subject:(swi snf)

1. 仲里, 秀次. Early-Stage Induction of SWI/SNF Mutations during Esophageal Squamous Cell Carcinogenesis : SIW/SNF遺伝子異常の食道扁平上皮がん発がんの早期における誘発.

Degree: 博士(医学), 2017, University of the Ryukyus / 琉球大学

URL: http://hdl.handle.net/20.500.12000/36588

► The SWI/SNF chromatin remodeling complex is frequently inactivated by somaticmutations of its various components in various types of cancers, and also by aberrant DNA methylation.… (more)

Subjects/Keywords: Epigenetics; SWI/SNF; mutation; ESCC

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

APA (6^th Edition):

仲里, �. (2017). Early-Stage Induction of SWI/SNF Mutations during Esophageal Squamous Cell Carcinogenesis : SIW/SNF遺伝子異常の食道扁平上皮がん発がんの早期における誘発. (Thesis). University of the Ryukyus / 琉球大学. Retrieved from http://hdl.handle.net/20.500.12000/36588

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):

仲里, 秀次. “Early-Stage Induction of SWI/SNF Mutations during Esophageal Squamous Cell Carcinogenesis : SIW/SNF遺伝子異常の食道扁平上皮がん発がんの早期における誘発.” 2017. Thesis, University of the Ryukyus / 琉球大学. Accessed January 17, 2021. http://hdl.handle.net/20.500.12000/36588.

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

MLA Handbook (7^th Edition):

仲里, 秀次. “Early-Stage Induction of SWI/SNF Mutations during Esophageal Squamous Cell Carcinogenesis : SIW/SNF遺伝子異常の食道扁平上皮がん発がんの早期における誘発.” 2017. Web. 17 Jan 2021.

Vancouver:

仲里 �. Early-Stage Induction of SWI/SNF Mutations during Esophageal Squamous Cell Carcinogenesis : SIW/SNF遺伝子異常の食道扁平上皮がん発がんの早期における誘発. [Internet] [Thesis]. University of the Ryukyus / 琉球大学; 2017. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/20.500.12000/36588.

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

Council of Science Editors:

仲里 �. Early-Stage Induction of SWI/SNF Mutations during Esophageal Squamous Cell Carcinogenesis : SIW/SNF遺伝子異常の食道扁平上皮がん発がんの早期における誘発. [Thesis]. University of the Ryukyus / 琉球大学; 2017. Available from: http://hdl.handle.net/20.500.12000/36588

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

2. AL-HUSSAIN, MOHAMED MUBARAK. Investigating chromatin remodelling by the Swi-Snf and Tup1-Cyc8 complexes.

Degree: School of Genetics & Microbiology. Discipline of Microbiology, 2020, Trinity College Dublin

URL: http://hdl.handle.net/2262/91851

► Swi-Snf is an ATP-dependent chromatin remodelling complex which generally acts as a co-activator of gene transcription via its removal of promoter nucleosomes. Conversely, Tup1-Cyc8 (Ssn6)… (more)

Subjects/Keywords: Chromatin; Swi-Snf; Tup1-Cyc8

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APA (6^th Edition):

AL-HUSSAIN, M. M. (2020). Investigating chromatin remodelling by the Swi-Snf and Tup1-Cyc8 complexes. (Thesis). Trinity College Dublin. Retrieved from http://hdl.handle.net/2262/91851

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):

AL-HUSSAIN, MOHAMED MUBARAK. “Investigating chromatin remodelling by the Swi-Snf and Tup1-Cyc8 complexes.” 2020. Thesis, Trinity College Dublin. Accessed January 17, 2021. http://hdl.handle.net/2262/91851.

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

MLA Handbook (7^th Edition):

AL-HUSSAIN, MOHAMED MUBARAK. “Investigating chromatin remodelling by the Swi-Snf and Tup1-Cyc8 complexes.” 2020. Web. 17 Jan 2021.

Vancouver:

AL-HUSSAIN MM. Investigating chromatin remodelling by the Swi-Snf and Tup1-Cyc8 complexes. [Internet] [Thesis]. Trinity College Dublin; 2020. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/2262/91851.

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

Council of Science Editors:

AL-HUSSAIN MM. Investigating chromatin remodelling by the Swi-Snf and Tup1-Cyc8 complexes. [Thesis]. Trinity College Dublin; 2020. Available from: http://hdl.handle.net/2262/91851

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

3. Masliah-Planchon, Julien. Complexe SWI/SNF et cancer _ Altérations génétiques et anomalies métaboliques : SWI/SNF Complexe in Oncogenesis _ Genetic Alterations and Metbolic Anomalies.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2018, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2018SACLS112

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Il y a presque 20 ans, la mise en évidence de mutations bi-alléliques inactivatrices du gène SMARCB1 dans les tumeurs rhabdoïdes établissait la première démonstration… (more)

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Il y a presque 20 ans, la mise en évidence de mutations bi-alléliques inactivatrices du gène SMARCB1 dans les tumeurs rhabdoïdes établissait la première démonstration d’altérations du complexe SWI/SNF de remodelage de la chromatine en oncologie. Depuis, l’avènement des techniques d’analyse moléculaire à haut débit appliquées à la cancérologie a permis de montrer que des altérations dans d’autres gènes du complexe SWI/SNF était présentes dans un très grand nombre de cancers. A travers la présentation de plusieurs types de tumeurs SWI/SNF déficientes et de nos modèles d’étude des tumeurs rhabdoïdes, nous montrons que la perte de SMARCB1 est associée à une augmentation de la biosynthèse de la sérine et des voies métaboliques en aval importantes pour l’oncogenèse. Ces résultats pourraient aboutir à une option thérapeutique pour les tumeurs rhabdoïdes voire, plus généralement, pour d’autres modèles de tumeurs SWI/SNF-déficientes. Enfin, la mise en perspective de ces changements métaboliques avec les altérations épigénétiques observées dans les tumeurs SWI/SNF déficientes pourrait se révéler pertinente pour continuer d’approfondir nos connaissances sur ces tumeurs.

Nearly 20 years ago, the demonstration of truncated bi-allelic mutations in the SMARCB1 gene in rhabdoid tumors established the first demonstration of alterations in the SWI/SNF chromatin remodeling complex in oncology. Since then, the advent of high-throughput molecular analysis techniques applied to oncology has shown that alterations in other genes of the SWI/SNF complex are present in a wide variety of cancers. Through the presentation of several types of SWI/SNF deficient tumors and our models of rhabdoid tumors, we show that the loss of SMARCB1 is associated with an increase of the serine biosynthesis pathway and the downstream metabolic pathways important for oncogenesis.These results could lead to a therapeutic option for rhabdoid tumors or, more generally, for other models of SWI/SNF-deficient tumors. Finally, the prospect of these metabolic changes with the epigenetic alterations observed in SWI / SNF deficient tumors may be relevant to continue to deepen our knowledge of these tumors.

Advisors/Committee Members: Delattre, Olivier (thesis director).

Subjects/Keywords: Complexe SWI/SNF; Cancer; Métabolisme; SWI/SNF complex; Cancer; Metabolism

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

APA (6^th Edition):

Masliah-Planchon, J. (2018). Complexe SWI/SNF et cancer _ Altérations génétiques et anomalies métaboliques : SWI/SNF Complexe in Oncogenesis _ Genetic Alterations and Metbolic Anomalies. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2018SACLS112

Chicago Manual of Style (16^th Edition):

Masliah-Planchon, Julien. “Complexe SWI/SNF et cancer _ Altérations génétiques et anomalies métaboliques : SWI/SNF Complexe in Oncogenesis _ Genetic Alterations and Metbolic Anomalies.” 2018. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed January 17, 2021. http://www.theses.fr/2018SACLS112.

MLA Handbook (7^th Edition):

Masliah-Planchon, Julien. “Complexe SWI/SNF et cancer _ Altérations génétiques et anomalies métaboliques : SWI/SNF Complexe in Oncogenesis _ Genetic Alterations and Metbolic Anomalies.” 2018. Web. 17 Jan 2021.

Vancouver:

Masliah-Planchon J. Complexe SWI/SNF et cancer _ Altérations génétiques et anomalies métaboliques : SWI/SNF Complexe in Oncogenesis _ Genetic Alterations and Metbolic Anomalies. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2018. [cited 2021 Jan 17]. Available from: http://www.theses.fr/2018SACLS112.

Council of Science Editors:

Masliah-Planchon J. Complexe SWI/SNF et cancer _ Altérations génétiques et anomalies métaboliques : SWI/SNF Complexe in Oncogenesis _ Genetic Alterations and Metbolic Anomalies. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2018. Available from: http://www.theses.fr/2018SACLS112

Vanderbilt University

4. McKenna, Brian Douglas. Investigations into islet pdx1 activity: contribution to mature β-cell identity and the identification and characterization of Pdx1 coregulators.

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

URL: http://hdl.handle.net/1803/12411

► Pdx1 is a transcription factor of fundamental importance to pancreas formation and adult islet β-cell function. However, little is known regarding its role in mature… (more)

Subjects/Keywords: swi/snf; diabetes; islet; Pdx1; coregulators

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APA (6^th Edition):

McKenna, B. D. (2015). Investigations into islet pdx1 activity: contribution to mature β-cell identity and the identification and characterization of Pdx1 coregulators. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/12411

Chicago Manual of Style (16^th Edition):

McKenna, Brian Douglas. “Investigations into islet pdx1 activity: contribution to mature β-cell identity and the identification and characterization of Pdx1 coregulators.” 2015. Doctoral Dissertation, Vanderbilt University. Accessed January 17, 2021. http://hdl.handle.net/1803/12411.

MLA Handbook (7^th Edition):

McKenna, Brian Douglas. “Investigations into islet pdx1 activity: contribution to mature β-cell identity and the identification and characterization of Pdx1 coregulators.” 2015. Web. 17 Jan 2021.

Vancouver:

McKenna BD. Investigations into islet pdx1 activity: contribution to mature β-cell identity and the identification and characterization of Pdx1 coregulators. [Internet] [Doctoral dissertation]. Vanderbilt University; 2015. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/1803/12411.

Council of Science Editors:

McKenna BD. Investigations into islet pdx1 activity: contribution to mature β-cell identity and the identification and characterization of Pdx1 coregulators. [Doctoral Dissertation]. Vanderbilt University; 2015. Available from: http://hdl.handle.net/1803/12411

University of Sydney

5. Farrell, Andrew William. The Role of Brm in Non-‐Melanoma Skin Cancer Progression .

Degree: 2016, University of Sydney

URL: http://hdl.handle.net/2123/16438

► Background: Australia has the highest incidence of non-melanoma skin cancer (NMSC) in the world. These cancers are predominantly caused by exposure to ultraviolet radiation (UVR)… (more)

▼ Background: Australia has the highest incidence of non-melanoma skin cancer (NMSC) in the world. These cancers are predominantly caused by exposure to ultraviolet radiation (UVR) in sunlight. Brm is an ATPase subunit that drives chromatin remodelling via the SWI/SNF complex. Thus, Brm is able to regulate access to transcription factors and repair enzymes to DNA, in addition to cell division. The loss of Brm has been observed in several cancer types, where its loss correlates with decreased patient survival. The loss of Brm has been identified in NMSC, but not pre-malignant lesions, suggesting Brm plays a role in the progression of a benign skin lesion into a malignant skin cancer. Brm-deficient mice also harbour excessive levels of epidermal hyperplasia as well as heightened tumour incidence following UVR as compared to mice with wildtype Brm. Moreover, a novel hotspot mutation of Brm (Q203K) has also been discovered in 17% of NMSC studied, which was the first mutation of Brm discovered in any type of cancer. Aims: This thesis aims to study the function of the Q203K mutation as compared to the loss of Brm in several key aspects of keratinocyte responses to UV-induced DNA damage: proliferation, cell cycle regulation, UVR-induced cell death and DNA repair. Methods: The loss of Brm was studied with keratinocytes grown ex vivo from neonatal Brm-/- mice and compared to keratinocytes grown from Brm+/+ mice. Further, a human keratinocyte cell line, HaCaT was also studied, in combination with Brm miRNAs to knockdown Brm expression in these cells. The overexpression of either wildtype or Q203K Brm was also studied in HaCaTs. These cells were treated with UV, and their responses were observed using assays for cell growth, cell death, cell cycle regulation and DNA repair. Results: In neonatal mouse keratinocytes, as well as HaCaT cells, the loss of Brm expression led to an altered cellular response to UVR. Cells lacking Brm exhibited increased proliferative potential following UVR due to a reduced time spent in G1 cell cycle arrest. Further, Brm-deficient cells displayed increased formation of UVR-induced cyclobutane pyrimidine dimers (CPDs) in the dark. Interestingly, when Brm was knocked down in the immortalised human keratinocyte cell line HaCaT, these cells were not as sensitive to the loss of Brm in combination with UVR, and showed less prominent effects on both cell cycle regulation and CPD formation. It was hypothesised that primary neonatal keratinocytes were more sensitive to UVR due to these cells being naïve, whereas HaCaT cells already exhibit several UVR-induced mutations, such as that of p53. Therefore, the loss of Brm in mouse neonatal keratinocytes was more catastrophic to the cell. Lastly, the mutation of Q203K did not lead to increased cellular sensitivity to UVR, suggesting the presence of this mutation in NMSC was most likely non-functional. However, increasing levels of Brm in HaCaT cells did lead to enhanced levels of cell viability at high density, which the Q203K mutation was able to reverse, suggesting…

Subjects/Keywords: Skin cancer; chromation remodelling; Brm; SWI/SNF

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

APA (6^th Edition):

Farrell, A. W. (2016). The Role of Brm in Non-‐Melanoma Skin Cancer Progression . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/16438

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):

Farrell, Andrew William. “The Role of Brm in Non-‐Melanoma Skin Cancer Progression .” 2016. Thesis, University of Sydney. Accessed January 17, 2021. http://hdl.handle.net/2123/16438.

