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You searched for subject:(Replication stress). Showing records 1 – 30 of 61 total matches.

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Vanderbilt University

1. Badu-Nkansah, Akosua Agyeman. Mechanisms of DNA Translocases in the Repair of Damaged Replication Forks.

Degree: PhD, Biochemistry, 2016, Vanderbilt University

 Genomic replication is a highly challenging task. The DNA replication machinery must precisely duplicate billions of base pairs while tolerating a multitude of obstacles including… (more)

Subjects/Keywords: DNA Repair; Replication Stress; Replication Forks; DNA Replication; DNA Damage

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APA (6th Edition):

Badu-Nkansah, A. A. (2016). Mechanisms of DNA Translocases in the Repair of Damaged Replication Forks. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-07192016-131516/ ;

Chicago Manual of Style (16th Edition):

Badu-Nkansah, Akosua Agyeman. “Mechanisms of DNA Translocases in the Repair of Damaged Replication Forks.” 2016. Doctoral Dissertation, Vanderbilt University. Accessed December 15, 2019. http://etd.library.vanderbilt.edu/available/etd-07192016-131516/ ;.

MLA Handbook (7th Edition):

Badu-Nkansah, Akosua Agyeman. “Mechanisms of DNA Translocases in the Repair of Damaged Replication Forks.” 2016. Web. 15 Dec 2019.

Vancouver:

Badu-Nkansah AA. Mechanisms of DNA Translocases in the Repair of Damaged Replication Forks. [Internet] [Doctoral dissertation]. Vanderbilt University; 2016. [cited 2019 Dec 15]. Available from: http://etd.library.vanderbilt.edu/available/etd-07192016-131516/ ;.

Council of Science Editors:

Badu-Nkansah AA. Mechanisms of DNA Translocases in the Repair of Damaged Replication Forks. [Doctoral Dissertation]. Vanderbilt University; 2016. Available from: http://etd.library.vanderbilt.edu/available/etd-07192016-131516/ ;


Vanderbilt University

2. Guler, Gulfem Dilek. Human DNA helicase B in replication fork surveillance and replication stress recovery.

Degree: PhD, Biological Sciences, 2012, Vanderbilt University

 Correct and faithful genome duplication is crucial for preserving genomic integrity. Genome duplication is, therefore, highly regulated through a complex network of proteins that accomplish… (more)

Subjects/Keywords: Replication protein A; RPA; DNA helicase; DNA replication; DNA repair; replication stress; HelB; HDHB

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APA (6th Edition):

Guler, G. D. (2012). Human DNA helicase B in replication fork surveillance and replication stress recovery. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu//available/etd-12292011-192757/ ;

Chicago Manual of Style (16th Edition):

Guler, Gulfem Dilek. “Human DNA helicase B in replication fork surveillance and replication stress recovery.” 2012. Doctoral Dissertation, Vanderbilt University. Accessed December 15, 2019. http://etd.library.vanderbilt.edu//available/etd-12292011-192757/ ;.

MLA Handbook (7th Edition):

Guler, Gulfem Dilek. “Human DNA helicase B in replication fork surveillance and replication stress recovery.” 2012. Web. 15 Dec 2019.

Vancouver:

Guler GD. Human DNA helicase B in replication fork surveillance and replication stress recovery. [Internet] [Doctoral dissertation]. Vanderbilt University; 2012. [cited 2019 Dec 15]. Available from: http://etd.library.vanderbilt.edu//available/etd-12292011-192757/ ;.

Council of Science Editors:

Guler GD. Human DNA helicase B in replication fork surveillance and replication stress recovery. [Doctoral Dissertation]. Vanderbilt University; 2012. Available from: http://etd.library.vanderbilt.edu//available/etd-12292011-192757/ ;

3. R. Choudhary. MECHANISMS CONTROLLING THE INTEGRITY OF CONVERGING FORKS DURING REPLICATION TERMINATION.

Degree: 2018, Università degli Studi di Milano

 During S phase, natural fork pausing elements including replication termination zones (TERs) and transcribed genes, can easily lead to genotoxicity and chromosome fragility at fragile… (more)

Subjects/Keywords: Replication termination; replication; checkpoints; Top2; Genomic instability replication stress; Settore BIO/11 - Biologia Molecolare

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APA (6th Edition):

Choudhary, R. (2018). MECHANISMS CONTROLLING THE INTEGRITY OF CONVERGING FORKS DURING REPLICATION TERMINATION. (Thesis). Università degli Studi di Milano. Retrieved from http://hdl.handle.net/2434/559540

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

Chicago Manual of Style (16th Edition):

Choudhary, R.. “MECHANISMS CONTROLLING THE INTEGRITY OF CONVERGING FORKS DURING REPLICATION TERMINATION.” 2018. Thesis, Università degli Studi di Milano. Accessed December 15, 2019. http://hdl.handle.net/2434/559540.

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

MLA Handbook (7th Edition):

Choudhary, R.. “MECHANISMS CONTROLLING THE INTEGRITY OF CONVERGING FORKS DURING REPLICATION TERMINATION.” 2018. Web. 15 Dec 2019.

Vancouver:

Choudhary R. MECHANISMS CONTROLLING THE INTEGRITY OF CONVERGING FORKS DURING REPLICATION TERMINATION. [Internet] [Thesis]. Università degli Studi di Milano; 2018. [cited 2019 Dec 15]. Available from: http://hdl.handle.net/2434/559540.

