through phagocytosis and production of reactive oxygen and nitrogen species. Activation of PRRs by pathogens constituents in macrophages triggers events of the innate immune response, activated by various intracellular signaling pathways. PI3Ks pathway is known to regulate several functions in the cell, such as regulation…

Advisors/Committee Members: Thiago Mattar Cunha, Vania Luiza Deperon Bonato Martins, Vanessa Pinho da Silva.

Subjects/Keywords: iNOS; NF-kB; NO; PI3K; iNOS; NF-kB; NO; PI3K

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

APA (6^th Edition):

Duarte, A. (2013). Participação da via PI3K/AKT na produção de óxido nítrico por macrófagos peritoneais. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/17/17147/tde-21102013-112320/

Chicago Manual of Style (16^th Edition):

Duarte, Andressa. “Participação da via PI3K/AKT na produção de óxido nítrico por macrófagos peritoneais.” 2013. Masters Thesis, University of São Paulo. Accessed April 17, 2021. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-21102013-112320/.

MLA Handbook (7^th Edition):

Duarte, Andressa. “Participação da via PI3K/AKT na produção de óxido nítrico por macrófagos peritoneais.” 2013. Web. 17 Apr 2021.

Vancouver:

Duarte A. Participação da via PI3K/AKT na produção de óxido nítrico por macrófagos peritoneais. [Internet] [Masters thesis]. University of São Paulo; 2013. [cited 2021 Apr 17]. Available from: http://www.teses.usp.br/teses/disponiveis/17/17147/tde-21102013-112320/.

Council of Science Editors:

Duarte A. Participação da via PI3K/AKT na produção de óxido nítrico por macrófagos peritoneais. [Masters Thesis]. University of São Paulo; 2013. Available from: http://www.teses.usp.br/teses/disponiveis/17/17147/tde-21102013-112320/

University of Ottawa

17. Phan, Michael. Viral Sensitizers Potentiate the Infection of Cancer Cells Via NF-kB .

Degree: 2020, University of Ottawa

URL: http://hdl.handle.net/10393/40524

► Genetically engineered oncolytic viruses (OVs) have been proven to be effective anti-cancer agents. However, the heterogeneity of tumours and obligate attenuation of OVs to achieve… (more)

Subjects/Keywords: Cancer; NF-kB; Oncolytic Virus; Cancer Immunotherapy; Mechanism of Action; Interferon; Antiviral Signalling

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

APA (6^th Edition):

Phan, M. (2020). Viral Sensitizers Potentiate the Infection of Cancer Cells Via NF-kB . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/40524

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):

Phan, Michael. “Viral Sensitizers Potentiate the Infection of Cancer Cells Via NF-kB .” 2020. Thesis, University of Ottawa. Accessed April 17, 2021. http://hdl.handle.net/10393/40524.

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

MLA Handbook (7^th Edition):

Phan, Michael. “Viral Sensitizers Potentiate the Infection of Cancer Cells Via NF-kB .” 2020. Web. 17 Apr 2021.

Vancouver:

Phan M. Viral Sensitizers Potentiate the Infection of Cancer Cells Via NF-kB . [Internet] [Thesis]. University of Ottawa; 2020. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10393/40524.

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

Council of Science Editors:

Phan M. Viral Sensitizers Potentiate the Infection of Cancer Cells Via NF-kB . [Thesis]. University of Ottawa; 2020. Available from: http://hdl.handle.net/10393/40524

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

University of Ottawa

18. Lejmi Mrad, Rim. Genetic and Pharmacologic Inhibition of Cellular Inhibitor of Apoptosis 1 (cIAP1) Protein Expression Protects Against Denervation-Induced Skeletal Muscle Atrophy In Vivo .

Degree: 2016, University of Ottawa

URL: http://hdl.handle.net/10393/34260

► Skeletal muscle atrophy is a debilitating condition caused by pathological conditions including cancer cachexia, disuse and denervation. Disuse atrophy is characterized by reduction in fiber… (more)

Subjects/Keywords: Cellular inhibitor of apoptosis; skeletal muscle atrophy; NF-kB signaling pathway; TWEAK/Fn14 system

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

APA (6^th Edition):

Lejmi Mrad, R. (2016). Genetic and Pharmacologic Inhibition of Cellular Inhibitor of Apoptosis 1 (cIAP1) Protein Expression Protects Against Denervation-Induced Skeletal Muscle Atrophy In Vivo . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/34260

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):

Lejmi Mrad, Rim. “Genetic and Pharmacologic Inhibition of Cellular Inhibitor of Apoptosis 1 (cIAP1) Protein Expression Protects Against Denervation-Induced Skeletal Muscle Atrophy In Vivo .” 2016. Thesis, University of Ottawa. Accessed April 17, 2021. http://hdl.handle.net/10393/34260.

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

MLA Handbook (7^th Edition):

Lejmi Mrad, Rim. “Genetic and Pharmacologic Inhibition of Cellular Inhibitor of Apoptosis 1 (cIAP1) Protein Expression Protects Against Denervation-Induced Skeletal Muscle Atrophy In Vivo .” 2016. Web. 17 Apr 2021.

Vancouver:

Lejmi Mrad R. Genetic and Pharmacologic Inhibition of Cellular Inhibitor of Apoptosis 1 (cIAP1) Protein Expression Protects Against Denervation-Induced Skeletal Muscle Atrophy In Vivo . [Internet] [Thesis]. University of Ottawa; 2016. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10393/34260.

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

Council of Science Editors:

Lejmi Mrad R. Genetic and Pharmacologic Inhibition of Cellular Inhibitor of Apoptosis 1 (cIAP1) Protein Expression Protects Against Denervation-Induced Skeletal Muscle Atrophy In Vivo . [Thesis]. University of Ottawa; 2016. Available from: http://hdl.handle.net/10393/34260

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

19. 山下, 恭德. RANKL pretreatment plays an important role in the differentiation of pit-forming osteoclasts induced by TNF-α on murine bone marrow macrophages : RANKL 前刺激はマウス骨髄マクロファージにおいてTNF-α 刺激による吸収活性を持つ破骨細胞の分化に重要な役割を持つ.