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

MLA Handbook (7^th Edition):

Farrell, Andrew William. “The Role of Brm in Non-‐Melanoma Skin Cancer Progression .” 2016. Web. 17 Jan 2021.

Vancouver:

Farrell AW. The Role of Brm in Non-‐Melanoma Skin Cancer Progression . [Internet] [Thesis]. University of Sydney; 2016. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/2123/16438.

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

Council of Science Editors:

Farrell AW. The Role of Brm in Non-‐Melanoma Skin Cancer Progression . [Thesis]. University of Sydney; 2016. Available from: http://hdl.handle.net/2123/16438

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

6. Κοταντάκη, Πανωραία. Δημιουργία ζώων μοντέλων για τη διερεύνηση του in vivo ρόλου της geminin : αδρανοποίηση του γονιδίου σε μύες με τη χρήση ολοδύναμων εμβρυονικών κυττάρων (knockout) και ιστοειδική υπερέκφραση σε διαγονιδιακούς μύες.

Degree: 2010, University of Patras

URL: http://nemertes.lis.upatras.gr/jspui/handle/10889/4356

► Η ανάπτυξη του ανοσοποιητικού συστήματος ξεκινά από πολυδύναμα αρχέγονα αιμοποιητικά κύτταρα, τα οποία διαδοχικά δίνουν γένεση σε ενδιάμεσους πληθυσμούς προγονικών κυττάρων οι οποίοι σταδιακά χάνουν… (more)

▼ Η ανάπτυξη του ανοσοποιητικού συστήματος ξεκινά από πολυδύναμα αρχέγονα αιμοποιητικά κύτταρα, τα οποία διαδοχικά δίνουν γένεση σε ενδιάμεσους πληθυσμούς προγονικών κυττάρων οι οποίοι σταδιακά χάνουν την ικανότητά τους για αυτοανανέωση και τελικά δίνουν γένεση στα πλήρως διαφοροποιημένα κύτταρα της μυελικής και λεμφικής σειράς. Η συγκεκριμένη διαδικασία στηρίζεται στο λεπτό συντονισμό της αυτοανανέωσης, αλλά και της διαφοροποίησης, απαιτεί δε την έκφραση διαφορετικών γονιδίων που σχετίζονται με τη ρύθμιση του κυτταρικού κύκλου, τη μεταγραφική ρύθμιση γονιδίων, αλλά και συμπλόκων αναδιοργάνωσης της δομής της χρωματίνης που εμπλέκονται στη διαφοροποίηση. Η geminin έχει προταθεί ότι ρυθμίζει την απόφαση ενός κυττάρου για πολλαπλασιασμό ή διαφοροποίηση. Αλληλεπιδρά με μεταγραφικούς παράγοντες, με σύμπλοκα αναδιάταξης της δομής της χρωματίνης, ρυθμίζοντας την έκφραση γονιδίων που ελέγχουν τη νευρωνική διαφοροποίηση. Παράλληλα, δρα σαν αναστολέας του κυτταρικού κύκλου, προσδενόμενη στο παράγοντα αδειοδότησης της αντιγραφής του DNA, CDT1. Στόχος μας ήταν να διερευνήσουμε τον in vivo ρόλο της Geminin στη διαφοροποίηση και τον πολλαπλασιασμό, στο ανοσοποιητικό σύστημα. Στα πλαίσια της διδακτορικής διατριβής, βασιζόμενοι στο σύστημα Cre-loxP, δημιουργήσαμε μύες που επιτρέπουν την υπό συνθήκη εξάλειψη (knockout) του γονιδίου της geminin, πλαισιώνοντας τα εξώνια 3 και 4 του γονιδίου της με θέσεις loxP. Η στόχευση του γονιδίου και η παρεμβολή των 3 loxP θέσεων πραγματοποιήθηκε σε pc3 εμβρυικά πολυδύναμα κύτταρα μυός, χρησιμοποιώντας κατάλληλο πλασμιδιακό knockout φορέα, που έφερε τη κασέτα επιλογής TKneo. Μετά από ένεση των ορθά ανασυνδυασμένων pc3 κλώνων σε βλαστοκύστεις, τη δημιουργία χιμαιρικών μυών που εκφράζουν την Cre ρεκομπινάση στη γαμετική σειρά, και την επακόλουθη διασταύρωσή τους με μύες αγρίου τύπου, δημιουργήθηκαν ετερόζυγοι μύες για το πλαισιωμένο με loxP θέσεις αλληλόμορφο της Geminin, που παράλληλα έφερε και τη κασέτα επιλογής TKneo («floxed-ΤΚneo»), το πλαισιωμένο με loxP θέσεις αλληλόμορφο της Geminin, που στερούνταν της κασέτας επιλογής TKneo (floxed), καθώς επίσης και το αλληλόμορφο που στερούνταν των εξωνίων 3 και 4 και είναι το πλήρες knockout (ΔGEM ΚΟ -null) αλληλόμορφο). Από διασταυρώσεις ετερόζυγων για το ΔGEM ΚΟ αλληλόμορφο της geminin, δεν προέκυψαν ομόζυγοι μύες για το ΔGEM ΚO αλληλόμορφο (-/-), τόσο μεταγεννητικά όσο και in utero. Η μειωμένη αντιπροσώπευση των ΔGEM+/- μυών σε συνδυασμό με την αύξηση των Thy1-/B220- κυττάρων σε σπλήνα και λεμφαδένες ενήλικων μυών, η σημαντική αύξηση των Thy1+ και ειδικότερα των CD8+ Τ κυττάρων, καθώς επίσης και η αισθητή μείωση των CD4+ Τ κυττάρων του σπλήνα σε ζώα ηλικίας 5 μηνών, προτείνει ένα είδος απλοανεπάρκειας των ετερόζυγων για Geminin μυών. Σε παραπλήσια αποτελέσματα οδηγηθήκαμε και μετά από την ανάλυση των GT KO για το γονίδιο της Geminin (GT) μυών με τη μεθοδολογία της παγίδευσης γονιδίων. Τα ετερόζυγα GT ζώα διασταυρώθηκαν με ετερόζυγα ζώα για το πλήρες ΚΟ του BRG1 (BRG) και με ετερόζυγα ζώα που υπερεκφράζουν μια επικρατούσα… Advisors/Committee Members: Ταραβήρας, Σταύρος, Kotantaki, Panoraia, Ταραβήρας, Σταύρος, Φλωρδέλλης, Χριστόδουλος, Βαράκης, Ιωάννης, Αθανασιάδου, Αγλαϊα, Κωστόπουλος, Γεώργιος, Πέτρου, Ελένη, Λυγερού, Ζωή.

Subjects/Keywords: Μύες; Αδρανοποίηση; Υπερέκφραση; Ανοσοποιητικό σύστημα; SWI/SNF σύμπλοκο; 616.079; Geminin; Cre-loxP; Knockout; Mice; Inactivation; Overexpression; Immune system; SWI/SNF complex

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

APA (6^th Edition):

Κοταντάκη, �. (2010). Δημιουργία ζώων μοντέλων για τη διερεύνηση του in vivo ρόλου της geminin : αδρανοποίηση του γονιδίου σε μύες με τη χρήση ολοδύναμων εμβρυονικών κυττάρων (knockout) και ιστοειδική υπερέκφραση σε διαγονιδιακούς μύες. (Doctoral Dissertation). University of Patras. Retrieved from http://nemertes.lis.upatras.gr/jspui/handle/10889/4356

Chicago Manual of Style (16^th Edition):

Κοταντάκη, Πανωραία. “Δημιουργία ζώων μοντέλων για τη διερεύνηση του in vivo ρόλου της geminin : αδρανοποίηση του γονιδίου σε μύες με τη χρήση ολοδύναμων εμβρυονικών κυττάρων (knockout) και ιστοειδική υπερέκφραση σε διαγονιδιακούς μύες.” 2010. Doctoral Dissertation, University of Patras. Accessed January 17, 2021. http://nemertes.lis.upatras.gr/jspui/handle/10889/4356.

MLA Handbook (7^th Edition):

Κοταντάκη, Πανωραία. “Δημιουργία ζώων μοντέλων για τη διερεύνηση του in vivo ρόλου της geminin : αδρανοποίηση του γονιδίου σε μύες με τη χρήση ολοδύναμων εμβρυονικών κυττάρων (knockout) και ιστοειδική υπερέκφραση σε διαγονιδιακούς μύες.” 2010. Web. 17 Jan 2021.

Vancouver:

Κοταντάκη �. Δημιουργία ζώων μοντέλων για τη διερεύνηση του in vivo ρόλου της geminin : αδρανοποίηση του γονιδίου σε μύες με τη χρήση ολοδύναμων εμβρυονικών κυττάρων (knockout) και ιστοειδική υπερέκφραση σε διαγονιδιακούς μύες. [Internet] [Doctoral dissertation]. University of Patras; 2010. [cited 2021 Jan 17]. Available from: http://nemertes.lis.upatras.gr/jspui/handle/10889/4356.

Council of Science Editors:

Κοταντάκη �. Δημιουργία ζώων μοντέλων για τη διερεύνηση του in vivo ρόλου της geminin : αδρανοποίηση του γονιδίου σε μύες με τη χρήση ολοδύναμων εμβρυονικών κυττάρων (knockout) και ιστοειδική υπερέκφραση σε διαγονιδιακούς μύες. [Doctoral Dissertation]. University of Patras; 2010. Available from: http://nemertes.lis.upatras.gr/jspui/handle/10889/4356

7. Ertl, Iris Elisabeth. Functional interplay of two SWI/SNF chromatin-remodeling accessory subunits during C. elegans development.

Degree: Departament de Ciències Experimentals i de la Salut, 2015, Universitat Pompeu Fabra

URL: http://hdl.handle.net/10803/286067

► SWI/SNF complexes are ATP-dependent chromatin remodelers highly conserved through evolution. By altering the chromatin state, these complexes can regulate the accessibility of a given genomic… (more)

Subjects/Keywords: Chromatin remodeler; SWI/SNF complexes; C. elegans; ham-3; swsn-2.2; Remodeladors de cromatina; Complexos SWI/SNF; 575

10 more images…

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APA (6^th Edition):

Ertl, I. E. (2015). Functional interplay of two SWI/SNF chromatin-remodeling accessory subunits during C. elegans development. (Thesis). Universitat Pompeu Fabra. Retrieved from http://hdl.handle.net/10803/286067

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):

Ertl, Iris Elisabeth. “Functional interplay of two SWI/SNF chromatin-remodeling accessory subunits during C. elegans development.” 2015. Thesis, Universitat Pompeu Fabra. Accessed January 17, 2021. http://hdl.handle.net/10803/286067.