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

Council of Science Editors:

Choudhary R. MECHANISMS CONTROLLING THE INTEGRITY OF CONVERGING FORKS DURING REPLICATION TERMINATION. [Thesis]. Università degli Studi di Milano; 2018. Available from: http://hdl.handle.net/2434/559540

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


Penn State University

4. Choe, Katherine Naeun. HUWE1 Interacts with PCNA to Alleviate Replication Stress.

Degree: PhD, Biomedical Sciences, 2016, Penn State University

 The integrity of the genome relies on the accurate and faithful duplication of genetic information from a parental cell to its progeny during each cellular… (more)

Subjects/Keywords: DNA replication; Genomic instability; H2AX; DNA Damage; HUWE1; PCNA; Replication stress

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APA (6th Edition):

Choe, K. N. (2016). HUWE1 Interacts with PCNA to Alleviate Replication Stress. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/13492kzc152

Chicago Manual of Style (16th Edition):

Choe, Katherine Naeun. “HUWE1 Interacts with PCNA to Alleviate Replication Stress.” 2016. Doctoral Dissertation, Penn State University. Accessed December 15, 2019. https://etda.libraries.psu.edu/catalog/13492kzc152.

MLA Handbook (7th Edition):

Choe, Katherine Naeun. “HUWE1 Interacts with PCNA to Alleviate Replication Stress.” 2016. Web. 15 Dec 2019.

Vancouver:

Choe KN. HUWE1 Interacts with PCNA to Alleviate Replication Stress. [Internet] [Doctoral dissertation]. Penn State University; 2016. [cited 2019 Dec 15]. Available from: https://etda.libraries.psu.edu/catalog/13492kzc152.

Council of Science Editors:

Choe KN. HUWE1 Interacts with PCNA to Alleviate Replication Stress. [Doctoral Dissertation]. Penn State University; 2016. Available from: https://etda.libraries.psu.edu/catalog/13492kzc152


Vanderbilt University

5. Luzwick, Jessica Whitney. Regulation of the ATR Pathway in the Replication Stress Response.

Degree: PhD, Biochemistry, 2016, Vanderbilt University

 Every cell divisions cycle, over 6.8 billion base pairs of DNA must be accurately replicated. To further complicate this process, the DNA is damaged at… (more)

Subjects/Keywords: replication; ATR inhibitor; DNA damage response; replication stress; ATR; ATRIP

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APA (6th Edition):

Luzwick, J. W. (2016). Regulation of the ATR Pathway in the Replication Stress Response. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-07152016-092619/ ;

Chicago Manual of Style (16th Edition):

Luzwick, Jessica Whitney. “Regulation of the ATR Pathway in the Replication Stress Response.” 2016. Doctoral Dissertation, Vanderbilt University. Accessed December 15, 2019. http://etd.library.vanderbilt.edu/available/etd-07152016-092619/ ;.

MLA Handbook (7th Edition):

Luzwick, Jessica Whitney. “Regulation of the ATR Pathway in the Replication Stress Response.” 2016. Web. 15 Dec 2019.

Vancouver:

Luzwick JW. Regulation of the ATR Pathway in the Replication Stress Response. [Internet] [Doctoral dissertation]. Vanderbilt University; 2016. [cited 2019 Dec 15]. Available from: http://etd.library.vanderbilt.edu/available/etd-07152016-092619/ ;.

Council of Science Editors:

Luzwick JW. Regulation of the ATR Pathway in the Replication Stress Response. [Doctoral Dissertation]. Vanderbilt University; 2016. Available from: http://etd.library.vanderbilt.edu/available/etd-07152016-092619/ ;


Boston University

6. Cox, Kelli. Replication stress and the alternative lengthening of telomeres pathway.

Degree: PhD, Pharmacology, 2016, Boston University

 In an effort to achieve replicative immortality, human cancer cells must avoid the constant telomere attrition that accompanies DNA replication. Cancer cells accomplish this by… (more)

Subjects/Keywords: Cellular biology; ALT; Cancer; Replication stress; Telomere

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APA (6th Edition):

Cox, K. (2016). Replication stress and the alternative lengthening of telomeres pathway. (Doctoral Dissertation). Boston University. Retrieved from http://hdl.handle.net/2144/16743

Chicago Manual of Style (16th Edition):

Cox, Kelli. “Replication stress and the alternative lengthening of telomeres pathway.” 2016. Doctoral Dissertation, Boston University. Accessed December 15, 2019. http://hdl.handle.net/2144/16743.

MLA Handbook (7th Edition):

Cox, Kelli. “Replication stress and the alternative lengthening of telomeres pathway.” 2016. Web. 15 Dec 2019.

Vancouver:

Cox K. Replication stress and the alternative lengthening of telomeres pathway. [Internet] [Doctoral dissertation]. Boston University; 2016. [cited 2019 Dec 15]. Available from: http://hdl.handle.net/2144/16743.

Council of Science Editors:

Cox K. Replication stress and the alternative lengthening of telomeres pathway. [Doctoral Dissertation]. Boston University; 2016. Available from: http://hdl.handle.net/2144/16743


Vanderbilt University

7. Robbins, Carol Bansbach. Identifying and defining the genome maintenance functions of SMARCAL1.

Degree: PhD, Biochemistry, 2012, Vanderbilt University

 In this dissertation I identify and define SWI/SNF, matrix-associated, actin-dependent regulator of chromatin, A-like 1 (SMARCAL1) as a genome maintenance protein. First, I introduce a… (more)

Subjects/Keywords: phosphorylation; DNA damage response; replication stress

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APA (6th Edition):

Robbins, C. B. (2012). Identifying and defining the genome maintenance functions of SMARCAL1. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-05252012-151148/ ;

Chicago Manual of Style (16th Edition):

Robbins, Carol Bansbach. “Identifying and defining the genome maintenance functions of SMARCAL1.” 2012. Doctoral Dissertation, Vanderbilt University. Accessed December 15, 2019. http://etd.library.vanderbilt.edu/available/etd-05252012-151148/ ;.