Degree: 博士(歯学), 2015, Nagasaki University / 長崎大学

URL: http://hdl.handle.net/10069/36049

► Background Osteoclasts differentiated from bone marrow macrophages (BMMs) induced by TNF-α alone do not have resorbing activity. When BMMs are stimulated with receptor activator of… (more)

Subjects/Keywords: Receptor activator of NF-κB ligand; Tumour necrosis factor-alpha; Osteoclast; Resorbing activity

…x29;:11394–9. 21. Jules J, Shi Z, Liu J, Xu D, Wang S, Feng X. Receptor activator of NF… …activation-induced cytokine/receptor activator of NF-kappa B ligand. J Immunol 2006;177(7)… …osteoclasts formed by TNF-a with or without OPG, which is a decoy receptor of RANKL. This result… …resorption activity in the presence of interleukin (IL)-1.11,12 The signals from RANK… …x28;the receptor of RANKL) or IL-1 receptors were reported to activate the pathway of…

3 more images…

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APA (6^th Edition):

山下, �. (2015). RANKL pretreatment plays an important role in the differentiation of pit-forming osteoclasts induced by TNF-α on murine bone marrow macrophages : RANKL 前刺激はマウス骨髄マクロファージにおいてTNF-α 刺激による吸収活性を持つ破骨細胞の分化に重要な役割を持つ. (Thesis). Nagasaki University / 長崎大学. Retrieved from http://hdl.handle.net/10069/36049

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):

山下, 恭德. “RANKL pretreatment plays an important role in the differentiation of pit-forming osteoclasts induced by TNF-α on murine bone marrow macrophages : RANKL 前刺激はマウス骨髄マクロファージにおいてTNF-α 刺激による吸収活性を持つ破骨細胞の分化に重要な役割を持つ.” 2015. Thesis, Nagasaki University / 長崎大学. Accessed April 17, 2021. http://hdl.handle.net/10069/36049.

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

MLA Handbook (7^th Edition):

山下, 恭德. “RANKL pretreatment plays an important role in the differentiation of pit-forming osteoclasts induced by TNF-α on murine bone marrow macrophages : RANKL 前刺激はマウス骨髄マクロファージにおいてTNF-α 刺激による吸収活性を持つ破骨細胞の分化に重要な役割を持つ.” 2015. Web. 17 Apr 2021.

Vancouver:

山下 �. RANKL pretreatment plays an important role in the differentiation of pit-forming osteoclasts induced by TNF-α on murine bone marrow macrophages : RANKL 前刺激はマウス骨髄マクロファージにおいてTNF-α 刺激による吸収活性を持つ破骨細胞の分化に重要な役割を持つ. [Internet] [Thesis]. Nagasaki University / 長崎大学; 2015. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/10069/36049.

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

Council of Science Editors:

山下 �. RANKL pretreatment plays an important role in the differentiation of pit-forming osteoclasts induced by TNF-α on murine bone marrow macrophages : RANKL 前刺激はマウス骨髄マクロファージにおいてTNF-α 刺激による吸収活性を持つ破骨細胞の分化に重要な役割を持つ. [Thesis]. Nagasaki University / 長崎大学; 2015. Available from: http://hdl.handle.net/10069/36049

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

20. LINDA WANG. Development of a novel Toll-like receptor-based two-hybrid assay for detecting protein-protein interactions and its application in the study of CD14 dimerization and FcyRIIA activation.

Degree: 2008, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/13133

Subjects/Keywords: Toll-like receptor; dimerization; CD14; Fcgamma receptor IIA; NF-kB

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APA (6^th Edition):

WANG, L. (2008). Development of a novel Toll-like receptor-based two-hybrid assay for detecting protein-protein interactions and its application in the study of CD14 dimerization and FcyRIIA activation. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/13133

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):

WANG, LINDA. “Development of a novel Toll-like receptor-based two-hybrid assay for detecting protein-protein interactions and its application in the study of CD14 dimerization and FcyRIIA activation.” 2008. Thesis, National University of Singapore. Accessed April 17, 2021. http://scholarbank.nus.edu.sg/handle/10635/13133.

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

MLA Handbook (7^th Edition):

WANG, LINDA. “Development of a novel Toll-like receptor-based two-hybrid assay for detecting protein-protein interactions and its application in the study of CD14 dimerization and FcyRIIA activation.” 2008. Web. 17 Apr 2021.

Vancouver:

WANG L. Development of a novel Toll-like receptor-based two-hybrid assay for detecting protein-protein interactions and its application in the study of CD14 dimerization and FcyRIIA activation. [Internet] [Thesis]. National University of Singapore; 2008. [cited 2021 Apr 17]. Available from: http://scholarbank.nus.edu.sg/handle/10635/13133.

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

Council of Science Editors:

WANG L. Development of a novel Toll-like receptor-based two-hybrid assay for detecting protein-protein interactions and its application in the study of CD14 dimerization and FcyRIIA activation. [Thesis]. National University of Singapore; 2008. Available from: http://scholarbank.nus.edu.sg/handle/10635/13133

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

Texas A&M University

21. Tong, Yanzheng. Functional Characterization of NLRC5 and DDX46 in the Regulation of Innate Immune Responses.

Degree: PhD, Medical Sciences, 2014, Texas A&M University

URL: http://hdl.handle.net/1969.1/186991

► The NOD-like receptor protein NLRC5 inhibits TLR-induced NF-ҡB and viral infection-mediated type I interferon signaling in vitro. In the first project, we generated NLRC5 knockout… (more)

▼ The NOD-like receptor protein NLRC5 inhibits TLR-induced NF-ҡB and viral infection-mediated type I interferon signaling in vitro. In the first project, we generated NLRC5 knockout mice to characterize the regulatory function of NLRC5. NLRC5 deficiency enhances Toll-like receptor-induced NF-ҡB signaling and type I IFN-mediated antiviral immunity in mouse embryonic fibroblasts (MEFs). NLRC5 deficiency also increases proinflammatory cytokine response and antiviral immunity in mouse immune cells. In addition, we confirmed that NLRC5 regulates the transcription of MHC class I gene. Our findings indicate that NLRC5 is a regulator with multiple functions by negatively regulating proinflammatory responses and positively regulating MHC class I gene expression. The inflammasome is a large protein complex that leads to apoptosis and proinflammatory responses. One of the well-studied inflammasome transduces the activation signal through NLRP3. NLRP3 inflammasome is known to be activated through ASC oligomerization induced by varieties of stimulations; however, the mechanism remains unknown. Some of the DDX family proteins have been reported to sense DNA or RNA to activate type I IFN signaling pathway. By screening DDX family proteins in 293T cells reconstituted with the inflammasome system, we found that DDX46 enhanced NLRP3 inflammasome activity. Knockdown of DDX46 in THP-1 cells reduces inflammasome activity and IL-1β release after crystalline stimulations. DDX46 is cleaved by activated caspase-3 after silica stimulation in mouse macrophages. Furthermore, cleaved DDX46 interacts with the NLRP-ASC complex following silica stimulation. The positive regulatory role of cleaved DDX46 in silica-mediated NLRP3 inflammasome activation was confirmed in the 293T cell system by its strong ability to interact with ASC. Together, our findings indicate that cleaved DDX46 acts as a bridge to promote the interaction between NLRP3 and ASC after crystalline stimulation. Advisors/Committee Members: Hook, Magnus (advisor), Wang, Rongfu (advisor), Chang, Jiang (committee member), Zhang, Dekai (committee member).