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

MLA Handbook (7^th Edition):

Ertl, Iris Elisabeth. “Functional interplay of two SWI/SNF chromatin-remodeling accessory subunits during C. elegans development.” 2015. Web. 17 Jan 2021.

Vancouver:

Ertl IE. Functional interplay of two SWI/SNF chromatin-remodeling accessory subunits during C. elegans development. [Internet] [Thesis]. Universitat Pompeu Fabra; 2015. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/10803/286067.

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

Council of Science Editors:

Ertl IE. Functional interplay of two SWI/SNF chromatin-remodeling accessory subunits during C. elegans development. [Thesis]. Universitat Pompeu Fabra; 2015. Available from: http://hdl.handle.net/10803/286067

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

University of Alberta

8. Minard, Laura. Chromatin regulation by histone chaperone Asf1.

Degree: PhD, Department of Biochemistry, 2010, University of Alberta

URL: https://era.library.ualberta.ca/files/44558d82z

► Asf1 is a conserved H3/H4 histone chaperone with multiple functions in chromatin modulation. Using budding yeast as a model, we identify new pathways of Asf1… (more)

▼ Asf1 is a conserved H3/H4 histone chaperone with multiple functions in chromatin modulation. Using budding yeast as a model, we identify new pathways of Asf1 function, and expand current knowledge regarding the known roles of Asf1. First, we uncover novel genetic interactions between ASF1 and genes encoding other chromatin regulators. We describe an interaction between ASF1 and SET2, which encodes a histone lysine methyltransferase, and show that Asf1 exists in a pathway to promote Set2-catalyzed H3K36 trimethylation. Second, we present evidence that Asf1 promotes transcriptional derepression of two DNA damage response (DDR) genes (RNR3 and HUG1), which is a hallmark event in the cellular response to replication stress or DNA damage. While Asf1 association with chromatin increases globally during replication stress, we find that direct binding of Asf1 to DDR gene promoters is not needed for their transcriptional derepression. Rather, the contribution of Asf1 is dependent on its ability to stimulate acetylation of H3K56 by the Rtt109 lysine acetyltransferase. This modification occurs in the globular domain of H3, is present on all newly synthesized histones and is lost after H3 incorporation into chromatin. Importantly, DDR gene promoters are occupied by H3K56-acetylated nucleosomes under repressing conditions, and the steady state level of H3K56 promoter acetylation does not change upon derepression. We propose that replication-coupled deposition of K56-acetylated H3 poises newly synthesized DDR genes for derepression. In this model, the known association of transcriptional repressors with DDR gene promoters would ensure that transcription remains minimal under normal conditions. Thirdly, we identify new functions for known Asf1 motifs and characterize key determinants for the constitutive and inducible association of Asf1 with chromatin. Finally, we identify new genetic, physical, and functional links between ASF1 and SNF2, the catalytic subunit of the SWI/SNF chromatin remodeller. Altogether, the research described in this report is consistent with the idea that Asf1 promotes genome stability through its ability to function in diverse pathways of chromatin regulation.

Subjects/Keywords: Asf1; SWI/SNF; histone chaperone; hydroxyurea; chromatin; DNA damage response

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

APA (6^th Edition):

Minard, L. (2010). Chromatin regulation by histone chaperone Asf1. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/44558d82z

Chicago Manual of Style (16^th Edition):

Minard, Laura. “Chromatin regulation by histone chaperone Asf1.” 2010. Doctoral Dissertation, University of Alberta. Accessed January 17, 2021. https://era.library.ualberta.ca/files/44558d82z.

MLA Handbook (7^th Edition):

Minard, Laura. “Chromatin regulation by histone chaperone Asf1.” 2010. Web. 17 Jan 2021.

Vancouver:

Minard L. Chromatin regulation by histone chaperone Asf1. [Internet] [Doctoral dissertation]. University of Alberta; 2010. [cited 2021 Jan 17]. Available from: https://era.library.ualberta.ca/files/44558d82z.

Council of Science Editors:

Minard L. Chromatin regulation by histone chaperone Asf1. [Doctoral Dissertation]. University of Alberta; 2010. Available from: https://era.library.ualberta.ca/files/44558d82z

Boston University

9. Buckshaw II, Robert S. Cloning and nextPBM analysis of the mediator and BRG1 associated factor complexes.

Degree: MS, Medical Sciences, 2020, Boston University

URL: http://hdl.handle.net/2144/41179

► Coordination of gene expression within the cell requires the integrated actions of various multi-protein, gene regulatory complexes. The Mediator and BRG1 Associate Factor (BAF) complexes… (more)

Subjects/Keywords: Systematic biology; BAF; Epigenetic regulation; Immunology; Mediator; PBM; SWI/SNF

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

APA (6^th Edition):

Buckshaw II, R. S. (2020). Cloning and nextPBM analysis of the mediator and BRG1 associated factor complexes. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/41179

Chicago Manual of Style (16^th Edition):

Buckshaw II, Robert S. “Cloning and nextPBM analysis of the mediator and BRG1 associated factor complexes.” 2020. Masters Thesis, Boston University. Accessed January 17, 2021. http://hdl.handle.net/2144/41179.

MLA Handbook (7^th Edition):

Buckshaw II, Robert S. “Cloning and nextPBM analysis of the mediator and BRG1 associated factor complexes.” 2020. Web. 17 Jan 2021.

Vancouver:

Buckshaw II RS. Cloning and nextPBM analysis of the mediator and BRG1 associated factor complexes. [Internet] [Masters thesis]. Boston University; 2020. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/2144/41179.

Council of Science Editors:

Buckshaw II RS. Cloning and nextPBM analysis of the mediator and BRG1 associated factor complexes. [Masters Thesis]. Boston University; 2020. Available from: http://hdl.handle.net/2144/41179

University of Vermont

10. Taber, Thomas Howland. Thyroid Hormone Receptor SS (trß) Regulation Of Runt-Related Transcription Factor 2 (runx2) In Thyroid Tumorigenesis: Determination Of The Trß Nuclear Protein Complexes That Associate With The Runx2 Gene.

Degree: MS, Pharmacology, 2017, University of Vermont

URL: https://scholarworks.uvm.edu/graddis/820

► Thyroid Tumorigenesis is typically a well understood process, with well delineated oncogenic factors. Follicular and papillary thyroid cancers are typically survivable, with 5-year survival… (more)

▼ Thyroid Tumorigenesis is typically a well understood process, with well delineated oncogenic factors. Follicular and papillary thyroid cancers are typically survivable, with 5-year survival rates being >95% for Stage I-III of both cancer types. Anaplastic thyroid cancer, in contrast, lacks this prognosis, and is the most lethal of all endocrine-related cancers. The median survival time after a diagnosis is generally between 6-8 months, with a 5-year survival rate of <10%. Current treatment for anaplastic thyroid cancers routinely meet roadblocks, as resistance is quickly developed. Even non-discriminatory kinase inactivators, such as sorafenib, which are generally considered a drug of last resort, are unable to effect survival rates. As such, there is a clear need for further investigation of the causes of anaplastic thyroid cancer mechanisms. Previous work in the Carr lab revealed a novel regulatory pathway of an oncogene that is associated with several other endocrine-related cancers, as well as other non-endocrine-related cancers. Specifically, the Runt-related transcription factor 2 (Runx2) was found to be suppressed via direct binding of the thyroid hormone receptor beta 1 isoform (TRß1) to its proximal promotor. Runx2 was previously shown to be associated with increasing malignancy, with Runx2 occurring at low-levels in indolent cell lines, whilst occurring at high-levels in more malignant cell lines. TRß1, conversely, exhibited the opposite relationship. Endogenous levels of TRß1 were found to be high in indolent cell lines and were depleted in malignant cell lines. These findings were further confirmed via tissue microarrays. Restoration of TRß1 in malignant cell lines diminished Runx2 mRNA and protein levels, which was corroborated by evidence from electrophoretic mobility-shift assays, and chromatin immunoprecipitations that TRß1 was able to directly bind Runx2 promotor 1. Current studies have investigated the nuclear protein profile that associates with TRß1 to alter Runx2 transcription. Through EMSA-to-Mass Spectrometry methodologies, as well as novel DNA pulldown techniques, binding partners have been elucidated. Findings have also been confirmed via classical immunoprecipitations. Specifically, our findings show that TRß1 complexes with the brahma-related gene 1 (BRG1) protein, the nuclear co-repressor (NCOR), and BRG1-associated protein 60 (BAF60). BRG1 functions by preferentially recruiting histone deacetylases (HDAC), with BRG1 and the HDAC’s acting to alter chromatin, and thus transcription. Future studies aim at examining whether other proteins complex with TRß1 to alter Runx2 transcription, and whether these complexes are altered in aggressive cell lines. Advisors/Committee Members: Frances E. Carr, Jeanne Harris.

Subjects/Keywords: Cancer; RUNX2; SWI/SNF; THRB; Thyroid; Thyroid Cancer; Cell Biology; Oncology

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

APA (6^th Edition):

Taber, T. H. (2017). Thyroid Hormone Receptor SS (trß) Regulation Of Runt-Related Transcription Factor 2 (runx2) In Thyroid Tumorigenesis: Determination Of The Trß Nuclear Protein Complexes That Associate With The Runx2 Gene. (Thesis). University of Vermont. Retrieved from https://scholarworks.uvm.edu/graddis/820

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):

Taber, Thomas Howland. “Thyroid Hormone Receptor SS (trß) Regulation Of Runt-Related Transcription Factor 2 (runx2) In Thyroid Tumorigenesis: Determination Of The Trß Nuclear Protein Complexes That Associate With The Runx2 Gene.” 2017. Thesis, University of Vermont. Accessed January 17, 2021. https://scholarworks.uvm.edu/graddis/820.

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

MLA Handbook (7^th Edition):

Taber, Thomas Howland. “Thyroid Hormone Receptor SS (trß) Regulation Of Runt-Related Transcription Factor 2 (runx2) In Thyroid Tumorigenesis: Determination Of The Trß Nuclear Protein Complexes That Associate With The Runx2 Gene.” 2017. Web. 17 Jan 2021.

Vancouver:

Taber TH. Thyroid Hormone Receptor SS (trß) Regulation Of Runt-Related Transcription Factor 2 (runx2) In Thyroid Tumorigenesis: Determination Of The Trß Nuclear Protein Complexes That Associate With The Runx2 Gene. [Internet] [Thesis]. University of Vermont; 2017. [cited 2021 Jan 17]. Available from: https://scholarworks.uvm.edu/graddis/820.

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

Council of Science Editors:

Taber TH. Thyroid Hormone Receptor SS (trß) Regulation Of Runt-Related Transcription Factor 2 (runx2) In Thyroid Tumorigenesis: Determination Of The Trß Nuclear Protein Complexes That Associate With The Runx2 Gene. [Thesis]. University of Vermont; 2017. Available from: https://scholarworks.uvm.edu/graddis/820

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

University of Ottawa

11. Nguyen, Thinh. CDX2 Regulates Gene Expression Through Recruitment of BRG1-Associated SWI/SNF Chromatin Remodeling Activity .

Degree: 2016, University of Ottawa

URL: http://hdl.handle.net/10393/35377

► The packaging of genomic DNA into nucleosomes creates a barrier to transcription which can be relieved through ATP-dependent chromatin remodeling via complexes such as the… (more)

Subjects/Keywords: Cdx2; transcription; Brg1; SWI/SNF; Chromatin Remodeling; development

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

APA (6^th Edition):

Nguyen, T. (2016). CDX2 Regulates Gene Expression Through Recruitment of BRG1-Associated SWI/SNF Chromatin Remodeling Activity . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/35377

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):

Nguyen, Thinh. “CDX2 Regulates Gene Expression Through Recruitment of BRG1-Associated SWI/SNF Chromatin Remodeling Activity .” 2016. Thesis, University of Ottawa. Accessed January 17, 2021. http://hdl.handle.net/10393/35377.

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

MLA Handbook (7^th Edition):

Nguyen, Thinh. “CDX2 Regulates Gene Expression Through Recruitment of BRG1-Associated SWI/SNF Chromatin Remodeling Activity .” 2016. Web. 17 Jan 2021.