MLA Handbook (7th Edition):

Robbins, Carol Bansbach. “Identifying and defining the genome maintenance functions of SMARCAL1.” 2012. Web. 15 Dec 2019.

Vancouver:

Robbins CB. Identifying and defining the genome maintenance functions of SMARCAL1. [Internet] [Doctoral dissertation]. Vanderbilt University; 2012. [cited 2019 Dec 15]. Available from: http://etd.library.vanderbilt.edu/available/etd-05252012-151148/ ;.

Council of Science Editors:

Robbins CB. Identifying and defining the genome maintenance functions of SMARCAL1. [Doctoral Dissertation]. Vanderbilt University; 2012. Available from: http://etd.library.vanderbilt.edu/available/etd-05252012-151148/ ;


Cornell University

8. Bai, Gongshi. Tumor Suppression By Regulation Of Mini-Chromosome Maintenance Expression In Response To Dna Replication Stress .

Degree: 2016, Cornell University

 DNA replication is an essential process during cell proliferation, when genomic information is completely and precisely duplicated. DNA replication machinery (replisome) is responsible for the… (more)

Subjects/Keywords: DNA replication and replication stress; Mini-chromosome maintenance (MCM); Genome integrity maintenance

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APA (6th Edition):

Bai, G. (2016). Tumor Suppression By Regulation Of Mini-Chromosome Maintenance Expression In Response To Dna Replication Stress . (Thesis). Cornell University. Retrieved from http://hdl.handle.net/1813/44309

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

Chicago Manual of Style (16th Edition):

Bai, Gongshi. “Tumor Suppression By Regulation Of Mini-Chromosome Maintenance Expression In Response To Dna Replication Stress .” 2016. Thesis, Cornell University. Accessed December 15, 2019. http://hdl.handle.net/1813/44309.

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

MLA Handbook (7th Edition):

Bai, Gongshi. “Tumor Suppression By Regulation Of Mini-Chromosome Maintenance Expression In Response To Dna Replication Stress .” 2016. Web. 15 Dec 2019.

Vancouver:

Bai G. Tumor Suppression By Regulation Of Mini-Chromosome Maintenance Expression In Response To Dna Replication Stress . [Internet] [Thesis]. Cornell University; 2016. [cited 2019 Dec 15]. Available from: http://hdl.handle.net/1813/44309.

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

Council of Science Editors:

Bai G. Tumor Suppression By Regulation Of Mini-Chromosome Maintenance Expression In Response To Dna Replication Stress . [Thesis]. Cornell University; 2016. Available from: http://hdl.handle.net/1813/44309

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

9. S.E. Rossi. INTERPLAY BETWEEN THE DNA HELICASES PIF1 AND RRM3, THE NUCLEASE DNA2 AND THE CHECKPOINT PATHWAYS IN THE MAINTENANCE OF THE DNA REPLICATION FORK INTEGRITY.

Degree: 2017, Università degli Studi di Milano

 Eukaryotic cells have evolved the ATR/hCHK1, MEC1/RAD53 kinase-mediated signal transduction pathway, known as replication checkpoint, to protect and stabilize stalled replication forks in human cells… (more)

Subjects/Keywords: Replication stress; replication fork; checkpoint; Rad53; Rrm3; Pif1; Dna2; Settore BIO/11 - Biologia Molecolare

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APA (6th Edition):

Rossi, S. (2017). INTERPLAY BETWEEN THE DNA HELICASES PIF1 AND RRM3, THE NUCLEASE DNA2 AND THE CHECKPOINT PATHWAYS IN THE MAINTENANCE OF THE DNA REPLICATION FORK INTEGRITY. (Thesis). Università degli Studi di Milano. Retrieved from http://hdl.handle.net/2434/471797

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

Chicago Manual of Style (16th Edition):

Rossi, S.E.. “INTERPLAY BETWEEN THE DNA HELICASES PIF1 AND RRM3, THE NUCLEASE DNA2 AND THE CHECKPOINT PATHWAYS IN THE MAINTENANCE OF THE DNA REPLICATION FORK INTEGRITY.” 2017. Thesis, Università degli Studi di Milano. Accessed December 15, 2019. http://hdl.handle.net/2434/471797.

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

MLA Handbook (7th Edition):

Rossi, S.E.. “INTERPLAY BETWEEN THE DNA HELICASES PIF1 AND RRM3, THE NUCLEASE DNA2 AND THE CHECKPOINT PATHWAYS IN THE MAINTENANCE OF THE DNA REPLICATION FORK INTEGRITY.” 2017. Web. 15 Dec 2019.

Vancouver:

Rossi S. INTERPLAY BETWEEN THE DNA HELICASES PIF1 AND RRM3, THE NUCLEASE DNA2 AND THE CHECKPOINT PATHWAYS IN THE MAINTENANCE OF THE DNA REPLICATION FORK INTEGRITY. [Internet] [Thesis]. Università degli Studi di Milano; 2017. [cited 2019 Dec 15]. Available from: http://hdl.handle.net/2434/471797.