Subjects/Keywords: innate immunity; NLRC5; inflammasome; NF-kB signaling

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

APA (6^th Edition):

Tong, Y. (2014). Functional Characterization of NLRC5 and DDX46 in the Regulation of Innate Immune Responses. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/186991

Chicago Manual of Style (16^th Edition):

Tong, Yanzheng. “Functional Characterization of NLRC5 and DDX46 in the Regulation of Innate Immune Responses.” 2014. Doctoral Dissertation, Texas A&M University. Accessed April 17, 2021. http://hdl.handle.net/1969.1/186991.

MLA Handbook (7^th Edition):

Tong, Yanzheng. “Functional Characterization of NLRC5 and DDX46 in the Regulation of Innate Immune Responses.” 2014. Web. 17 Apr 2021.

Vancouver:

Tong Y. Functional Characterization of NLRC5 and DDX46 in the Regulation of Innate Immune Responses. [Internet] [Doctoral dissertation]. Texas A&M University; 2014. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/1969.1/186991.

Council of Science Editors:

Tong Y. Functional Characterization of NLRC5 and DDX46 in the Regulation of Innate Immune Responses. [Doctoral Dissertation]. Texas A&M University; 2014. Available from: http://hdl.handle.net/1969.1/186991

University of Illinois – Urbana-Champaign

22. Lamb, Acacia. New insights into a complex host-pathogen interaction: mechanisms of Helicobacter pylori activation of NF-κB.

Degree: PhD, 0318, 2012, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/31951

► Helicobacter pylori infection is the main cause of chronic gastritis, gastric ulcers and gastric cancer. The gram-negative spirochete, which infects more than half of the… (more)

▼ Helicobacter pylori infection is the main cause of chronic gastritis, gastric ulcers and gastric cancer. The gram-negative spirochete, which infects more than half of the world’s population, is recognized by the International Agency for Research on Cancer as a group 1 carcinogen. The mechanism by which H. pylori induces carcinogenesis is believed to be its ability to cause chronic inflammation, creating an environment suitable to tumor initiation and progression. Many different strains of H. pylori exist, but those strains harboring the cag pathogenicity island (cagPAI) have been found to be more virulent, with more carcinomas associated with infection by these strains. Significantly, higher levels of H. pylori-initiated chronic gastritis is characterized by the cagPAI-dependent up-regulation of proinflammatory cytokines, which are largely mediated by the transcription factor nuclear factor (NF)-κB. The goal of this work is to better define the bacterial proteins and the cellular signaling molecules involved in H. pylori-induced NF-κB activation. The H. pylori virulence factor CagA, encoded by the cagPAI, is injected into host cells via a type 4 secretion system, where it interacts with a number of different signaling pathways leading to inflammation and cell scattering. While a number of these interactions have been defined, the role of CagA in NF-κB activation and in immune response remains unclear. In this work, CagA is shown to be crucial in the activation of NF-κB by H. pylori infection. Once inside the cell, CagA utilizes host proteins to induce NF-κB activity. CagA associates with transforming growth factor β-activated kinase 1 (TAK1), a MAP kinase involved in the NF-κB, AP-1 and JNK signaling pathways, and enhances the polyubiquitination and iii activation of the kinase. This lysine 63-linked ubiquitination is mediated by E3 ligase tumor necrosis factor receptor-associated factor 6 (TRAF6) and E2 Ubc13. These findings show that polyubiquitination of TAK1 regulates the activation of NF-κB, which in turn is used by H. pylori CagA for the H. pylori-induced inflammatory response. Advisors/Committee Members: Chen, Lin-Feng (advisor), Chen, Lin-Feng (Committee Chair), Shapiro, David J. (committee member), Fratti, Rutilio A. (committee member), Huang, Raven H. (committee member).

Subjects/Keywords: Helicobacter pylori; NF-kB; TAK1; ubiquitination

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APA (6^th Edition):

Lamb, A. (2012). New insights into a complex host-pathogen interaction: mechanisms of Helicobacter pylori activation of NF-κB. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/31951

Chicago Manual of Style (16^th Edition):

Lamb, Acacia. “New insights into a complex host-pathogen interaction: mechanisms of Helicobacter pylori activation of NF-κB.” 2012. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed April 17, 2021. http://hdl.handle.net/2142/31951.

MLA Handbook (7^th Edition):

Lamb, Acacia. “New insights into a complex host-pathogen interaction: mechanisms of Helicobacter pylori activation of NF-κB.” 2012. Web. 17 Apr 2021.

Vancouver:

Lamb A. New insights into a complex host-pathogen interaction: mechanisms of Helicobacter pylori activation of NF-κB. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2012. [cited 2021 Apr 17]. Available from: http://hdl.handle.net/2142/31951.

Council of Science Editors:

Lamb A. New insights into a complex host-pathogen interaction: mechanisms of Helicobacter pylori activation of NF-κB. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2012. Available from: http://hdl.handle.net/2142/31951

University of Southern California

23. Narula, Mansi. Effect of hepatitis C virus infection on signal transduction adaptor protein: TRAF6.

Degree: MS, Molecular Microbiology and Immunology, 2013, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/280450/rec/2179

► Hepatitis C virus (HCV) is a major cause of chronic liver disease and evasion of the host immune system by HCV plays a key role… (more)

Subjects/Keywords: HCV; TRAF6; polyubiquitination; apoptosis; autophagy; NF-kB

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APA (6^th Edition):

Narula, M. (2013). Effect of hepatitis C virus infection on signal transduction adaptor protein: TRAF6. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/280450/rec/2179

Chicago Manual of Style (16^th Edition):

Narula, Mansi. “Effect of hepatitis C virus infection on signal transduction adaptor protein: TRAF6.” 2013. Masters Thesis, University of Southern California. Accessed April 17, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/280450/rec/2179.

MLA Handbook (7^th Edition):

Narula, Mansi. “Effect of hepatitis C virus infection on signal transduction adaptor protein: TRAF6.” 2013. Web. 17 Apr 2021.

Vancouver:

Narula M. Effect of hepatitis C virus infection on signal transduction adaptor protein: TRAF6. [Internet] [Masters thesis]. University of Southern California; 2013. [cited 2021 Apr 17]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/280450/rec/2179.

Council of Science Editors:

Narula M. Effect of hepatitis C virus infection on signal transduction adaptor protein: TRAF6. [Masters Thesis]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/280450/rec/2179

Louisiana State University

24. Verhoeve, Victoria Irene. Identification and Characterization of a Relish-type NF-kB, DvRelish in Dermacentor variabilis, the American Dog Tick.