Vancouver:

Nguyen T. CDX2 Regulates Gene Expression Through Recruitment of BRG1-Associated SWI/SNF Chromatin Remodeling Activity . [Internet] [Thesis]. University of Ottawa; 2016. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/10393/35377.

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

Council of Science Editors:

Nguyen T. CDX2 Regulates Gene Expression Through Recruitment of BRG1-Associated SWI/SNF Chromatin Remodeling Activity . [Thesis]. University of Ottawa; 2016. Available from: http://hdl.handle.net/10393/35377

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

University of Toronto

12. Tu, William Bo Chen. Chromatin Regulators of MYC Oncoprotein Activity in Cancer.

Degree: PhD, 2017, University of Toronto

URL: http://hdl.handle.net/1807/88986

►

The MYC oncoprotein is a key contributor to the development of virtually all cancer types. MYC is known as a global regulator of transcription that… (more)

▼

The MYC oncoprotein is a key contributor to the development of virtually all cancer types. MYC is known as a global regulator of transcription that controls diverse physiological and oncogenic functions. Though there are 35 yearsâ worth of research on this protein, mechanistic understanding and therapeutic targeting of MYC are still needed. We hypothesize that chromatin interactors are critical for MYC to achieve transcriptional control and biological outcomes. Our proteomic study of the MYC interactome yielded chromatin complexes and epigenetic regulators. In this thesis, we investigated two MYC-interacting complexes and defined the chromatin landscape of the MYC interactome. We characterized the novel interaction of MYC and the G9a histone methyltransferase and demonstrated their coordinated regulation of genome-wide transcriptional repression. This interaction and their resulting gene expression output support breast cancer growth, which is impaired with G9a inhibition. This study underscores the crucial role of epigenetics and epigenetic regulators in modulating MYC activity; this serves as the basis for a compelling strategy to target oncogenic MYC. We also interrogated the interaction of MYC and the SWI/SNF chromatin remodeling complex, whose many components are inactivated in a multitude of cancer types. We specifically showed the direct interaction of MYC and the INI1 subunit and their antagonistic relationship in regulating transcription and biological functions. Combining our proteomic approach with genome-wide resources, we established the chromatin landscape of the MYC interactome, defining chromatin profiles and target gene networks of known and novel MYC interactors. Collectively, these studies brought new insights to the understanding of MYC through the identification of novel chromatin interactors of MYC, their coordinated roles in regulating transcriptional activation and repression, their contributions to MYC-driven oncogenesis, and their therapeutic potential.

2018-06-19 00:00:00

Advisors/Committee Members: Penn, Linda Z, Medical Biophysics.

Subjects/Keywords: Cancer; Epigenetics; G9a; MYC; SWI/SNF; Transcription; 0307

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

APA (6^th Edition):

Tu, W. B. C. (2017). Chromatin Regulators of MYC Oncoprotein Activity in Cancer. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/88986

Chicago Manual of Style (16^th Edition):

Tu, William Bo Chen. “Chromatin Regulators of MYC Oncoprotein Activity in Cancer.” 2017. Doctoral Dissertation, University of Toronto. Accessed January 17, 2021. http://hdl.handle.net/1807/88986.

MLA Handbook (7^th Edition):

Tu, William Bo Chen. “Chromatin Regulators of MYC Oncoprotein Activity in Cancer.” 2017. Web. 17 Jan 2021.

Vancouver:

Tu WBC. Chromatin Regulators of MYC Oncoprotein Activity in Cancer. [Internet] [Doctoral dissertation]. University of Toronto; 2017. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/1807/88986.

Council of Science Editors:

Tu WBC. Chromatin Regulators of MYC Oncoprotein Activity in Cancer. [Doctoral Dissertation]. University of Toronto; 2017. Available from: http://hdl.handle.net/1807/88986

Université Paris-Sud – Paris XI

13. Jégu, Teddy. Rôle du facteur de remodelage de la chromatine BAF60 au cours de la progression du cycle cellulaire et du développement chez Arabidopsis thaliana : Role of BAF60, a chromatin-remodeling factor, during cell cycle progression and development of Arabidopsis thaliana.

Degree: Docteur es, Biologie, 2015, Université Paris-Sud – Paris XI

URL: http://www.theses.fr/2015PA112088

►

Bien que l’ADN contenu dans les cellules eucaryotes permette le stockage de l’information génétique, c’est l’empaquetage de l’ADN en chromatine qui permet d’organiser finement cette… (more)

▼

Bien que l’ADN contenu dans les cellules eucaryotes permette le stockage de l’information génétique, c’est l’empaquetage de l’ADN en chromatine qui permet d’organiser finement cette information au cours du développement des organismes. Cependant cette structure constitue une barrière pour l’accessibilité de séquences d’ADN régulatrices. Ainsi, il existe différents mécanismes qui permettent de moduler la structure de la chromatine afin de définir le programme transcriptionnel spécifique de chaque cellule durant le développement des organismes. Dans cette étude nous avons montré que BAF60, une sous unité des complexes de remodelage de la chromatine de type SWI/SNF, favorise la transition florale en réprimant l’expression du gène FLC, répresseur de la floraison, et en contrôlant la formation d’une boucle intra-génique sur ce gène via la modulation de la condensation de la chromatine, la composition en histone et la régulation de marques épigénétiques au niveau de ce locus. De plus, nous avons mis en évidence que BAF60 agit sur la croissance des racines en régulant négativement la production de cytokinines et en favorisant la progression du cycle cellulaire grâce à son rôle sur l’architecture chromatinienne. Nous avons également montré que BAF60 se fixe préférentiellement sur les G-box des gènes actifs au niveau des régions sans nucléosome. BAF60 est exprimé durant le jour et favorise la répression de gènes impliqués dans l’élongation de l’hypocotyle. L’ensemble des résultats obtenus dans cette étude a montré que BAF60 régule des étapes clés du développement d’Arabidopsis thaliana en modulant l’architecture chromatinienne afin de réguler l’expression de nombreux gènes indispensables à différentes voies développementales de la plante. Comprendre comment BAF60 peut réguler l’organisation chromatinienne au sein de tissus spécifiques constituera le prochain défi.

Although DNA in eukaryotic cells allows storage of genetic information, it is its packaging into chromatin which allows to finely organize this information throughout the development of organisms. Chromatin constitutes a barrier to regulatory DNA sequences accessibility. Different mechanisms modulate chromatin structure in order to set the specific transcriptional program for each cell type during development. In this study, we have shown that BAF60, a subunit of SWI/SNF complexes, promotes flowering, by repressing the expression of FLC, a key flowering repressor. BAF60 regulates FLC by controlling gene loop formation via modulation of chromatin condensation, histone composition and post-translational modifications. Furthermore, we have demonstrated that BAF60 acts on root growth by negatively regulating cytokinin production and by promoting cell cycle progression through its role in chromatin architecture. We have also shown that BAF60 binds preferentially G-box of active genes at nucleosome-free region. BAF60 is expressed during the day to promote repression of genes involved in hypocotyl elongation. All together these results have shown that BAF60 regulates…

Advisors/Committee Members: Benhamed, Moussa (thesis director).

Subjects/Keywords: Epigénétique; Chromatine; Complexe de remodelage de la chromatine dépendants de l’ATP de type SWI/SNF; Cycle cellulaire; Développement; Epigenetic; Chromatin; SWI/SNF; Cell cycle; Development

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

APA (6^th Edition):

Jégu, T. (2015). Rôle du facteur de remodelage de la chromatine BAF60 au cours de la progression du cycle cellulaire et du développement chez Arabidopsis thaliana : Role of BAF60, a chromatin-remodeling factor, during cell cycle progression and development of Arabidopsis thaliana. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2015PA112088

Chicago Manual of Style (16^th Edition):

Jégu, Teddy. “Rôle du facteur de remodelage de la chromatine BAF60 au cours de la progression du cycle cellulaire et du développement chez Arabidopsis thaliana : Role of BAF60, a chromatin-remodeling factor, during cell cycle progression and development of Arabidopsis thaliana.” 2015. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed January 17, 2021. http://www.theses.fr/2015PA112088.

MLA Handbook (7^th Edition):

Jégu, Teddy. “Rôle du facteur de remodelage de la chromatine BAF60 au cours de la progression du cycle cellulaire et du développement chez Arabidopsis thaliana : Role of BAF60, a chromatin-remodeling factor, during cell cycle progression and development of Arabidopsis thaliana.” 2015. Web. 17 Jan 2021.

Vancouver:

Jégu T. Rôle du facteur de remodelage de la chromatine BAF60 au cours de la progression du cycle cellulaire et du développement chez Arabidopsis thaliana : Role of BAF60, a chromatin-remodeling factor, during cell cycle progression and development of Arabidopsis thaliana. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2015. [cited 2021 Jan 17]. Available from: http://www.theses.fr/2015PA112088.

Council of Science Editors:

Jégu T. Rôle du facteur de remodelage de la chromatine BAF60 au cours de la progression du cycle cellulaire et du développement chez Arabidopsis thaliana : Role of BAF60, a chromatin-remodeling factor, during cell cycle progression and development of Arabidopsis thaliana. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2015. Available from: http://www.theses.fr/2015PA112088

14. Lesbats, Paul. Architecture fonctionnelle du complexe d’integration du vih-1 : Functional architecture of the hiv-1 integration complex.

Degree: Docteur es, Sciences, technologie, santé. Microbiologie, 2011, Université de Bordeaux Segalen

URL: http://www.theses.fr/2011BOR21879

►

L’intégrase (IN) du VIH-1 est une enzyme clé catalysant l’insertion de l’ADN proviral dans le génome cellulaire au sein d’un complexe nucléoprotéique d’intégration.Les nombreux efforts… (more)

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L’intégrase (IN) du VIH-1 est une enzyme clé catalysant l’insertion de l’ADN proviral dans le génome cellulaire au sein d’un complexe nucléoprotéique d’intégration.Les nombreux efforts apportés à l’étude du mécanisme d’intégration ont permis d’accumuler de multiples données sur ce processus complexe. Cependant plusieurs questions essentielles demeurent sans réponses en particulier concernant l’architecture fonctionnelle des complexes d’intégration de VIH-1. En effet même si les complexes actifs pour l’intégration sont relativement bien définis leur chronologie précoce de formation demeure inconnue. De même les phases tardives de leur association au substrat naturel d’intégration que constitue la chromatine restent floues. Enfin le rôle des facteurs du complexe de préintégration (CPI) dans la régulation des ces mécanismes doit être déterminé.Mon travail de thèse s’est reposé sur trois axes s’articulant autour de ces questions:-Comment est régulée la dynamique des phases précoces d’attachement des oligomères d’intégrase sur les extrémités virales ?-Quel est l’impact de la structure de l’ADN cible et de la chromatine sur l’association active des complexes d’intégration ?-Quel(s) rôle(s) joue(nt) les facteurs du CPI dans ces phases ?

HIV-1 integrase (IN) is a key enzyme catalyzing the proviral DNA insertion into the cellular genome within a nucleoprotein integration complex.The numerous efforts made on the mechanism of integration have led to the accumulation of substantial data on this process. However many important questions are still open particularly on the functional architecture of the HIV-1 integration complexes. Indeed even if the active complexes involved in the catalysis of the integration are well described, the chronology of their early formation is still unknown. Moreover, the late association of these complexes with the host chromatin is also obscure. Finally the involvement of the IN cofactors inside the preintegration complex on these steps has to be elucidated.The project of my PhD relied on three axis articulated on these questions:-What is the dynamic of the IN oligomers association on the DNA viral ends?-What is the impact of the target DNA chromatin structure on the functional association of the integration complexes?-Involvement of the PIC factors on these steps?

Advisors/Committee Members: Parissi, Vincent (thesis director).

Subjects/Keywords: Rétrovirus; VIH; Intégrase; Complexe d’intégration; Structure-fonction; Oligomérisation; Chromatine; SWI/SNF; Retrovirus; HIV; Integrase; Integration complex; Structure-function; Oligomerization; Chromatin; SWI/SNF

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

APA (6^th Edition):

Lesbats, P. (2011). Architecture fonctionnelle du complexe d’integration du vih-1 : Functional architecture of the hiv-1 integration complex. (Doctoral Dissertation). Université de Bordeaux Segalen. Retrieved from http://www.theses.fr/2011BOR21879

Chicago Manual of Style (16^th Edition):

Lesbats, Paul. “Architecture fonctionnelle du complexe d’integration du vih-1 : Functional architecture of the hiv-1 integration complex.” 2011. Doctoral Dissertation, Université de Bordeaux Segalen. Accessed January 17, 2021. http://www.theses.fr/2011BOR21879.