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

Council of Science Editors:

Rossi S. INTERPLAY BETWEEN THE DNA HELICASES PIF1 AND RRM3, THE NUCLEASE DNA2 AND THE CHECKPOINT PATHWAYS IN THE MAINTENANCE OF THE DNA REPLICATION FORK INTEGRITY. [Thesis]. Università degli Studi di Milano; 2017. Available from: http://hdl.handle.net/2434/471797

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


Vanderbilt University

10. Couch, Frank Benjamin IV. Regulation of Stalled Replication Forks by ATR.

Degree: PhD, Biochemistry, 2014, Vanderbilt University

 Errors during DNA replication lead to mutations which contribute to cancer development. To deal with these challenges, cells contain an innate machinery known as the… (more)

Subjects/Keywords: cell cycle checkpoint; SMARCAL1; replication stress; DNA replication; DNA damage response; ATR

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APA (6th Edition):

Couch, F. B. I. (2014). Regulation of Stalled Replication Forks by ATR. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu//available/etd-03252014-150303/ ;

Chicago Manual of Style (16th Edition):

Couch, Frank Benjamin IV. “Regulation of Stalled Replication Forks by ATR.” 2014. Doctoral Dissertation, Vanderbilt University. Accessed December 15, 2019. http://etd.library.vanderbilt.edu//available/etd-03252014-150303/ ;.

MLA Handbook (7th Edition):

Couch, Frank Benjamin IV. “Regulation of Stalled Replication Forks by ATR.” 2014. Web. 15 Dec 2019.

Vancouver:

Couch FBI. Regulation of Stalled Replication Forks by ATR. [Internet] [Doctoral dissertation]. Vanderbilt University; 2014. [cited 2019 Dec 15]. Available from: http://etd.library.vanderbilt.edu//available/etd-03252014-150303/ ;.

Council of Science Editors:

Couch FBI. Regulation of Stalled Replication Forks by ATR. [Doctoral Dissertation]. Vanderbilt University; 2014. Available from: http://etd.library.vanderbilt.edu//available/etd-03252014-150303/ ;


University of New Mexico

11. De Haro, Leyma. The role of metnase in DNA replication fork stress response and DNA damage.

Degree: Biomedical Sciences Graduate Program, 2009, University of New Mexico

 Metnase is a recently evolved human protein with methylase (SET) and nuclease domains that is widely expressed, especially in proliferating tissues. Metnase promotes plasmid and… (more)

Subjects/Keywords: Metnase; DNA replication stress; DNA damage; non-homologous end joining; hydroxyurea; replication fork

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APA (6th Edition):

De Haro, L. (2009). The role of metnase in DNA replication fork stress response and DNA damage. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/10

Chicago Manual of Style (16th Edition):

De Haro, Leyma. “The role of metnase in DNA replication fork stress response and DNA damage.” 2009. Doctoral Dissertation, University of New Mexico. Accessed December 15, 2019. https://digitalrepository.unm.edu/biom_etds/10.

MLA Handbook (7th Edition):

De Haro, Leyma. “The role of metnase in DNA replication fork stress response and DNA damage.” 2009. Web. 15 Dec 2019.

Vancouver:

De Haro L. The role of metnase in DNA replication fork stress response and DNA damage. [Internet] [Doctoral dissertation]. University of New Mexico; 2009. [cited 2019 Dec 15]. Available from: https://digitalrepository.unm.edu/biom_etds/10.

Council of Science Editors:

De Haro L. The role of metnase in DNA replication fork stress response and DNA damage. [Doctoral Dissertation]. University of New Mexico; 2009. Available from: https://digitalrepository.unm.edu/biom_etds/10

12. Ait Saada, Anissia. Mécanismes par lesquels la recombinaison homologue prévient les défauts mitotiques induits par le stress réplicatif : Mechanisms by which homologous recombination prevents mitotic defects in response to replication stress.

Degree: Docteur es, Sciences de la vie et de la santé, 2018, Paris Saclay

Des stress réplicatifs sont rencontrés à chaque phase S du cycle cellulaire et différents mécanismes permettent leur prise en charge. La recombinaison homologue (RH) tient… (more)

Subjects/Keywords: Recombinaison homologue; Réplication; Défauts mitotiques; Stress Réplicatif; Protection des fourches de réplication; Homologous recombination; Replication; Mitotic defects; Replication Stress; Fork Protection

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

APA (6th Edition):

Ait Saada, A. (2018). Mécanismes par lesquels la recombinaison homologue prévient les défauts mitotiques induits par le stress réplicatif : Mechanisms by which homologous recombination prevents mitotic defects in response to replication stress. (Doctoral Dissertation). Paris Saclay. Retrieved from http://www.theses.fr/2018SACLS167

Chicago Manual of Style (16th Edition):

Ait Saada, Anissia. “Mécanismes par lesquels la recombinaison homologue prévient les défauts mitotiques induits par le stress réplicatif : Mechanisms by which homologous recombination prevents mitotic defects in response to replication stress.” 2018. Doctoral Dissertation, Paris Saclay. Accessed December 15, 2019. http://www.theses.fr/2018SACLS167.

MLA Handbook (7th Edition):

Ait Saada, Anissia. “Mécanismes par lesquels la recombinaison homologue prévient les défauts mitotiques induits par le stress réplicatif : Mechanisms by which homologous recombination prevents mitotic defects in response to replication stress.” 2018. Web. 15 Dec 2019.

Vancouver:

Ait Saada A. Mécanismes par lesquels la recombinaison homologue prévient les défauts mitotiques induits par le stress réplicatif : Mechanisms by which homologous recombination prevents mitotic defects in response to replication stress. [Internet] [Doctoral dissertation]. Paris Saclay; 2018. [cited 2019 Dec 15]. Available from: http://www.theses.fr/2018SACLS167.