Degree: PhD, Veterinary Pathology and Pathobiology, 2016, Louisiana State University

URL: etd-04062016-103735 ; https://digitalcommons.lsu.edu/gradschool_dissertations/1179

► Ticks are important worldwide as vectors of bacteria, viruses, and parasites. Pathogenic and non-pathogenic Spotted fever group (SFG) Rickettsia are maintained and transmitted by ticks… (more)

▼ Ticks are important worldwide as vectors of bacteria, viruses, and parasites. Pathogenic and non-pathogenic Spotted fever group (SFG) Rickettsia are maintained and transmitted by ticks with specific hard tick-Rickettsia pairings evident in nature. The pathogenic SFG Rickettsia rickettsii is transmitted by the hard tick Dermacentor variabilis. In response to infection, D. variabilis is known differentially respond to SFG Rickettsia infection. The mechanisms of differential immune induction are currently unknown, and are likely involved in the establishment of specific tick-SFG Rickettsia pairings. It was hypothesized that the level of response by D. variabilis to SFG Rickettsia occurs in a species-specific manner, and that this response drives vector competence. To this end, we report the isolation of an mRNA transcript, dvrelish, using RACE-PCR. Conserved domain analysis of dvrelish identified a Rel-homolgy domain, allowing for its identification as encoding a putative Relish-type NF-κB protein. DvRelish was identified via Western blot, immunofluorescence assay and MALDI-TOF/TOF mass-spectrometry. Tick infection assays were performed using microinjection and capillary feeding technique methodologies to identify dvrelish expression in response to SFG Rickettsia infection. Microinjection of 107 R. rickettsii induced the increased expression of dvrelish in hemocytes at 1 hour post injection, and in combined tissues at 6 hours post injected. Injection with similar and lower doses of P. aeruginosa and Rickettsia parkeri did not significantly change dvrelish expression. When capillary fed R. rickettsii, dvrelish expression increased in hemocytes after 1 hour exposure and decreased after a 3 hour exposure. Together, the expression of dvrelish was dose and tissues specific in response to SFG Rickettsia challenge. Understanding the molecular regulation of immunological response to rickettsial infection in ticks may better define the mechanisms of vector competence and the epidemiology of SFG rickettsioses.

Subjects/Keywords: Rickettsia; immune response; NF-kB; tick

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APA (6^th Edition):

Verhoeve, V. I. (2016). Identification and Characterization of a Relish-type NF-kB, DvRelish in Dermacentor variabilis, the American Dog Tick. (Doctoral Dissertation). Louisiana State University. Retrieved from etd-04062016-103735 ; https://digitalcommons.lsu.edu/gradschool_dissertations/1179

Chicago Manual of Style (16^th Edition):

Verhoeve, Victoria Irene. “Identification and Characterization of a Relish-type NF-kB, DvRelish in Dermacentor variabilis, the American Dog Tick.” 2016. Doctoral Dissertation, Louisiana State University. Accessed April 17, 2021. etd-04062016-103735 ; https://digitalcommons.lsu.edu/gradschool_dissertations/1179.

MLA Handbook (7^th Edition):

Verhoeve, Victoria Irene. “Identification and Characterization of a Relish-type NF-kB, DvRelish in Dermacentor variabilis, the American Dog Tick.” 2016. Web. 17 Apr 2021.

Vancouver:

Verhoeve VI. Identification and Characterization of a Relish-type NF-kB, DvRelish in Dermacentor variabilis, the American Dog Tick. [Internet] [Doctoral dissertation]. Louisiana State University; 2016. [cited 2021 Apr 17]. Available from: etd-04062016-103735 ; https://digitalcommons.lsu.edu/gradschool_dissertations/1179.

Council of Science Editors:

Verhoeve VI. Identification and Characterization of a Relish-type NF-kB, DvRelish in Dermacentor variabilis, the American Dog Tick. [Doctoral Dissertation]. Louisiana State University; 2016. Available from: etd-04062016-103735 ; https://digitalcommons.lsu.edu/gradschool_dissertations/1179

University of Texas Medical Branch – Galveston

25. [No author]. ATM REGULATES THE NF-kB PATHWAY VIA RELA SER 276 PHOSPHORYLATION .

Degree: University of Texas Medical Branch – Galveston

URL: http://hdl.handle.net/2152.3/11201

► Ataxia-Telangiectasia Mutated (ATM), a member of the phosphatidylinositol 3 kinase-like kinase family, is a master regulator of the double strand DNA break-repair pathway after genotoxic… (more)

▼ Ataxia-Telangiectasia Mutated (ATM), a member of the phosphatidylinositol 3 kinase-like kinase family, is a master regulator of the double strand DNA break-repair pathway after genotoxic stress. Here we found ATM serves as an essential regulator of TNF-and RSV- induced NF-kB pathway. We observed that TNF exposure of cells rapidly induced DNA double strand breaks and activates ATM. TNF-induced ROS promote nuclear IKKr-ubiquitin association and complex formation with ATM for nuclear export. Activated cytoplasmic ATM is involved in the selective recruitment of the E3-ubiquitin ligase b-TrCP to phospho-IkBa proteosomal degradation. Importantly, ATM binds and activates the catalytic subunit of protein kinase A (PKAc), a ribosmal S6 kinase that controls RelA Ser 276 phosphorylation. In ATM knockdown cells, TNF-induced RelA Ser 276 phosphorylation is significantly decreased. We further observed decreased binding and recruitment of the transcriptional elongation complex containing cyclin dependent kinase-9 (CDK9; a kinase necessary for triggering transcriptional elongation) to promoters of NF-kB-dependent immediate early cytokine genes, in ATM knockdown cells. We conclude that ATM is a nuclear damage-response signal modulator of TNF-induced NF-kB activation that plays a key scaffolding role in IkBa degradation and RelA Ser 276 phosphorylation. In the antiviral response pathway, we observed RSV infection activates ATM and ATM is also required for RSV induced RelA Ser 276 phosphorylation. We further demonstrated that IRF7 gene expression is pRelA Ser 276 dependent and IRF7 is a essential regulator of RIG-I gene expression. Depletion of ATM results in an increased RSV proliferation and reduced IFN and ISG gene expression, indicating the significance of resynthesized RIG-I regulated by IRF7. These results demonstrate a RSV- phospho-Ser 276 RelA-IRF7-RIG-I pathway mediated by ATM. Taken together, our study provides a mechanistic explanation of decreased innate immune response associated with A-T mutation. Advisors/Committee Members: Choudhary, Sanjeev (advisor), Brasier , Allan (committeeMember), Boldogh, Istvan (committeeMember), Hazra, Tapas (committeeMember), Wu, Zhaohui (committeeMember).