MLA Handbook (7^th Edition):

Lesbats, Paul. “Architecture fonctionnelle du complexe d’integration du vih-1 : Functional architecture of the hiv-1 integration complex.” 2011. Web. 17 Jan 2021.

Vancouver:

Lesbats P. Architecture fonctionnelle du complexe d’integration du vih-1 : Functional architecture of the hiv-1 integration complex. [Internet] [Doctoral dissertation]. Université de Bordeaux Segalen; 2011. [cited 2021 Jan 17]. Available from: http://www.theses.fr/2011BOR21879.

Council of Science Editors:

Lesbats P. Architecture fonctionnelle du complexe d’integration du vih-1 : Functional architecture of the hiv-1 integration complex. [Doctoral Dissertation]. Université de Bordeaux Segalen; 2011. Available from: http://www.theses.fr/2011BOR21879

15. Leruste, Amaury. Immune context of malignant rhabdoid tumors : description and identification of new therapeutic targets : Contexte immunitaire des tumeurs rhabdoïdes : description et identification de nouvelles cibles thérapeutiques.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2019, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2019SACLS050

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Les tumeurs rhabdoïdes (TR) constituent un rare cancer indifférencié du jeune enfant et du nourrisson, avec un âge médian au diagnostic de 20 mois. Ces… (more)

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Les tumeurs rhabdoïdes (TR) constituent un rare cancer indifférencié du jeune enfant et du nourrisson, avec un âge médian au diagnostic de 20 mois. Ces tumeurs sont caractérisées par une inactivation biallélique du gène suppresseur de tumeur SMARCB1, un des membres du complexe SWI/SNF, acteur majeur du remodelage de la chromatine, sans autre altération génomique récurrente. Le pronostic des TR est péjoratif, le taux de survie globale atteignant 30% dans la plupart des séries, malgré des approches thérapeutiques conventionnelles particulièrement agressives. Les approches d’immunothérapies ont obtenu un succès certain dans certains cancers de l’adulte, et récentes analyses de l’infiltrat immun des cancers pédiatriques ne montrent pas un fort taux de tumeurs infiltrées à l’exception de rare types de cancers dont les TR intracrâniennes. Nous avons donc procédé à une analyse multimodale de l’infiltrat immun de cohortes de patients ainsi que d’un modèle de TR murines établi dans notre laboratoire. Nous avons identifié une forte proportion de tumeurs infiltrées dans certains sous-groupes de TR. Cet infiltrat était composé à la fois de cellules myéloïdes incluant des populations au phénotype immunosuppresseur, et lymphocytaires T notamment de phénotype résident mémoire caractérisées par une forte expansion clonale probablement spécifique d’un antigène tumoral. Nous avons identifié des cibles thérapeutiques communes aux tumeurs humaines et au modèle murin syngénique, et trouvé que cibler l’infiltrat lymphocytaire T ou myéloïde était susceptible d’induire une réponse tumorale complète avec induction d’une mémoire immunitaire, confirmant le caractère immunogénique des TR, et apportant de nouvelles stratégies thérapeutiques utiles en clinique. Enfin, nous avons identifié que les TR étaient le site d’une réexpression de rétrovirus endogènes, dépendante de celle de SMARCB1, avec activation des voies de l’interféron, apportant une base à une immunogénicité des TR issue du génome non codant.

Rhabdoid tumors (RT) are highly undifferentiated cancers occurring in infancy and early childhood, with a median age at diagnosis about 20 months. These tumors are characterized by the biallelic inactivation of SMARCB1 tumor suppressor gene, core member of the SWI/SNF complex, one major chromatin remodeling actor, in an otherwise highly stable genome. The prognosis of RT is dismal with overall survival hardly reaching 30% in most series, despite particularly aggressive conventional treatment. Immunotherapy approaches has gained a striking success within some adult cancer types and recent analyses of immune cell content of pediatric cancers don’t reveal a high rate of infiltrated tumors, except in few tumor types such as intracranial rhabdoid tumors. Then, we conducted a comprehensive analysis of the immune context of both human RT cohorts and a mouse RT model, including at single cell level. We identified a high recurrence of infiltrated tumors, in a RT-subgroup related manner, composed of both myeloid cells including cells with immune…

Advisors/Committee Members: Bourdeaut, Franck (thesis director), Piaggio, Eliane (thesis director).

Subjects/Keywords: Microenvironnement tumoral; Immunothérapie; Récepteur T; Swi/snf; Tumeurs rhabdoïdes; Rétrovirus endogènes; Tumor microenvironment; Immunotherapy; T cell receptor; Swi/snf; Rhabdoid tumors; Endogenous retroviruses

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APA (6^th Edition):

Leruste, A. (2019). Immune context of malignant rhabdoid tumors : description and identification of new therapeutic targets : Contexte immunitaire des tumeurs rhabdoïdes : description et identification de nouvelles cibles thérapeutiques. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2019SACLS050

Chicago Manual of Style (16^th Edition):

Leruste, Amaury. “Immune context of malignant rhabdoid tumors : description and identification of new therapeutic targets : Contexte immunitaire des tumeurs rhabdoïdes : description et identification de nouvelles cibles thérapeutiques.” 2019. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed January 17, 2021. http://www.theses.fr/2019SACLS050.

MLA Handbook (7^th Edition):

Leruste, Amaury. “Immune context of malignant rhabdoid tumors : description and identification of new therapeutic targets : Contexte immunitaire des tumeurs rhabdoïdes : description et identification de nouvelles cibles thérapeutiques.” 2019. Web. 17 Jan 2021.

Vancouver:

Leruste A. Immune context of malignant rhabdoid tumors : description and identification of new therapeutic targets : Contexte immunitaire des tumeurs rhabdoïdes : description et identification de nouvelles cibles thérapeutiques. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2019. [cited 2021 Jan 17]. Available from: http://www.theses.fr/2019SACLS050.

Council of Science Editors:

Leruste A. Immune context of malignant rhabdoid tumors : description and identification of new therapeutic targets : Contexte immunitaire des tumeurs rhabdoïdes : description et identification de nouvelles cibles thérapeutiques. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2019. Available from: http://www.theses.fr/2019SACLS050

Cornell University

16. Hah, Nasun. Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses.

Degree: PhD, Biochemistry, 2011, Cornell University

URL: http://hdl.handle.net/1813/33589

► Estrogens play crucial roles in regulating gene expression in physiological and disease states. Estrogens acts through estrogen receptors (ERs) and their binding sites in genomic… (more)

▼ Estrogens play crucial roles in regulating gene expression in physiological and disease states. Estrogens acts through estrogen receptors (ERs) and their binding sites in genomic DNA to modulate transcription by RNA polymerase II. Although recent gene-specific and genomic analyses have provided considerable information about of estrogen-dependent transcription, many aspects of the estrogen signaling network have not yet been elucidated. The goal of my studies was to uncover new information about the immediate and direct effects of estrogen signaling at the cell membrane, in the cytoplasm, and in the nucleus to elucidate the underlying regulatory networks. First, I investigated an ER transcriptional coregulators, SWI/SNF, an ATPdependent chromatin remodeling complex. I explored the molecular functions of the BAF57 and BAF180 subunits of SWI/SNF using a quantitative proteomic approach called SILAC (Stable Isotope Labeling by Amino Acids in Cell Culture). I found that depletion of BAF57 results in a significant depletion of BAF180 from the SWI/SNF complex without decreasing the total cellular BAF180 levels, resulting in an accumulation of cells in the G2/M phase. Knockdown of BAF57 also causes transcriptional misregulation of cell cycle-related genes involved in the late G2 checkpoint. Collectively, these studies have elucidated the role of BAF57 and BAF180 in the transcriptional control of cell proliferation. Second, I have used GRO-Seq (Global Nuclear Run-On and Massively Parallel Sequencing) to explore the immediate effects of estrogen signaling on the transcriptome of breast cancer cells. I found that estrogen directly regulates a strikingly large fraction of the transcriptome in a rapid, robust, and unexpectedly transient manner. In addition to protein coding genes, estrogen regulates the distribution and activity of all three RNA polymerases, and virtually every class of non-coding RNA that has been described to date. I also identified a large number of previously undetected estrogen-regulated intergenic transcripts, many of which are found proximal to ER[alpha] binding sites. These results provide the most comprehensive measurement of the primary and immediate estrogen effects to date. I expect that genome-wide inferences based on the direct estrogen-regulated transcriptome in combination with estrogen-regulated signaling pathway will be useful for understanding estrogen biology. Advisors/Committee Members: Kraus, William Lee (chair), Collins, Ruth N. (committee member), Lis, John T (committee member).

Subjects/Keywords: estrogen; estrogen receptor; GRO-seq; swi/snf; baf57; baf180; silac; proteomic; enhancer; edc; estrogen signaling

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APA (6^th Edition):

Hah, N. (2011). Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/33589

Chicago Manual of Style (16^th Edition):

Hah, Nasun. “Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses.” 2011. Doctoral Dissertation, Cornell University. Accessed January 17, 2021. http://hdl.handle.net/1813/33589.

MLA Handbook (7^th Edition):

Hah, Nasun. “Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses.” 2011. Web. 17 Jan 2021.

Vancouver:

Hah N. Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses. [Internet] [Doctoral dissertation]. Cornell University; 2011. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/1813/33589.

Council of Science Editors:

Hah N. Signal Regulated Gene Expression: Defining The Effects Of Estrogen Signaling Through Genomic And Proteomic Analyses. [Doctoral Dissertation]. Cornell University; 2011. Available from: http://hdl.handle.net/1813/33589

Penn State University

17. Chandy, Mark. HISTONE MODIFICATIONS INFLUENCE CHROMATIN MODIFYING AND CHROMATIN REMODELING COMPLEXES .

Degree: 2008, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/6926

► Chromatin condenses DNA and packages it into the nucleus. The fundamental unit of chromatin is the nucleosome, which compacts and forms higher order structures. Chromatin… (more)

▼ Chromatin condenses DNA and packages it into the nucleus. The fundamental unit of chromatin is the nucleosome, which compacts and forms higher order structures. Chromatin structure affects transcription, DNA replication and DNA repair. For gene expression, chromatin is dynamically modulated by chromatin modifying complexes and chromatin remodeling complexes. The histone code hypothesis predicts that modifications not only dictate the inheritance of chromatin states, but also that combinations of modifications recognized by protein-interaction domains are important for recruiting cofactors that alter chromatin structure. For over 40 years, histone acetylation has been associated with gene activation. Moreover, the discovery of histone acetyl transferase (HAT) complexes has implicated acetylation in transcription, DNA repair and even silencing. The SAGA complex is a 1.8 MDa multisubunit HAT complex that is recruited by activator at promoters. As the catalytic subunit of SAGA, Gcn5 acetylates promoter nucleosomes and produces a peaked acetylation profile upon gene induction. Moreover, the Gcn5 bromodomain is required for retention on acetylated nucleosomes. We test the importance of the Gcn5 bromodomain in restricting SAGA acetylation to the promoter using the scanning in vitro chromatin immunoprecipitation assay. The Gcn5 bromodomain does not significantly affect the nucleosomal acetylation profile of SAGA, even when the activator is removed from the array. While the Spt7 bromodomain does not retain SAGA on acetylated nucleosomes in vitro, its evolutionary conservation in yeast suggests that it may help retain SAGA on acetylated nucleosomes in vivo. When tested on phenotypic screens, the Spt7 bromodomain mutant and the Spt7 and Gcn5 double bromodomain mutant have a slight phenotype. The accumulation of acetylated histones at the promoter signals for the recruitment of other cofactors. SAGA and the ATP dependent chromatin remodeler, SWI/SNF functioned cooperatively in the activation of several genes in budding yeast. At the PHO5 promoter, both SAGA and SWI/SNF are important for timely removal of nucleosomes from the promoter. The loss of SWI/SNF results in the accumulation of H3K9 acetylated histones at this promoter, which is also an acetylation site for SAGA. Thus, SAGA acetylation at the promoter may recruit SWI/SNF and promote the displacement of acetylated nucleosomes. We directly test the influence of SAGA acetylation on SWI/SNF nucleosome displacement using several assays on the immobilized nucleosome array in vitro. SWI/SNF not only displaces acetylated nucleosomes, but it also targets promoter acetylated nucleosomes in the absence of activator. More important, SWI/SNF displacement of acetylated nucleosomes correlates with an increase in accessible DNA at the promoter. Advisors/Committee Members: James E Hopper, Committee Chair/Co-Chair, Sergei A Grigoryev, Committee Member, Michael G Fried, Committee Member, Laura Carrel, Committee Member, Jerry L Workman, Committee Chair/Co-Chair, Robert G Levenson, Committee Member.