Council of Science Editors:

Ait Saada A. Mécanismes par lesquels la recombinaison homologue prévient les défauts mitotiques induits par le stress réplicatif : Mechanisms by which homologous recombination prevents mitotic defects in response to replication stress. [Doctoral Dissertation]. Paris Saclay; 2018. Available from: http://www.theses.fr/2018SACLS167

13. Guitton-Sert, Laure. Identification de nouveaux mécanismes de régulation temporelle des origines de réplication dans les cellules humaines : Identification of new mechanisms of temporal regulation of DNA replication origins in human cells.

Degree: Docteur es, Cancérologie, 2015, Université Toulouse III – Paul Sabatier

La duplication de l'ADN au cours de la phase S est initiée à partir de l'activation de plusieurs dizaines de milliers d'origines de réplication. La… (more)

Subjects/Keywords: Réplication de l'ADN; Timing de réplication; Origines de réplication; ADN polymérase Thêta; Stress réplicatif; DNA replication; Replication timing; DNA replication origins; DNA polymerase Theta; Replicative stress

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APA (6th Edition):

Guitton-Sert, L. (2015). Identification de nouveaux mécanismes de régulation temporelle des origines de réplication dans les cellules humaines : Identification of new mechanisms of temporal regulation of DNA replication origins in human cells. (Doctoral Dissertation). Université Toulouse III – Paul Sabatier. Retrieved from http://www.theses.fr/2015TOU30350

Chicago Manual of Style (16th Edition):

Guitton-Sert, Laure. “Identification de nouveaux mécanismes de régulation temporelle des origines de réplication dans les cellules humaines : Identification of new mechanisms of temporal regulation of DNA replication origins in human cells.” 2015. Doctoral Dissertation, Université Toulouse III – Paul Sabatier. Accessed December 15, 2019. http://www.theses.fr/2015TOU30350.

MLA Handbook (7th Edition):

Guitton-Sert, Laure. “Identification de nouveaux mécanismes de régulation temporelle des origines de réplication dans les cellules humaines : Identification of new mechanisms of temporal regulation of DNA replication origins in human cells.” 2015. Web. 15 Dec 2019.

Vancouver:

Guitton-Sert L. Identification de nouveaux mécanismes de régulation temporelle des origines de réplication dans les cellules humaines : Identification of new mechanisms of temporal regulation of DNA replication origins in human cells. [Internet] [Doctoral dissertation]. Université Toulouse III – Paul Sabatier; 2015. [cited 2019 Dec 15]. Available from: http://www.theses.fr/2015TOU30350.

Council of Science Editors:

Guitton-Sert L. Identification de nouveaux mécanismes de régulation temporelle des origines de réplication dans les cellules humaines : Identification of new mechanisms of temporal regulation of DNA replication origins in human cells. [Doctoral Dissertation]. Université Toulouse III – Paul Sabatier; 2015. Available from: http://www.theses.fr/2015TOU30350


Université Paris-Sud – Paris XI

14. Wilhelm, Therese. Homologous recombination protects against mitotic defects and unbalanced chromosome segregation caused by spontaneous replication stress : Recombinaison homologue protège contre les défauts de la mitose et la ségrégation des chromosomes déséquilibre causé par le stress de réplication spontanée.

Degree: Docteur es, Biologie, 2011, Université Paris-Sud – Paris XI

 Les cellules déficientes pour la recombinaison homologue (RH) présentent un ralentissement des fourches de réplication, un nombre aberrant de centrosomes et une aneuploïdie même en… (more)

Subjects/Keywords: RECOMBINAISON HOMOLOGUE; STRESS DE REPLICATION; DEFECTS DE CENTROSOME; DEFECTS DE SEGREGATION DE CHROMOSOME; STRESS OXIDATIVE; HOMOLOGOUS RECOMBINATION; REPLICATION STRESS; CENTROSOME DEFECTS; CHROMOSOME SEGREGATION DEFECTS; OXIDATIVE STRESS

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APA (6th Edition):

Wilhelm, T. (2011). Homologous recombination protects against mitotic defects and unbalanced chromosome segregation caused by spontaneous replication stress : Recombinaison homologue protège contre les défauts de la mitose et la ségrégation des chromosomes déséquilibre causé par le stress de réplication spontanée. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2011PA112059

Chicago Manual of Style (16th Edition):

Wilhelm, Therese. “Homologous recombination protects against mitotic defects and unbalanced chromosome segregation caused by spontaneous replication stress : Recombinaison homologue protège contre les défauts de la mitose et la ségrégation des chromosomes déséquilibre causé par le stress de réplication spontanée.” 2011. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed December 15, 2019. http://www.theses.fr/2011PA112059.

MLA Handbook (7th Edition):

Wilhelm, Therese. “Homologous recombination protects against mitotic defects and unbalanced chromosome segregation caused by spontaneous replication stress : Recombinaison homologue protège contre les défauts de la mitose et la ségrégation des chromosomes déséquilibre causé par le stress de réplication spontanée.” 2011. Web. 15 Dec 2019.

Vancouver:

Wilhelm T. Homologous recombination protects against mitotic defects and unbalanced chromosome segregation caused by spontaneous replication stress : Recombinaison homologue protège contre les défauts de la mitose et la ségrégation des chromosomes déséquilibre causé par le stress de réplication spontanée. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2011. [cited 2019 Dec 15]. Available from: http://www.theses.fr/2011PA112059.