Subjects/Keywords: NF-kB ATM

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

APA (6^th Edition):

author], [. (n.d.). ATM REGULATES THE NF-kB PATHWAY VIA RELA SER 276 PHOSPHORYLATION . (Thesis). University of Texas Medical Branch – Galveston. Retrieved from http://hdl.handle.net/2152.3/11201

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

author], [No. “ATM REGULATES THE NF-kB PATHWAY VIA RELA SER 276 PHOSPHORYLATION .” Thesis, University of Texas Medical Branch – Galveston. Accessed April 17, 2021. http://hdl.handle.net/2152.3/11201.

Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

author], [No. “ATM REGULATES THE NF-kB PATHWAY VIA RELA SER 276 PHOSPHORYLATION .” Web. 17 Apr 2021.

Note: this citation may be lacking information needed for this citation format:
No year of publication.

Vancouver:

author] [. ATM REGULATES THE NF-kB PATHWAY VIA RELA SER 276 PHOSPHORYLATION . [Internet] [Thesis]. University of Texas Medical Branch – Galveston; [cited 2021 Apr 17]. Available from: http://hdl.handle.net/2152.3/11201.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Council of Science Editors:

author] [. ATM REGULATES THE NF-kB PATHWAY VIA RELA SER 276 PHOSPHORYLATION . [Thesis]. University of Texas Medical Branch – Galveston; Available from: http://hdl.handle.net/2152.3/11201

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

University of Canterbury

26. Tino, Alexandria. An investigation into the anti-tumour properties and underlying mechanisms of natural polyphenols against ovarian cancer.

Degree: MS, Cellular and Molecular Biology, 2014, University of Canterbury

URL: http://dx.doi.org/10.26021/7096

► Ovarian cancer is the deadliest gynaecologic cancer in New Zealand. Its high mortality rate is due to the fact that it is usually diagnosed at… (more)

▼ Ovarian cancer is the deadliest gynaecologic cancer in New Zealand. Its high mortality rate is due to the fact that it is usually diagnosed at an advanced stage. Advanced ovarian cancer is less responsive to current cytotoxic treatment. Thus, there is an urgent need for novel anti-cancer drugs that can improve patient longevity and quality of life. One of the clinical features of advanced ovarian cancer is the growth of secondary tumours due to the highly metastatic nature of the disease. Cancer cells disseminate from the ovary, some form cell clusters that travel through the abdominal cavity by physiological movement of body fluid and then deposit on the abdominal wall and internal organs to generate secondary tumours. The exact mechanisms of how these cells metastasize are unclear, but prognosis typically worsens if levels of vascular endothelial growth factor (VEGF) are elevated. This study investigated the anti-tumour activities of naturally occurring food compounds resveratrol, acetyl resveratrol and (-)-Epicatechin-3-gallate (EGCG), in cell spheroids/clusters of ovarian cancer. It also examined the protein expression of various proteins involved in the NF-κB signalling pathway. This pathway has been suggested to mediate the secretion of VEGF and is a possible target for the naturally occurring compounds. Results show that resveratrol and acetyl resveratrol reduce cell growth and cellular metabolism in a dose-, time- and cell line- dependent fashion. In addition, the reduction of VEGF is also dose-, time- and cell line- dependent. Paradoxically, another angiogenic protein interleukin-8 (IL-8) secretion is increased. Resveratrol and acetyl resveratrol attenuate the expression of NF-κB but this effect is cell line specific. EGCG has limited effect on cell growth, cellular metabolism and the secretion of VEGF and IL-8. These findings suggest that resveratrol and its derivative may have the ability to supress the angiogenic activity of ovarian cancer cells and warrant further in vivo study.

Subjects/Keywords: ovarian cancer; resveratrol; EGCG; NF-kB

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APA (6^th Edition):

Tino, A. (2014). An investigation into the anti-tumour properties and underlying mechanisms of natural polyphenols against ovarian cancer. (Masters Thesis). University of Canterbury. Retrieved from http://dx.doi.org/10.26021/7096

Chicago Manual of Style (16^th Edition):

Tino, Alexandria. “An investigation into the anti-tumour properties and underlying mechanisms of natural polyphenols against ovarian cancer.” 2014. Masters Thesis, University of Canterbury. Accessed April 17, 2021. http://dx.doi.org/10.26021/7096.

MLA Handbook (7^th Edition):

Tino, Alexandria. “An investigation into the anti-tumour properties and underlying mechanisms of natural polyphenols against ovarian cancer.” 2014. Web. 17 Apr 2021.

Vancouver:

Tino A. An investigation into the anti-tumour properties and underlying mechanisms of natural polyphenols against ovarian cancer. [Internet] [Masters thesis]. University of Canterbury; 2014. [cited 2021 Apr 17]. Available from: http://dx.doi.org/10.26021/7096.

Council of Science Editors:

Tino A. An investigation into the anti-tumour properties and underlying mechanisms of natural polyphenols against ovarian cancer. [Masters Thesis]. University of Canterbury; 2014. Available from: http://dx.doi.org/10.26021/7096

Université Paris-Sud – Paris XI

27. Poalas, Konstantinos. Ubiquitinylation and deubiquitinylation in the regulation of the transcription factor NF-kB activation : Ubiquitinylation et déubiquitinylation dans la régulation de l’activation du facteur de transcription NF-kB.

Degree: Docteur es, Biochimie, Biologie Cellulaire et Moléculaire, 2013, Université Paris-Sud – Paris XI

URL: http://www.theses.fr/2013PA11T058

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L’activation de la signalisation NF-κB par de nombreux immunorécepteurs met en jeu un large signalosome. Afin de propager cette signalisation en réponse à différents stimuli,… (more)

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L’activation de la signalisation NF-κB par de nombreux immunorécepteurs met en jeu un large signalosome. Afin de propager cette signalisation en réponse à différents stimuli, l’oligomérisation d’adaptateurs pourvus de domaines d’interaction protéine-protéine est nécessaire. Alors que certains adapteurs sont communs d’autres sont spécifiques à un immunorécepteur donné. Une des principales caractéristiques partagées par toutes ses protéines est leur capacité à être poly-ubiquitinylé de façon non-dégradative afin d’aboutir à une activation optimale de NF-κB. Ce projet avait pour objectif d’identifier de nouvelles déubiquitinylases impliquées dans la signalisation NF-κB. C’est ainsi que nous avons identifié USP34 comme étant un régulateur négatif de la signalisation NF-κB induite par le TCR dans des cellules Jurkats, une lignée de lymphocytes T immortalisés. Nos données suggèrent un modèle dans lequel USP34 permet d’éviter l’activation excessive de NF-κB, en agissant directement ou indirectement sur les dimères NF-κB/IκBα, en aval d’IKK, et en modulant l’affinité du facteur de transcription pour l’ADN. Parallèlement, l’étude du microenvironnement des membranes endocellulaires responsables du recrutement des signalosomes formés en réponse à l’activation du TCR, du TNFR et du CD40 a permis l’identification d’une protéine - clé de la signalisation NF-κB, la MTDH. Cette protéine du RE s’est révélée être un relais déterminant pour l’activation d’IKK et donc la propagation du signal NF-κB.