Subjects/Keywords: SAGA; SWI/SNF; chromatin remodeling; bromodomain

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APA (6^th Edition):

Chandy, M. (2008). HISTONE MODIFICATIONS INFLUENCE CHROMATIN MODIFYING AND CHROMATIN REMODELING COMPLEXES . (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/6926

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):

Chandy, Mark. “HISTONE MODIFICATIONS INFLUENCE CHROMATIN MODIFYING AND CHROMATIN REMODELING COMPLEXES .” 2008. Thesis, Penn State University. Accessed January 17, 2021. https://submit-etda.libraries.psu.edu/catalog/6926.

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

MLA Handbook (7^th Edition):

Chandy, Mark. “HISTONE MODIFICATIONS INFLUENCE CHROMATIN MODIFYING AND CHROMATIN REMODELING COMPLEXES .” 2008. Web. 17 Jan 2021.

Vancouver:

Chandy M. HISTONE MODIFICATIONS INFLUENCE CHROMATIN MODIFYING AND CHROMATIN REMODELING COMPLEXES . [Internet] [Thesis]. Penn State University; 2008. [cited 2021 Jan 17]. Available from: https://submit-etda.libraries.psu.edu/catalog/6926.

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

Council of Science Editors:

Chandy M. HISTONE MODIFICATIONS INFLUENCE CHROMATIN MODIFYING AND CHROMATIN REMODELING COMPLEXES . [Thesis]. Penn State University; 2008. Available from: https://submit-etda.libraries.psu.edu/catalog/6926

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

Texas Medical Center

18. Kwan, Suet Yan. REGULATION OF THE OXIDATIVE STRESS RESPONSE BY ARID1A.

Degree: PhD, 2015, Texas Medical Center

URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/608

► SWI/SNF is mutated in about 20% of all human cancers; in particular ARID1A is the most frequently mutated SWI/SNF subunit. ARID1A is a tumor… (more)

▼ SWI/SNF is mutated in about 20% of all human cancers; in particular ARID1A is the most frequently mutated SWI/SNF subunit. ARID1A is a tumor suppressor gene, inactivating mutations in ARID1A are most frequently found in ovarian and endometrial cancers, specifically uterine corpus endometrioid carcinomas (UCEC), ovarian clear cell carcinomas (OCCC) and ovarian endometrioid carcinomas (OEC). The functional roles of ARID1A are not completely understood and there are limited therapeutic strategies that specifically target ARID1A-mutant cancers. Given that ARID1A expression is lost in cancer, ARID1A mutations cannot be targeted directly and novel therapeutic strategies are required to target ARID1A-mutant cancers. In this study, drug responses between ARID1A-wildtype and ARID1A-mutant cell lines were compared using the ‘Genomics of Drug Sensitivities in Cancer’ database. From this analysis, I found that ARID1A-mutant cell lines are more sensitive to elesclomol, which is a reactive oxygen species (ROS)-inducing agent. This finding was validated using a panel of ovarian and endometrial cancer cell lines, where ARID1A-mutant cell lines exhibited lower IC50 values and higher apoptotic rates when treated with elesclomol. Knockdown and re-expression of ARID1A in ovarian cancer cells showed that ARID1A is required to protect cancer cells from oxidative stress. In the absence of ARID1A, intracellular ROS levels were increased, and this increase was required for increased cell growth upon ARID1A depletion. Next, I investigated the relationship between ARID1A and NRF2, the major regulator of the antioxidant response in the cell. I found that ARID1A negatively regulates the expression of NRF2. Knockdown of NRF2 in ovarian cancer cell lines revealed that NRF2 expression may be preferentially required for protection from oxidative stress and cell proliferation in ARID1A-mutant cells. Analysis using The Cancer Genome Atlas (TCGA) UCEC dataset revealed that ARID1A-mutant tumor samples have higher expression of NRF2 and NRF2-target genes. In summary, this study revealed novel roles of ARID1A in protecting ovarian cancer cells against oxidative stress. In the absence of ARID1A, NRF2 is up-regulated and may be required to compensate for ARID1A deficiency. These findings suggest that ROS-inducing agents and NRF2 inhibitors may be used as therapeutic strategies in targeting ARID1A-mutant ovarian cancer cells. Advisors/Committee Members: Kwong-Kwok Wong, Russell Broaddus, Joya Chandra.

Subjects/Keywords: ARID1A; SWI/SNF; oxidative stress; ROS; NRF2; elesclomol; Medicine and Health Sciences; Oncology

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APA (6^th Edition):

Kwan, S. Y. (2015). REGULATION OF THE OXIDATIVE STRESS RESPONSE BY ARID1A. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/608

Chicago Manual of Style (16^th Edition):

Kwan, Suet Yan. “REGULATION OF THE OXIDATIVE STRESS RESPONSE BY ARID1A.” 2015. Doctoral Dissertation, Texas Medical Center. Accessed January 17, 2021. https://digitalcommons.library.tmc.edu/utgsbs_dissertations/608.

MLA Handbook (7^th Edition):

Kwan, Suet Yan. “REGULATION OF THE OXIDATIVE STRESS RESPONSE BY ARID1A.” 2015. Web. 17 Jan 2021.

Vancouver:

Kwan SY. REGULATION OF THE OXIDATIVE STRESS RESPONSE BY ARID1A. [Internet] [Doctoral dissertation]. Texas Medical Center; 2015. [cited 2021 Jan 17]. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/608.

Council of Science Editors:

Kwan SY. REGULATION OF THE OXIDATIVE STRESS RESPONSE BY ARID1A. [Doctoral Dissertation]. Texas Medical Center; 2015. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/608

University of California – San Francisco

19. Stewart, Kathleen Marie. The Role of SWI/SNF Chromatin Remodeling in Breast Tumorigenesis.

Degree: Biomedical Sciences, 2010, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/0645d0zw

► Mammary epithelial cell (MEC)-extracellular matrix (ECM) interactions are critical for normal breast tissue development, differentiation and homeostasis by engaging a repertoire of ECM adhesion receptors… (more)

▼ Mammary epithelial cell (MEC)-extracellular matrix (ECM) interactions are critical for normal breast tissue development, differentiation and homeostasis by engaging a repertoire of ECM adhesion receptors including integrins to activate signaling processes that control MEC differentiation, proliferation and survival. Malignant progression alters MEC responsiveness to ECM cues and is highlighted by the observation that the expression of integrins is altered during breast tumor progression. The molecular basis for altered integrins in breast tumors and the regulation of integrin changes during malignant transformation are less understood. The goal of my thesis is to test the hypothesis that oncogene-dependent transformation promotes breast tumor progression through regulating changes in ECM responsiveness via α5 integrin through targeting of the SWI/SNF chromatin remodeling protein BRM. I found that oncogene-driven transformation depends upon increased expression of α5 integrin to promote MEC growth and survival in three-dimensional (3D) cultures and implicates the SWI/SNF chromatin remodeling protein, Brahma (BRM) in the regulation of tumor-driven ECM responsiveness changes. I also observed decreased BRM expression in breast cancer cell lines and abrogation of BRM in non-malignant MECs enhanced cell motility and anchorage independent growth and upregulated a gene program associated with breast tumor progression. Microarray analysis of breast cancer patient samples revealed that reduced BRM expression correlated with increased disease recurrence and morbidity. Whether BRM is a bona fide tumor suppressor in breast cancers and whether targeting the re-expression of BRM in breast tumors is a viable therapeutic target remains an area of active research. Nevertheless, regaining ECM responsiveness in breast tumor cells by manipulating chromatin is without precedent and forms the foundation for future investigations into the epigenetic mechanisms governing ECM responsiveness and may lead to the discovery of novel molecular targets in the treatment of breast cancer.

Subjects/Keywords: Biology, Cell; Biology, Molecular; Breast; Breast Cancer; Chromatin remodeling; Integrin; SWI/SNF

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APA (6^th Edition):

Stewart, K. M. (2010). The Role of SWI/SNF Chromatin Remodeling in Breast Tumorigenesis. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/0645d0zw

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):

Stewart, Kathleen Marie. “The Role of SWI/SNF Chromatin Remodeling in Breast Tumorigenesis.” 2010. Thesis, University of California – San Francisco. Accessed January 17, 2021. http://www.escholarship.org/uc/item/0645d0zw.

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

MLA Handbook (7^th Edition):

Stewart, Kathleen Marie. “The Role of SWI/SNF Chromatin Remodeling in Breast Tumorigenesis.” 2010. Web. 17 Jan 2021.

Vancouver:

Stewart KM. The Role of SWI/SNF Chromatin Remodeling in Breast Tumorigenesis. [Internet] [Thesis]. University of California – San Francisco; 2010. [cited 2021 Jan 17]. Available from: http://www.escholarship.org/uc/item/0645d0zw.

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

Council of Science Editors:

Stewart KM. The Role of SWI/SNF Chromatin Remodeling in Breast Tumorigenesis. [Thesis]. University of California – San Francisco; 2010. Available from: http://www.escholarship.org/uc/item/0645d0zw

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

University of California – San Francisco

20. Engel, Karin Buser. Participation of Regulatory Factors and the Coregulator Brm in the Combinatorial Control of Transcription.

Degree: Chemistry and Chemical Biology, 2011, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/1c55146w

► Metazoan transcriptional regulation is governed by combinatorial control, in which distinct multifactor regulatory complexes composed of various combinations of factors assemble at different genomic sites.… (more)

Subjects/Keywords: Molecular Biology; chromatin remodeling; combinatorial control; glucocorticoid receptor; NFkappaB; Swi/Snf; transcriptional regulation

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APA (6^th Edition):

Engel, K. B. (2011). Participation of Regulatory Factors and the Coregulator Brm in the Combinatorial Control of Transcription. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/1c55146w

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):

Engel, Karin Buser. “Participation of Regulatory Factors and the Coregulator Brm in the Combinatorial Control of Transcription.” 2011. Thesis, University of California – San Francisco. Accessed January 17, 2021. http://www.escholarship.org/uc/item/1c55146w.

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

MLA Handbook (7^th Edition):

Engel, Karin Buser. “Participation of Regulatory Factors and the Coregulator Brm in the Combinatorial Control of Transcription.” 2011. Web. 17 Jan 2021.

Vancouver:

Engel KB. Participation of Regulatory Factors and the Coregulator Brm in the Combinatorial Control of Transcription. [Internet] [Thesis]. University of California – San Francisco; 2011. [cited 2021 Jan 17]. Available from: http://www.escholarship.org/uc/item/1c55146w.

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

Council of Science Editors:

Engel KB. Participation of Regulatory Factors and the Coregulator Brm in the Combinatorial Control of Transcription. [Thesis]. University of California – San Francisco; 2011. Available from: http://www.escholarship.org/uc/item/1c55146w

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

University of Western Ontario

21. Chubak, Melissa C. Role of the SWI/SNF Chromatin Remodelling Complex in the Axon Development of the Drosophila Mushroom Body.

Degree: 2017, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/4911

► The SWI/SNF complex is an evolutionarily conserved ATP-dependent chromatin remodelling complex that has been implicated in the aetiology of intellectual disability (ID). Among the dominant… (more)

Subjects/Keywords: Drosophila melanogaster; SWI/SNF complex; mushroom body; epigenetics; chromatin remodelling; axon development; Developmental Neuroscience

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APA (6^th Edition):

Chubak, M. C. (2017). Role of the SWI/SNF Chromatin Remodelling Complex in the Axon Development of the Drosophila Mushroom Body. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/4911

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):

Chubak, Melissa C. “Role of the SWI/SNF Chromatin Remodelling Complex in the Axon Development of the Drosophila Mushroom Body.” 2017. Thesis, University of Western Ontario. Accessed January 17, 2021. https://ir.lib.uwo.ca/etd/4911.