Council of Science Editors:

Wilhelm T. Homologous recombination protects against mitotic defects and unbalanced chromosome segregation caused by spontaneous replication stress : Recombinaison homologue protège contre les défauts de la mitose et la ségrégation des chromosomes déséquilibre causé par le stress de réplication spontanée. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2011. Available from: http://www.theses.fr/2011PA112059


Universiteit Utrecht

15. Slaats, G.G.G. Looking beyond cilia in renal ciliopathies.

Degree: 2015, Universiteit Utrecht

 In this work, I have investigated the group of inherited diseases called “ciliopathies”, involving defects in proteins localizing to the cilium or associated complexes and… (more)

Subjects/Keywords: kidney; cilia; cysts; fibrosis; DNA damage; replication stress; ciliopathies; treatment

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APA (6th Edition):

Slaats, G. G. G. (2015). Looking beyond cilia in renal ciliopathies. (Doctoral Dissertation). Universiteit Utrecht. Retrieved from http://dspace.library.uu.nl:8080/handle/1874/318641

Chicago Manual of Style (16th Edition):

Slaats, G G G. “Looking beyond cilia in renal ciliopathies.” 2015. Doctoral Dissertation, Universiteit Utrecht. Accessed December 15, 2019. http://dspace.library.uu.nl:8080/handle/1874/318641.

MLA Handbook (7th Edition):

Slaats, G G G. “Looking beyond cilia in renal ciliopathies.” 2015. Web. 15 Dec 2019.

Vancouver:

Slaats GGG. Looking beyond cilia in renal ciliopathies. [Internet] [Doctoral dissertation]. Universiteit Utrecht; 2015. [cited 2019 Dec 15]. Available from: http://dspace.library.uu.nl:8080/handle/1874/318641.

Council of Science Editors:

Slaats GGG. Looking beyond cilia in renal ciliopathies. [Doctoral Dissertation]. Universiteit Utrecht; 2015. Available from: http://dspace.library.uu.nl:8080/handle/1874/318641

16. A. Ajazi. ATG6/BECLIN 1 COUPLES THE REPLICATION STRESS RESPONSE TO AMINO ACID METABOLISM.

Degree: 2017, Università degli Studi di Milano

 In the budding yeast Saccharomices Cerevisiae, Atg6 is a non-catalytic component of the phosphatidylinositol (PtdIns) kinase complex Vps34-Vps15-Atg6, which phosphorylates PtdIns to produce phosphatidylinositol 3-phosphate… (more)

Subjects/Keywords: DNA replication stress; metabolism; amino acids; Settore BIO/11 - Biologia Molecolare

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APA (6th Edition):

Ajazi, A. (2017). ATG6/BECLIN 1 COUPLES THE REPLICATION STRESS RESPONSE TO AMINO ACID METABOLISM. (Thesis). Università degli Studi di Milano. Retrieved from http://hdl.handle.net/2434/471447

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

Chicago Manual of Style (16th Edition):

Ajazi, A.. “ATG6/BECLIN 1 COUPLES THE REPLICATION STRESS RESPONSE TO AMINO ACID METABOLISM.” 2017. Thesis, Università degli Studi di Milano. Accessed December 15, 2019. http://hdl.handle.net/2434/471447.

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

MLA Handbook (7th Edition):

Ajazi, A.. “ATG6/BECLIN 1 COUPLES THE REPLICATION STRESS RESPONSE TO AMINO ACID METABOLISM.” 2017. Web. 15 Dec 2019.

Vancouver:

Ajazi A. ATG6/BECLIN 1 COUPLES THE REPLICATION STRESS RESPONSE TO AMINO ACID METABOLISM. [Internet] [Thesis]. Università degli Studi di Milano; 2017. [cited 2019 Dec 15]. Available from: http://hdl.handle.net/2434/471447.

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

Council of Science Editors:

Ajazi A. ATG6/BECLIN 1 COUPLES THE REPLICATION STRESS RESPONSE TO AMINO ACID METABOLISM. [Thesis]. Università degli Studi di Milano; 2017. Available from: http://hdl.handle.net/2434/471447

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


Vanderbilt University

17. Nam, Edward Adam. Phospho-regulation of the DNA Damage Response Kinase ATR.

Degree: PhD, Cancer Biology, 2011, Vanderbilt University

 Understanding how cells maintain genome integrity is necessary to gain insight into the pathology of cancer and to identify therapeutic targets and biomarkers. The DNA… (more)

Subjects/Keywords: replication stress; DNA-PK; ATR; ATM; DNA damage

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APA (6th Edition):

Nam, E. A. (2011). Phospho-regulation of the DNA Damage Response Kinase ATR. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-09032011-100056/ ;

Chicago Manual of Style (16th Edition):

Nam, Edward Adam. “Phospho-regulation of the DNA Damage Response Kinase ATR.” 2011. Doctoral Dissertation, Vanderbilt University. Accessed December 15, 2019. http://etd.library.vanderbilt.edu/available/etd-09032011-100056/ ;.

MLA Handbook (7th Edition):

Nam, Edward Adam. “Phospho-regulation of the DNA Damage Response Kinase ATR.” 2011. Web. 15 Dec 2019.

Vancouver:

Nam EA. Phospho-regulation of the DNA Damage Response Kinase ATR. [Internet] [Doctoral dissertation]. Vanderbilt University; 2011. [cited 2019 Dec 15]. Available from: http://etd.library.vanderbilt.edu/available/etd-09032011-100056/ ;.