Large signalosome assembly is a prerequisite for NF-κB signaling upon engagement of various immunoreceptors. Adaptor proteins containing protein-protein interaction domains oligomerise in response to such stimuli in order to propagate signaling. Each immunoreceptor uses distinct adaptors, as well as common ones, to achieve that. The main characteristic shared by these proteins is their ability to undergo poly-ubiquitinylation in a non-degradative manner, leading to optimal NF-κB activation. In this work, we aimed to identify novel deubiquitinylating enzymes that control ubiquitinylation status. That is how USP34 came up to be a negative regulator of NF-κB signaling in TCR-activated Jurkat cells, a T lymphocyte cell line. Our data suggest a model whereby USP34 prevents excessive NF-κB activation by acting rather late, directly or indirectly on the NF-κB:IκBα dimers, downstream of IKK, altering transcription factor DNA binding affinity. In parallel, studies of the endocellular membrane microenvironment that hosts mature signalosomes in response to TCR-, TNFR- and CD40 ligation led to the identification of an ER-residing protein, Metadherin (MTDH), which seems to globally integrate signaling before forwarding it to downstream pathway components able to activate IKK.

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

Subjects/Keywords: NF-kB; TCR; Ubiquitinylation; Déubiquitinylation; USP34; MTDH; NF-kB; TCR; Ubiquitinylation; Deubiquitinylation; USP34; MTDH

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

Poalas, K. (2013). Ubiquitinylation and deubiquitinylation in the regulation of the transcription factor NF-kB activation : Ubiquitinylation et déubiquitinylation dans la régulation de l’activation du facteur de transcription NF-kB. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2013PA11T058

Chicago Manual of Style (16^th Edition):

Poalas, Konstantinos. “Ubiquitinylation and deubiquitinylation in the regulation of the transcription factor NF-kB activation : Ubiquitinylation et déubiquitinylation dans la régulation de l’activation du facteur de transcription NF-kB.” 2013. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed April 17, 2021. http://www.theses.fr/2013PA11T058.

MLA Handbook (7^th Edition):

Poalas, Konstantinos. “Ubiquitinylation and deubiquitinylation in the regulation of the transcription factor NF-kB activation : Ubiquitinylation et déubiquitinylation dans la régulation de l’activation du facteur de transcription NF-kB.” 2013. Web. 17 Apr 2021.

Vancouver:

Poalas K. Ubiquitinylation and deubiquitinylation in the regulation of the transcription factor NF-kB activation : Ubiquitinylation et déubiquitinylation dans la régulation de l’activation du facteur de transcription NF-kB. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2013. [cited 2021 Apr 17]. Available from: http://www.theses.fr/2013PA11T058.

Council of Science Editors:

Poalas K. Ubiquitinylation and deubiquitinylation in the regulation of the transcription factor NF-kB activation : Ubiquitinylation et déubiquitinylation dans la régulation de l’activation du facteur de transcription NF-kB. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2013. Available from: http://www.theses.fr/2013PA11T058

28. Senegas, Anna. Caractérisation des défauts cérébraux chez le modèle murin d'Incontinentia Pigmenti, maladie génétique liée à la voie NF-kB : Brain defects characterization of the mouse model of Incontinentia Pigmenti, a NF-kB-related genetic disease.

Degree: Docteur es, Neurosciences - Neurobiologie, 2016, Université Grenoble Alpes (ComUE)

URL: http://www.theses.fr/2016GREAV075

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Incontinentia pigmenti (IP, OMIM 308300) est une maladie génétique liée au chromosome X qui est létale chez les garçons. Chez les filles, une dermatose débute… (more)

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Incontinentia pigmenti (IP, OMIM 308300) est une maladie génétique liée au chromosome X qui est létale chez les garçons. Chez les filles, une dermatose débute peu après la naissance et évolue selon une séquence complexe d’événements associant de l’inflammation, de l’hyperprolifération cellulaire et de l’apoptose. En dehors de ce problème cutané, les patientes IP peuvent aussi souffrir d’anomalies oculaires, dentaires et cérébrales. Les défauts cérébraux affectent environ 30% des patientes et se caractérisent par de l’épilepsie et des troubles cognitifs et/ou moteurs. Le gène causant IP code pour la protéine NEMO, un composant essentiel de la voie de signalisation NF-kB, qui régule les processus immunitaires, inflammatoires, ainsi que la prolifération et la mort cellulaire. Chez approximativement 70% des patientes IP, le même réarrangement chromosomique élimine presque intégralement le gène NEMO, générant une perte d’activation de la voie NF-kB. L’invalidation du gène Nemo chez la souris (femelles Nemo +/-) fournit un modèle pour l’étude de la dermatose associée à IP en récapitulant les événements cutanés observés chez les patientes.Dans le but de mieux définir les anomalies cérébrales des patientes IP ainsi que leur origine qui reste obscure, nous avons analysé le cerveau des souris Nemo +/-. Nous montrons ici, en utilisant un protocole d’IRM adapté à des cerveaux de sept jours (P7), que des anomalies sont détectées dans une fraction des échantillons. Ces anomalies sont hétérogènes et localisées de manière aspécifique, comme chez l’Homme. Elles incluent des zones hémorragiques diffuses, des cavités et de l’atrophie du corps calleux. Cela démontre l’utilité du système murin Nemo +/- pour étudier également les défauts cérébraux des patientes IP. De manière intéressante, ces lésions cérébrales peuvent être détectées avant la naissance, au jour 18 du développement, et ne sont pas causées par un dysfonctionnement neuronal, astrocytaire ou des oligodendrocytes. Utilisant une approche immunitaire couplée à une analyse in toto de cerveaux P7 après mise en transparence (Technique 3DISCO), nous avons détecté des anomalies vasculaires qui suggèrent que ce compartiment serait à l’origine des défauts cérébraux des patientes IP.