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

MLA Handbook (7^th Edition):

Chubak, Melissa C. “Role of the SWI/SNF Chromatin Remodelling Complex in the Axon Development of the Drosophila Mushroom Body.” 2017. Web. 17 Jan 2021.

Vancouver:

Chubak MC. Role of the SWI/SNF Chromatin Remodelling Complex in the Axon Development of the Drosophila Mushroom Body. [Internet] [Thesis]. University of Western Ontario; 2017. [cited 2021 Jan 17]. Available from: https://ir.lib.uwo.ca/etd/4911.

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

Council of Science Editors:

Chubak MC. Role of the SWI/SNF Chromatin Remodelling Complex in the Axon Development of the Drosophila Mushroom Body. [Thesis]. University of Western Ontario; 2017. Available from: https://ir.lib.uwo.ca/etd/4911

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

University of New Mexico

22. Wiest, Nathaniel E. MAINTENANCE OF GENETIC AND EPIGENETIC STABILITY DURING DNA DOUBLE-STRAND BREAK REPAIR AND DNA REPLICATION.

Degree: Biomedical Sciences Graduate Program, 2019, University of New Mexico

URL: https://digitalrepository.unm.edu/biom_etds/191

► Eukaryotic genomes are assembled into a complex of DNA and proteins known as chromatin. The packaging of DNA into chromatin is the foundational strategy… (more)

▼ Eukaryotic genomes are assembled into a complex of DNA and proteins known as chromatin. The packaging of DNA into chromatin is the foundational strategy that cells use to both compress genomic DNA into nuclei and regulate access to its contents. The basic repeating subunit of chromatin is the nucleosome, composed of an octamer of two copies of each of the core histone proteins H2A, H2B, H3, and H4 around which 146 bp of DNA are tightly wrapped. While the compaction of genomes into chromatin offers cells significant advantages, it also presents serious challenges to fundamental processes that maintain genome integrity, including DNA repair and replication. Nucleosomes must be disrupted to allow access to damaged DNA by repair factors. Additionally, the millions of nucleosomes that package genomic DNA are displaced during DNA replication. After their displacement, nucleosomes must be faithfully restored to preserve proper chromatin compaction and regulation of access to DNA that underlie transcriptional programs and cellular identity. Thus, the processes that maintain genome and epigenome stability are intricately linked. In the first aim of this dissertation, I examined the role of the conserved SWI/SNF ATP-dependent nucleosome remodeler in the repair of DNA double-strand breaks (DSBs) in yeast. I demonstrated that SWI/SNF facilitates the actions of the MRX complex at the DSB, including the eviction of KU, initiation of DNA end resection, recruitment of long-range resection factors, and activation of the DNA damage response. Furthermore, I showed that this activity of SWI/SNF is related to its role in the efficient eviction of nucleosomes near a DSB. This study contributes to an understanding of the roles of the clinically relevant SWI/SNF complex in mediating accurate repair of DSBs in the context of chromatin. In the second aim, I examined the role of DNA Ligase I (Lig1) in coordinating chromatin assembly and maturation on newly replicated DNA in mammalian cells. I accumulated preliminary data demonstrating that Lig1 may influence the deposition of the linker histone H1 on DNA during replication, and that that Lig1 may also contribute to the recruitment of DNA methylation machinery. These combined studies provide novel information on two critical processes that maintain genetic and epigenetic stability in eukaryotes. Advisors/Committee Members: Alan E Tomkinson, PhD, Mary Ann Osley, PhD, Diane S Lidke, PhD, David Y Lee, MD/PhD.

Subjects/Keywords: Chromatin; SWI/SNF; Double-Strand Break Repair; DNA Replication; DNA Ligase; Genome Stability; Molecular Genetics

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

APA (6^th Edition):

Wiest, N. E. (2019). MAINTENANCE OF GENETIC AND EPIGENETIC STABILITY DURING DNA DOUBLE-STRAND BREAK REPAIR AND DNA REPLICATION. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/191

Chicago Manual of Style (16^th Edition):

Wiest, Nathaniel E. “MAINTENANCE OF GENETIC AND EPIGENETIC STABILITY DURING DNA DOUBLE-STRAND BREAK REPAIR AND DNA REPLICATION.” 2019. Doctoral Dissertation, University of New Mexico. Accessed January 17, 2021. https://digitalrepository.unm.edu/biom_etds/191.

MLA Handbook (7^th Edition):

Wiest, Nathaniel E. “MAINTENANCE OF GENETIC AND EPIGENETIC STABILITY DURING DNA DOUBLE-STRAND BREAK REPAIR AND DNA REPLICATION.” 2019. Web. 17 Jan 2021.

Vancouver:

Wiest NE. MAINTENANCE OF GENETIC AND EPIGENETIC STABILITY DURING DNA DOUBLE-STRAND BREAK REPAIR AND DNA REPLICATION. [Internet] [Doctoral dissertation]. University of New Mexico; 2019. [cited 2021 Jan 17]. Available from: https://digitalrepository.unm.edu/biom_etds/191.

Council of Science Editors:

Wiest NE. MAINTENANCE OF GENETIC AND EPIGENETIC STABILITY DURING DNA DOUBLE-STRAND BREAK REPAIR AND DNA REPLICATION. [Doctoral Dissertation]. University of New Mexico; 2019. Available from: https://digitalrepository.unm.edu/biom_etds/191

University of Toledo Health Science Campus

23. Saladi, SrinivasVinod. SWI/SNF Chromatin Remodeling Enzymes: Epigenetic Modulators in Melanoma Invasiveness and Survival.

Degree: PhD, College of Medicine, 2011, University of Toledo Health Science Campus

URL: http://rave.ohiolink.edu/etdc/view?acc_num=mco1310065995

► SWI/SNF enzymes are multi subunit complexes consisting of an ATPase subunit, either BRG1 or BRM. They act as epigenetic modulators and remodel the chromatin in… (more)

▼ SWI/SNF enzymes are multi subunit complexes consisting of an ATPase subunit, either BRG1 or BRM. They act as epigenetic modulators and remodel the chromatin in an ATP dependent manner. The SWI/SNF complex has 9-12 BRG1 or BRM associated factors called (BAFs). Earlier studies from our lab showed that BRG1 interacts with Microphthalmia associated transcription factor (MITF) to promote melanocyte differentiation. MITF is a lineage addiction oncogene in melanoma that regulates melanoma proliferation and metastasis. Several of the SWI/SNF subunits have been demonstrated to behave as tumor suppressors in mice and been found to be down regulated in many forms of cancer. However, our lab has shown that although, BRG1 or BRM is down-regulated in a small subset of melanoma cell lines, one catalytic subunit is always retained and the other SWI/SNF subunits are expressed at high levels compared to normal melanocytes. This has led to the hypothesis, that in melanoma, SWI/SNF enzymes interact with MITF and other transcription factors to modulate melanoma metastasis and survival. In the first study we demonstrate that BRG1 is significantly upregulated in stage IV metastatic melanomas compared to stage III melanoma and normal skin. We found that BRG1 modulates the expression of genes that code for components of the extracellular matrix and regulators of adhesion. We found that BRG1 promotes adhesion of melanoma cells to laminin and collagen but inhibits adhesion to fibronectin. Furthermore, in vitro BRG1 promotes the invasive potential of the cells by upregulating matrix metalloproteinase 2 (MMP2) expression at the transcriptional level. Thus, our studies demonstrate that BRG1 epigenetically modulates melanoma invasive ability in vitro, suggesting that BRG1 plays a role in melanoma metastasis.SWI/SNF enzymes have been demonstrated to regulate the response to DNA damage by promoting DNA repair and cell cycle checkpoint controls. Earlier studies from the lab showed that BRG1 promotes melanoma resistance to the DNA damaging agent, cisplatin. In the present study we determined that BRG1 also promotes survival in response to DNA damage induced by UVB radiation. We found that in addition to promoting DNA repair and regulating cell cycle proteins, BRG1 directly modulates the apoptotic pathway by activating expression of the melanoma-inhibitor of apoptosis gene (ML-IAP). ML-IAP is a potent inhibitor of the apoptotic pathway, and a potential target for melanoma treatment. In melanoma cells, ML-IAP expression is regulated by a cooperative activation loop involving BRG1 and MITF that promotes permissive chromatin structure and an active epigenetic signature on the ML-IAP promoter. Our studies suggest that an effective option for treating melanoma may be the use of epigenetic drugs that target either BRG1 or chromatin remodeling enzymes that function in concert with BRG1. Advisors/Committee Members: de la Serna, Ivana (Committee Co-Chair), Chin, Khew-Voon (Committee Co-Chair).

Subjects/Keywords: Biomedical Research; Cellular Biology; Molecular Biology; SWI/SNF; Chromatin remodeling; DNA repair; Invasion; Apoptosis

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APA (6^th Edition):

Saladi, S. (2011). SWI/SNF Chromatin Remodeling Enzymes: Epigenetic Modulators in Melanoma Invasiveness and Survival. (Doctoral Dissertation). University of Toledo Health Science Campus. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=mco1310065995

Chicago Manual of Style (16^th Edition):

Saladi, SrinivasVinod. “SWI/SNF Chromatin Remodeling Enzymes: Epigenetic Modulators in Melanoma Invasiveness and Survival.” 2011. Doctoral Dissertation, University of Toledo Health Science Campus. Accessed January 17, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=mco1310065995.

MLA Handbook (7^th Edition):

Saladi, SrinivasVinod. “SWI/SNF Chromatin Remodeling Enzymes: Epigenetic Modulators in Melanoma Invasiveness and Survival.” 2011. Web. 17 Jan 2021.

Vancouver:

Saladi S. SWI/SNF Chromatin Remodeling Enzymes: Epigenetic Modulators in Melanoma Invasiveness and Survival. [Internet] [Doctoral dissertation]. University of Toledo Health Science Campus; 2011. [cited 2021 Jan 17]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1310065995.

Council of Science Editors:

Saladi S. SWI/SNF Chromatin Remodeling Enzymes: Epigenetic Modulators in Melanoma Invasiveness and Survival. [Doctoral Dissertation]. University of Toledo Health Science Campus; 2011. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=mco1310065995

Texas A&M University

24. Dhasarathy, Archana. Interplay between promoter occupancy and chromatin remodeling requirements in transactivation of the S.cerevisiae PHO5 gene.

Degree: PhD, Genetics, 2006, Texas A&M University

URL: http://hdl.handle.net/1969.1/3272

► In higher eukaryotes, DNA is packaged with histones and other proteins into chromatin. While this is important in the control of unwanted gene expression, chromatin… (more)

Subjects/Keywords: chromatin; Gcn5; PHO5; gene expression; SAGA; SWI/SNF

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

APA (6^th Edition):

Dhasarathy, A. (2006). Interplay between promoter occupancy and chromatin remodeling requirements in transactivation of the S.cerevisiae PHO5 gene. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/3272

Chicago Manual of Style (16^th Edition):

Dhasarathy, Archana. “Interplay between promoter occupancy and chromatin remodeling requirements in transactivation of the S.cerevisiae PHO5 gene.” 2006. Doctoral Dissertation, Texas A&M University. Accessed January 17, 2021. http://hdl.handle.net/1969.1/3272.

MLA Handbook (7^th Edition):

Dhasarathy, Archana. “Interplay between promoter occupancy and chromatin remodeling requirements in transactivation of the S.cerevisiae PHO5 gene.” 2006. Web. 17 Jan 2021.

Vancouver:

Dhasarathy A. Interplay between promoter occupancy and chromatin remodeling requirements in transactivation of the S.cerevisiae PHO5 gene. [Internet] [Doctoral dissertation]. Texas A&M University; 2006. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/1969.1/3272.

Council of Science Editors:

Dhasarathy A. Interplay between promoter occupancy and chromatin remodeling requirements in transactivation of the S.cerevisiae PHO5 gene. [Doctoral Dissertation]. Texas A&M University; 2006. Available from: http://hdl.handle.net/1969.1/3272

University of Washington

25. Fawcett, Emily Marie. A beneficial toxin: The response to hydrogen sulfide improves survival in a changing environment.