Council of Science Editors:

Nam EA. Phospho-regulation of the DNA Damage Response Kinase ATR. [Doctoral Dissertation]. Vanderbilt University; 2011. Available from: http://etd.library.vanderbilt.edu/available/etd-09032011-100056/ ;


Vanderbilt University

18. Chavez, Diana Andrea. Replication Fork Remodeling by Helicase-Like Transcription Factor.

Degree: PhD, Biological Sciences, 2018, Vanderbilt University

 During DNA replication, a moving replication fork can encounter various sources of replication stress that can lead the moving fork to stall. Organisms have developed… (more)

Subjects/Keywords: DNA repair; fork remodeling; HIRAN; replication stress; HLTF; x-ray crystallography

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APA (6th Edition):

Chavez, D. A. (2018). Replication Fork Remodeling by Helicase-Like Transcription Factor. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-06252018-151636/ ;

Chicago Manual of Style (16th Edition):

Chavez, Diana Andrea. “Replication Fork Remodeling by Helicase-Like Transcription Factor.” 2018. Doctoral Dissertation, Vanderbilt University. Accessed December 15, 2019. http://etd.library.vanderbilt.edu/available/etd-06252018-151636/ ;.

MLA Handbook (7th Edition):

Chavez, Diana Andrea. “Replication Fork Remodeling by Helicase-Like Transcription Factor.” 2018. Web. 15 Dec 2019.

Vancouver:

Chavez DA. Replication Fork Remodeling by Helicase-Like Transcription Factor. [Internet] [Doctoral dissertation]. Vanderbilt University; 2018. [cited 2019 Dec 15]. Available from: http://etd.library.vanderbilt.edu/available/etd-06252018-151636/ ;.

Council of Science Editors:

Chavez DA. Replication Fork Remodeling by Helicase-Like Transcription Factor. [Doctoral Dissertation]. Vanderbilt University; 2018. Available from: http://etd.library.vanderbilt.edu/available/etd-06252018-151636/ ;


Vanderbilt University

19. Bass, Thomas Edwin. ETAA1 promotes genome stability through activation of ATR.

Degree: PhD, Biochemistry, 2018, Vanderbilt University

 The ATR kinase controls cell cycle transitions and the DNA damage response. Budding yeast contain three activators of Mec1ATR; however, only TOPBP1 is known to… (more)

Subjects/Keywords: ETAA1; TOPBP1; ATR activator; ATR; DNA damage; Replication stress

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APA (6th Edition):

Bass, T. E. (2018). ETAA1 promotes genome stability through activation of ATR. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-11162018-121040/ ;

Chicago Manual of Style (16th Edition):

Bass, Thomas Edwin. “ETAA1 promotes genome stability through activation of ATR.” 2018. Doctoral Dissertation, Vanderbilt University. Accessed December 15, 2019. http://etd.library.vanderbilt.edu/available/etd-11162018-121040/ ;.

MLA Handbook (7th Edition):

Bass, Thomas Edwin. “ETAA1 promotes genome stability through activation of ATR.” 2018. Web. 15 Dec 2019.

Vancouver:

Bass TE. ETAA1 promotes genome stability through activation of ATR. [Internet] [Doctoral dissertation]. Vanderbilt University; 2018. [cited 2019 Dec 15]. Available from: http://etd.library.vanderbilt.edu/available/etd-11162018-121040/ ;.

Council of Science Editors:

Bass TE. ETAA1 promotes genome stability through activation of ATR. [Doctoral Dissertation]. Vanderbilt University; 2018. Available from: http://etd.library.vanderbilt.edu/available/etd-11162018-121040/ ;


Université Paris-Sud – Paris XI

20. Bellini, Angela. Rôle des voies de réponse au stress dans le maintien de la stabilité génomique chez la levure Schizosaccharomyces pombe : Role of the stress response pathway in genome stability maintenance in Schizosaccharomyces pombe yeast.

Degree: Docteur es, Biologie cellulaire et moléculaire, 2012, Université Paris-Sud – Paris XI

Le génome est sans cesse menacé dans sa structure par des stress génotoxiques d’origine endogène (stress oxydant, blocage de la réplication…) ou exogène (irradiations, produits… (more)

Subjects/Keywords: Stress oxydant; Recombinaison; Réplication; MAPK; SAPK; Rad52; Oxidative stress; Recombination; Replication; MAPK; SAPK; Rad52

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

APA (6th Edition):

Bellini, A. (2012). Rôle des voies de réponse au stress dans le maintien de la stabilité génomique chez la levure Schizosaccharomyces pombe : Role of the stress response pathway in genome stability maintenance in Schizosaccharomyces pombe yeast. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2012PA11T048

Chicago Manual of Style (16th Edition):

Bellini, Angela. “Rôle des voies de réponse au stress dans le maintien de la stabilité génomique chez la levure Schizosaccharomyces pombe : Role of the stress response pathway in genome stability maintenance in Schizosaccharomyces pombe yeast.” 2012. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed December 15, 2019. http://www.theses.fr/2012PA11T048.

MLA Handbook (7th Edition):

Bellini, Angela. “Rôle des voies de réponse au stress dans le maintien de la stabilité génomique chez la levure Schizosaccharomyces pombe : Role of the stress response pathway in genome stability maintenance in Schizosaccharomyces pombe yeast.” 2012. Web. 15 Dec 2019.

Vancouver:

Bellini A. Rôle des voies de réponse au stress dans le maintien de la stabilité génomique chez la levure Schizosaccharomyces pombe : Role of the stress response pathway in genome stability maintenance in Schizosaccharomyces pombe yeast. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2012. [cited 2019 Dec 15]. Available from: http://www.theses.fr/2012PA11T048.