Incontinentia pigmenti (IP, OMIM # 308300) is an X-linked genetic disease which is lethal in boys. In girls, it causes a skin disease that begins soon after birth and evolves along a complex sequence of events involving inflammation, cell hyperproliferation and apoptosis. IP patients can also suffer from ocular, dental and brain anomalies. Brain defects affect about 30% of patients and are characterized by epilepsy and/or cognitive/motor disorders. The IP-causing gene encodes the protein NEMO, an essential component of the signaling pathway NF-kB that regulates immunity, inflammation, proliferation and cell death process. In approximately 70% of IP patients, the same chromosomal rearrangement eliminates almost completely the NEMO gene, generating a loss of activation of the NF-kB pathway. Invalidation…

Advisors/Committee Members: Courtois, Gilles (thesis director).

Subjects/Keywords: Incontinentia pigmenti; Nemo; NF-KB; Neurobiologie; Incontinentia pigmenti; Nemo; NF-KB; Neurobiology

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

APA (6^th Edition):

Senegas, A. (2016). Caractérisation des défauts cérébraux chez le modèle murin d'Incontinentia Pigmenti, maladie génétique liée à la voie NF-kB : Brain defects characterization of the mouse model of Incontinentia Pigmenti, a NF-kB-related genetic disease. (Doctoral Dissertation). Université Grenoble Alpes (ComUE). Retrieved from http://www.theses.fr/2016GREAV075

Chicago Manual of Style (16^th Edition):

Senegas, Anna. “Caractérisation des défauts cérébraux chez le modèle murin d'Incontinentia Pigmenti, maladie génétique liée à la voie NF-kB : Brain defects characterization of the mouse model of Incontinentia Pigmenti, a NF-kB-related genetic disease.” 2016. Doctoral Dissertation, Université Grenoble Alpes (ComUE). Accessed April 17, 2021. http://www.theses.fr/2016GREAV075.

MLA Handbook (7^th Edition):

Senegas, Anna. “Caractérisation des défauts cérébraux chez le modèle murin d'Incontinentia Pigmenti, maladie génétique liée à la voie NF-kB : Brain defects characterization of the mouse model of Incontinentia Pigmenti, a NF-kB-related genetic disease.” 2016. Web. 17 Apr 2021.

Vancouver:

Senegas A. Caractérisation des défauts cérébraux chez le modèle murin d'Incontinentia Pigmenti, maladie génétique liée à la voie NF-kB : Brain defects characterization of the mouse model of Incontinentia Pigmenti, a NF-kB-related genetic disease. [Internet] [Doctoral dissertation]. Université Grenoble Alpes (ComUE); 2016. [cited 2021 Apr 17]. Available from: http://www.theses.fr/2016GREAV075.

Council of Science Editors:

Senegas A. Caractérisation des défauts cérébraux chez le modèle murin d'Incontinentia Pigmenti, maladie génétique liée à la voie NF-kB : Brain defects characterization of the mouse model of Incontinentia Pigmenti, a NF-kB-related genetic disease. [Doctoral Dissertation]. Université Grenoble Alpes (ComUE); 2016. Available from: http://www.theses.fr/2016GREAV075

29. Ronin, Émilie. Etude du rôle de NF-kB dans les lymphocytes T régulateurs chez la souris : Investigation of the role of NF-kB in mouse regulatory T cells.

Degree: Docteur es, Immunologie, 2017, Université Pierre et Marie Curie – Paris VI

URL: http://www.theses.fr/2017PA066222

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Les lymphocytes T CD4+FoxP3+ régulateurs (Tregs) jouent un rôle majeur dans l'homéostasie du système immunitaire et la prévention des maladies auto-immunes en régulant les réponses… (more)

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Les lymphocytes T CD4+FoxP3+ régulateurs (Tregs) jouent un rôle majeur dans l'homéostasie du système immunitaire et la prévention des maladies auto-immunes en régulant les réponses immunitaires. Aussi bien chez la souris que chez l'homme, il est établi que des mutations de Foxp3 entraînent une déficience en Tregs qui induit un syndrome auto-immun conduisant à la mort. Bien que Foxp3 soit essentiel à la différenciation, la fonction et la stabilité des Tregs, ce n'est pas le seul facteur de transcription impliqué dans ces processus. De plus en plus d'études suggèrent notamment un rôle important de NF- B dans le développement et la fonction des Tregs mais celui-ci reste mal défini. Nous avons donc généré des souris ayant une délétion spécifique des sous-unités RelA ou RelB de NF- KB dans les Tregs. L'invalidation de RelA dans les Tregs conduit au développement d'un syndrome auto-immun sévère qui s'explique par un défaut fonctionnel et de stabilité des Tregs. L'invalidation de RelB dans les Tregs semble, quant à elle, augmenter leur fonction suppressive. Nous montrons ainsi un rôle majeur de NF- KB dans la fonction des Tregs ouvrant la voie à de nouveaux traitements qui stimuleraient ou inhiberaient les Tregs en modulant l'activation de NF- KB.

CD4+ Foxp3+ regulatory T cells (Tregs) play a critical role in immune homeostasis and in the prevention of autoimmune diseases by regulating immune responses. In humans and mice, it is well established that Foxp3 deficiency conducts to the development of an autoimmune syndrome leading to early death. Although Foxp3 plays a critical role in differentiation, suppressive function and stability of Tregs, other transcription factors are also involved in different aspects of their biology. Even though increasing evidence shows an important role of NF-KB transcription factors in Treg cells development and function, their role is still poorly defined. To address this question we have generated conditional knock-out mice for RelA or RelB subunits of NF-KB only in Tregs. We show that the deficiency of RelA in Tregs leads to the development of a spontaneous severe autoimmune syndrome that could be explained by a defect in Tregs activation and stability. However, the deficiency of RelB seems to increase their suppressive function. Altogether, our data show a major role of NF-KB in Treg biology. This work could lead to new treatments that would stimulate or inhibit Tregs through the modulation of NF-KB activation.

Advisors/Committee Members: Salomon, Benoît (thesis director).

Subjects/Keywords: Tregs; NF- KB; TNF; Auto-immunité; Cancer; Souris; Tregs; NF-KB; Autoimmunity; 616.994

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

APA (6^th Edition):

Ronin, E. (2017). Etude du rôle de NF-kB dans les lymphocytes T régulateurs chez la souris : Investigation of the role of NF-kB in mouse regulatory T cells. (Doctoral Dissertation). Université Pierre et Marie Curie – Paris VI. Retrieved from http://www.theses.fr/2017PA066222

Chicago Manual of Style (16^th Edition):

Ronin, Émilie. “Etude du rôle de NF-kB dans les lymphocytes T régulateurs chez la souris : Investigation of the role of NF-kB in mouse regulatory T cells.” 2017. Doctoral Dissertation, Université Pierre et Marie Curie – Paris VI. Accessed April 17, 2021. http://www.theses.fr/2017PA066222.

MLA Handbook (7^th Edition):

Ronin, Émilie. “Etude du rôle de NF-kB dans les lymphocytes T régulateurs chez la souris : Investigation of the role of NF-kB in mouse regulatory T cells.” 2017. Web. 17 Apr 2021.