Degree: PhD, 2015, University of Washington

URL: http://hdl.handle.net/1773/34061

► Fluctuations in environmental conditions can be deadly. The ability to rapidly and appropriately respond to stressful conditions can mean the difference between life and death.… (more)

▼ Fluctuations in environmental conditions can be deadly. The ability to rapidly and appropriately respond to stressful conditions can mean the difference between life and death. The toxic gas hydrogen sulfide (H2S) is a common workplace toxin that, at low doses, can protect against hypoxic damage in mammals and extend lifespan in nematodes. However, the enduring implications of exposure to H2S are largely unknown. In my dissertation research, I discovered that the response to H2S in the nematode C. elegans results in long-term and stable changes to cellular physiology that helps protect the animal in an ever-changing environment. Utilizing a new method that we developed for reliable and reproducible delivery of gases at defined concentrations, I discovered that H2S protects against hypoxia-induced disruption of proteostasis. Excitingly, treatment with H2S after hypoxic injury was still effective in reestablishing proteostasis, highlighting new potential for H2S as a therapy after ischemia reperfusion injuries. One strategy that animals use to survive in a changing environment is to predict the onset and pre-emptively respond to stressful conditions based on prior life experiences. There is emerging evidence that this strategy, known as cellular bookmarking, is established through changes to the epigenetic landscape. I discovered that the response to low levels of H2S forms a cellular bookmark that is maintained through development and protects against otherwise lethal doses of H2S later in life. A network of histone modifiers and chromatin remodeling complexes are required for the maintenance of a bookmark of H2S. In the future, these two uniquely tractable models can be leveraged to define mechanisms that allow animals to code changes of environmental conditions into chromatin modifications in a tightly controlled manner. I propose that these coded changes will help to explain, at least partially, differences in sensitivity between individuals to drugs, stress, and even aging. Advisors/Committee Members: Miller, Dana L (advisor).

Subjects/Keywords: bookmark; C. elegans; epigenetics; H3K4me; hydrogen sulfide; SWI/SNF; Cellular biology; Biochemistry; Molecular biology; molecular and cellular biology

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

APA (6^th Edition):

Fawcett, E. M. (2015). A beneficial toxin: The response to hydrogen sulfide improves survival in a changing environment. (Doctoral Dissertation). University of Washington. Retrieved from http://hdl.handle.net/1773/34061

Chicago Manual of Style (16^th Edition):

Fawcett, Emily Marie. “A beneficial toxin: The response to hydrogen sulfide improves survival in a changing environment.” 2015. Doctoral Dissertation, University of Washington. Accessed January 17, 2021. http://hdl.handle.net/1773/34061.

MLA Handbook (7^th Edition):

Fawcett, Emily Marie. “A beneficial toxin: The response to hydrogen sulfide improves survival in a changing environment.” 2015. Web. 17 Jan 2021.

Vancouver:

Fawcett EM. A beneficial toxin: The response to hydrogen sulfide improves survival in a changing environment. [Internet] [Doctoral dissertation]. University of Washington; 2015. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/1773/34061.

Council of Science Editors:

Fawcett EM. A beneficial toxin: The response to hydrogen sulfide improves survival in a changing environment. [Doctoral Dissertation]. University of Washington; 2015. Available from: http://hdl.handle.net/1773/34061

University of Western Ontario

26. Nixon, Kevin CJ. Mushroom body-specific gene regulation by the SWI/SNF chromatin remodeling complex.

Degree: 2020, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/6818

► Over the lifetime of an organism, neurons must establish, remodel, and maintain precise connections in order to form neural circuits that are required for proper… (more)

Subjects/Keywords: Drosophila; SWI/SNF complex; mushroom body; neurodevelopment; chromatin remodeling; epigenetics; Bioinformatics; Biology; Developmental Biology; Genetics; Molecular and Cellular Neuroscience

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

APA (6^th Edition):

Nixon, K. C. (2020). Mushroom body-specific gene regulation by the SWI/SNF chromatin remodeling complex. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/6818

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):

Nixon, Kevin CJ. “Mushroom body-specific gene regulation by the SWI/SNF chromatin remodeling complex.” 2020. Thesis, University of Western Ontario. Accessed January 17, 2021. https://ir.lib.uwo.ca/etd/6818.

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

MLA Handbook (7^th Edition):

Nixon, Kevin CJ. “Mushroom body-specific gene regulation by the SWI/SNF chromatin remodeling complex.” 2020. Web. 17 Jan 2021.

Vancouver:

Nixon KC. Mushroom body-specific gene regulation by the SWI/SNF chromatin remodeling complex. [Internet] [Thesis]. University of Western Ontario; 2020. [cited 2021 Jan 17]. Available from: https://ir.lib.uwo.ca/etd/6818.

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

Council of Science Editors:

Nixon KC. Mushroom body-specific gene regulation by the SWI/SNF chromatin remodeling complex. [Thesis]. University of Western Ontario; 2020. Available from: https://ir.lib.uwo.ca/etd/6818

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

University of Western Ontario

27. Stone, Max H. Regulation of Learning and Memory by the Drosophila melanogaster SWI/SNF complex.

Degree: 2017, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/4753

► The SWI/SNF complex is a highly-conserved ATP-dependent chromatin remodelling complex that is important in the etiology of intellectual disability (ID). I systematically investigated the overall… (more)

Subjects/Keywords: Drosophila melanogaster; SWI/SNF complex; learning and memory; courtship conditioning; epigenetics; intellectual disability; Biology; Life Sciences

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APA (6^th Edition):

Stone, M. H. (2017). Regulation of Learning and Memory by the Drosophila melanogaster SWI/SNF complex. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/4753

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):

Stone, Max H. “Regulation of Learning and Memory by the Drosophila melanogaster SWI/SNF complex.” 2017. Thesis, University of Western Ontario. Accessed January 17, 2021. https://ir.lib.uwo.ca/etd/4753.

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

MLA Handbook (7^th Edition):

Stone, Max H. “Regulation of Learning and Memory by the Drosophila melanogaster SWI/SNF complex.” 2017. Web. 17 Jan 2021.

Vancouver:

Stone MH. Regulation of Learning and Memory by the Drosophila melanogaster SWI/SNF complex. [Internet] [Thesis]. University of Western Ontario; 2017. [cited 2021 Jan 17]. Available from: https://ir.lib.uwo.ca/etd/4753.

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

Council of Science Editors:

Stone MH. Regulation of Learning and Memory by the Drosophila melanogaster SWI/SNF complex. [Thesis]. University of Western Ontario; 2017. Available from: https://ir.lib.uwo.ca/etd/4753

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

28. FONG HEI TUNG. LDB-1 AND SWI/SNF CHROMATIN REMODELING COMPLEX PARTICIPATE IN THE TRANSCRIPTIONAL ACTIVATION BY C. ELEGANS BLIMP1/PRDM1.

Degree: 2019, National University of Singapore

URL: https://scholarbank.nus.edu.sg/handle/10635/154990

Subjects/Keywords: LDB-1; SWI/SNF; BLIMP1; PRDM1; C. elegans; transcription

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

APA (6^th Edition):

TUNG, F. H. (2019). LDB-1 AND SWI/SNF CHROMATIN REMODELING COMPLEX PARTICIPATE IN THE TRANSCRIPTIONAL ACTIVATION BY C. ELEGANS BLIMP1/PRDM1. (Thesis). National University of Singapore. Retrieved from https://scholarbank.nus.edu.sg/handle/10635/154990

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):

TUNG, FONG HEI. “LDB-1 AND SWI/SNF CHROMATIN REMODELING COMPLEX PARTICIPATE IN THE TRANSCRIPTIONAL ACTIVATION BY C. ELEGANS BLIMP1/PRDM1.” 2019. Thesis, National University of Singapore. Accessed January 17, 2021. https://scholarbank.nus.edu.sg/handle/10635/154990.

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

MLA Handbook (7^th Edition):

TUNG, FONG HEI. “LDB-1 AND SWI/SNF CHROMATIN REMODELING COMPLEX PARTICIPATE IN THE TRANSCRIPTIONAL ACTIVATION BY C. ELEGANS BLIMP1/PRDM1.” 2019. Web. 17 Jan 2021.

Vancouver:

TUNG FH. LDB-1 AND SWI/SNF CHROMATIN REMODELING COMPLEX PARTICIPATE IN THE TRANSCRIPTIONAL ACTIVATION BY C. ELEGANS BLIMP1/PRDM1. [Internet] [Thesis]. National University of Singapore; 2019. [cited 2021 Jan 17]. Available from: https://scholarbank.nus.edu.sg/handle/10635/154990.

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

Council of Science Editors:

TUNG FH. LDB-1 AND SWI/SNF CHROMATIN REMODELING COMPLEX PARTICIPATE IN THE TRANSCRIPTIONAL ACTIVATION BY C. ELEGANS BLIMP1/PRDM1. [Thesis]. National University of Singapore; 2019. Available from: https://scholarbank.nus.edu.sg/handle/10635/154990

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

29. LEE PEI. THE STUDY OF THE EFFECTS OF A CHANGE IN THE EXPRESSION OF MIXED LINEAGE LEUKEMIA 5 ON TRANSCRIPTION REGULATION.

Degree: 2012, National University of Singapore

URL: http://scholarbank.nus.edu.sg/handle/10635/32363

Subjects/Keywords: MLL5; SC35; RNAPII; transcription; splicing; SWI/SNF

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

APA (6^th Edition):

PEI, L. (2012). THE STUDY OF THE EFFECTS OF A CHANGE IN THE EXPRESSION OF MIXED LINEAGE LEUKEMIA 5 ON TRANSCRIPTION REGULATION. (Thesis). National University of Singapore. Retrieved from http://scholarbank.nus.edu.sg/handle/10635/32363

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):

PEI, LEE. “THE STUDY OF THE EFFECTS OF A CHANGE IN THE EXPRESSION OF MIXED LINEAGE LEUKEMIA 5 ON TRANSCRIPTION REGULATION.” 2012. Thesis, National University of Singapore. Accessed January 17, 2021. http://scholarbank.nus.edu.sg/handle/10635/32363.

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

MLA Handbook (7^th Edition):

PEI, LEE. “THE STUDY OF THE EFFECTS OF A CHANGE IN THE EXPRESSION OF MIXED LINEAGE LEUKEMIA 5 ON TRANSCRIPTION REGULATION.” 2012. Web. 17 Jan 2021.

Vancouver:

PEI L. THE STUDY OF THE EFFECTS OF A CHANGE IN THE EXPRESSION OF MIXED LINEAGE LEUKEMIA 5 ON TRANSCRIPTION REGULATION. [Internet] [Thesis]. National University of Singapore; 2012. [cited 2021 Jan 17]. Available from: http://scholarbank.nus.edu.sg/handle/10635/32363.

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

Council of Science Editors:

PEI L. THE STUDY OF THE EFFECTS OF A CHANGE IN THE EXPRESSION OF MIXED LINEAGE LEUKEMIA 5 ON TRANSCRIPTION REGULATION. [Thesis]. National University of Singapore; 2012. Available from: http://scholarbank.nus.edu.sg/handle/10635/32363

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

Kyoto University

30. Tsuda, Motoyuki. The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis .

Degree: 2019, Kyoto University

URL: http://hdl.handle.net/2433/242378

Subjects/Keywords: BRG1; SWI/SNF; pancreatic cancer; PanIN; SOX9

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

APA (6^th Edition):

Tsuda, M. (2019). The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis . (Thesis). Kyoto University. Retrieved from http://hdl.handle.net/2433/242378

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):

Tsuda, Motoyuki. “The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis .” 2019. Thesis, Kyoto University. Accessed January 17, 2021. http://hdl.handle.net/2433/242378.

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

MLA Handbook (7^th Edition):

Tsuda, Motoyuki. “The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis .” 2019. Web. 17 Jan 2021.

Vancouver:

Tsuda M. The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis . [Internet] [Thesis]. Kyoto University; 2019. [cited 2021 Jan 17]. Available from: http://hdl.handle.net/2433/242378.

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

Council of Science Editors:

Tsuda M. The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis . [Thesis]. Kyoto University; 2019. Available from: http://hdl.handle.net/2433/242378

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

Open Access Theses and Dissertations