Vancouver:

Ronin E. Etude du rôle de NF-kB dans les lymphocytes T régulateurs chez la souris : Investigation of the role of NF-kB in mouse regulatory T cells. [Internet] [Doctoral dissertation]. Université Pierre et Marie Curie – Paris VI; 2017. [cited 2021 Apr 17]. Available from: http://www.theses.fr/2017PA066222.

Council of Science Editors:

Ronin E. Etude du rôle de NF-kB dans les lymphocytes T régulateurs chez la souris : Investigation of the role of NF-kB in mouse regulatory T cells. [Doctoral Dissertation]. Université Pierre et Marie Curie – Paris VI; 2017. Available from: http://www.theses.fr/2017PA066222

30. Mhaidly, Rana. Effet de la surexpression de la glycéraldéhyde 3-phosphate déshydrogénase (GAPDH) sur le développement et la fonction des lymphocytes T : Impact of GAPH overexpression on T cell development and function.

Degree: Docteur es, Sciences de la vie et de la santé, 2019, Université Côte d'Azur (ComUE)

URL: http://www.theses.fr/2019AZUR6021

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L’activation des lymphocytes T (LT) et l’acquisition des fonctions effectrices sont des phénomènes récemment décrits pour être régulés par le métabolisme cellulaire, introduisant ainsi la… (more)

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L’activation des lymphocytes T (LT) et l’acquisition des fonctions effectrices sont des phénomènes récemment décrits pour être régulés par le métabolisme cellulaire, introduisant ainsi la notion d’« immunométabolisme » dans de nombreuses études biologiques.Dix enzymes métaboliques participent à la conversion du glucose en énergie cellulaire (glycolyse). Parmi celles-ci, des études récentes ont fait émerger la glycéraldéhyde 3-phosphate déshydrogénase (GAPDH) comme un acteur principal de la survie et de la différenciation des LT. Dans ce rôle, la balance entre ses fonctions glycolytiques (associées à la catalyse du glycéraldéhyde-3-phosphate en le 1,3-bisphosphoglycérate) et non-glycolytiques (stabilité des ARNm des cytokines et activation des voies de signalisation) est un phénomène majeur contrôlant la sélection et l’activation des LT.Afin d’étudier les fonctions glycolytiques et non-glycolytiques de la GAPDH dans le développement lymphocytaire, nous avons généré un modèle de souris transgéniques surexprimant la GAPDH exclusivement dans les LT (plck-GAPDH). Une première caractérisation de ces souris montre que la surexpression de la GAPDH n’a pas d’effet sur les stades précoces de développement des LT. De façon intéressante, nous avons observé dans les souris âgées (>18 mois) des changements phénotypiques évidents, notamment : une splénomégalie, des ganglions lymphatiques hypertrophiés et une infiltration lymphocytaire majeure au niveau du foie et de la moelle osseuse. Un immunophénotypage détaillé de ces tissus a montré une augmentation de la proportion des LT folliculaires helpers (Tfh) CD4+ Bcl-6+CXCR5+ PD-1high. De plus, ces cellules, fortement prolifératives et clonales, interagissent avec les lymphocytes B CD95+ GL7+ du centre germinatif, eux-mêmes associés à des cellules dendritiques folliculaires, formant ainsi un microenvironnement tumoral dans notre modèle plck-GAPDH. À la recherche d'un équivalent humain à notre modèle, nous avons découvert que les caractéristiques pathologiques, l’immunophénotypage et le profil génétique des souris plck-GAPDH correspondaient étroitement au lymphome T angio-immunoblastique humain (AITL). Il s’agit d’une hémopathie maligne rare pour laquelle aucune stratégie thérapeutique n’a été clairement décrite. Nous avons également mis en évidence dans les souris plck-GAPDH une activation de la voie NF-kB non canonique, également activée chez les patients AITL. Le ciblage de cette voie par un nouvel inhibiteur associé à une immunothérapie anti-PD1 a augmenté la survie des souris. Ce traitement permet une induction efficace de la réponse immunitaire anticancéreuse et représente une nouvelle perspective thérapeutique pour les patients atteints d’AITL.En conclusion, ce nouveau modèle de souris AITL capable de mimer étroitement les caractéristiques du lymphome humain, permettra d’élucider l'origine possible de la maladie, d’identifier d’autres voies de signalisation impliquées et de tester de nouvelles lignes thérapeutiques.

Fundamental metabolic changes are implemented by cancer cells…

Advisors/Committee Members: Verhoeyen, Els (thesis director).

Subjects/Keywords: GAPDH; AITL; Lymphocytes T; NF-kB; GAPDH; AITL; T cell Lymphocyte; NF-kB pathway

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

Mhaidly, R. (2019). Effet de la surexpression de la glycéraldéhyde 3-phosphate déshydrogénase (GAPDH) sur le développement et la fonction des lymphocytes T : Impact of GAPH overexpression on T cell development and function. (Doctoral Dissertation). Université Côte d'Azur (ComUE). Retrieved from http://www.theses.fr/2019AZUR6021

Chicago Manual of Style (16^th Edition):

Mhaidly, Rana. “Effet de la surexpression de la glycéraldéhyde 3-phosphate déshydrogénase (GAPDH) sur le développement et la fonction des lymphocytes T : Impact of GAPH overexpression on T cell development and function.” 2019. Doctoral Dissertation, Université Côte d'Azur (ComUE). Accessed April 17, 2021. http://www.theses.fr/2019AZUR6021.

MLA Handbook (7^th Edition):

Mhaidly, Rana. “Effet de la surexpression de la glycéraldéhyde 3-phosphate déshydrogénase (GAPDH) sur le développement et la fonction des lymphocytes T : Impact of GAPH overexpression on T cell development and function.” 2019. Web. 17 Apr 2021.

Vancouver:

Mhaidly R. Effet de la surexpression de la glycéraldéhyde 3-phosphate déshydrogénase (GAPDH) sur le développement et la fonction des lymphocytes T : Impact of GAPH overexpression on T cell development and function. [Internet] [Doctoral dissertation]. Université Côte d'Azur (ComUE); 2019. [cited 2021 Apr 17]. Available from: http://www.theses.fr/2019AZUR6021.

Council of Science Editors:

Mhaidly R. Effet de la surexpression de la glycéraldéhyde 3-phosphate déshydrogénase (GAPDH) sur le développement et la fonction des lymphocytes T : Impact of GAPH overexpression on T cell development and function. [Doctoral Dissertation]. Université Côte d'Azur (ComUE); 2019. Available from: http://www.theses.fr/2019AZUR6021

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Open Access Theses and Dissertations