Council of Science Editors:

Bellini A. Rôle des voies de réponse au stress dans le maintien de la stabilité génomique chez la levure Schizosaccharomyces pombe : Role of the stress response pathway in genome stability maintenance in Schizosaccharomyces pombe yeast. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2012. Available from: http://www.theses.fr/2012PA11T048


Georgia State University

21. Liu, Hsuan. Further Analysis of the Interaction of the Cellular Protein TIAR with the 3' Terminal Stem-Loop of the West Nile Virus (WNV) Minus-Strand RNA.

Degree: PhD, Biology, 2013, Georgia State University

  Cellular T-cell intracellular antigen-1 related protein (TIAR) binds to the 3' terminal stem-loop of the West Nile virus minus-strand RNA [WNV 3'(-) SL RNA].… (more)

Subjects/Keywords: West Nile virus; Flavivirus; TIAR; TIA-1; Viral RNA replication; Stress granules

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APA (6th Edition):

Liu, H. (2013). Further Analysis of the Interaction of the Cellular Protein TIAR with the 3' Terminal Stem-Loop of the West Nile Virus (WNV) Minus-Strand RNA. (Doctoral Dissertation). Georgia State University. Retrieved from https://scholarworks.gsu.edu/biology_diss/138

Chicago Manual of Style (16th Edition):

Liu, Hsuan. “Further Analysis of the Interaction of the Cellular Protein TIAR with the 3' Terminal Stem-Loop of the West Nile Virus (WNV) Minus-Strand RNA.” 2013. Doctoral Dissertation, Georgia State University. Accessed December 15, 2019. https://scholarworks.gsu.edu/biology_diss/138.

MLA Handbook (7th Edition):

Liu, Hsuan. “Further Analysis of the Interaction of the Cellular Protein TIAR with the 3' Terminal Stem-Loop of the West Nile Virus (WNV) Minus-Strand RNA.” 2013. Web. 15 Dec 2019.

Vancouver:

Liu H. Further Analysis of the Interaction of the Cellular Protein TIAR with the 3' Terminal Stem-Loop of the West Nile Virus (WNV) Minus-Strand RNA. [Internet] [Doctoral dissertation]. Georgia State University; 2013. [cited 2019 Dec 15]. Available from: https://scholarworks.gsu.edu/biology_diss/138.

Council of Science Editors:

Liu H. Further Analysis of the Interaction of the Cellular Protein TIAR with the 3' Terminal Stem-Loop of the West Nile Virus (WNV) Minus-Strand RNA. [Doctoral Dissertation]. Georgia State University; 2013. Available from: https://scholarworks.gsu.edu/biology_diss/138


University of Sydney

22. Masamsetti, Venkata Sai Durga Pragathi. Replication stress induces mitotic cell death through cohesion fatigue and telomere deprotection .

Degree: 2018, University of Sydney

 Inducing DNA replication stress or targeting pathways that respond to replication stress is a prominent approach for chemotherapeutic cancer treatment. Lethal replication stress has previously… (more)

Subjects/Keywords: Replication stress; mitotic cell death; telomeres; sister chromatid cohesion; DNA damage response; apoptosis

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APA (6th Edition):

Masamsetti, V. S. D. P. (2018). Replication stress induces mitotic cell death through cohesion fatigue and telomere deprotection . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/18591

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

Chicago Manual of Style (16th Edition):

Masamsetti, Venkata Sai Durga Pragathi. “Replication stress induces mitotic cell death through cohesion fatigue and telomere deprotection .” 2018. Thesis, University of Sydney. Accessed December 15, 2019. http://hdl.handle.net/2123/18591.

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

MLA Handbook (7th Edition):

Masamsetti, Venkata Sai Durga Pragathi. “Replication stress induces mitotic cell death through cohesion fatigue and telomere deprotection .” 2018. Web. 15 Dec 2019.

Vancouver:

Masamsetti VSDP. Replication stress induces mitotic cell death through cohesion fatigue and telomere deprotection . [Internet] [Thesis]. University of Sydney; 2018. [cited 2019 Dec 15]. Available from: http://hdl.handle.net/2123/18591.

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

Council of Science Editors:

Masamsetti VSDP. Replication stress induces mitotic cell death through cohesion fatigue and telomere deprotection . [Thesis]. University of Sydney; 2018. Available from: http://hdl.handle.net/2123/18591

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


University of South Carolina

23. Brady, Kathryn. INVESTIGATION OF THE RESPONSE AND REPAIR OF REPLICATION.

Degree: MS, Pharmacology, Physiology and Neuroscience, 2014, University of South Carolina

  When a mammalian cell suffers DNA damage, DNA damage signaling responses and repair pathways are invoked. The phosphorylation of histone variant H2AX (γH2AX) and… (more)

Subjects/Keywords: Medicine and Health Sciences; Pharmacy and Pharmaceutical Sciences; H2AX; PLK1; pRPA; RAD51; Replication Stress

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APA (6th Edition):

Brady, K. (2014). INVESTIGATION OF THE RESPONSE AND REPAIR OF REPLICATION. (Masters Thesis). University of South Carolina. Retrieved from https://scholarcommons.sc.edu/etd/2776

Chicago Manual of Style (16th Edition):

Brady, Kathryn. “INVESTIGATION OF THE RESPONSE AND REPAIR OF REPLICATION.” 2014. Masters Thesis, University of South Carolina. Accessed December 15, 2019. https://scholarcommons.sc.edu/etd/2776.

MLA Handbook (7th Edition):

Brady, Kathryn. “INVESTIGATION OF THE RESPONSE AND REPAIR OF REPLICATION.” 2014. Web. 15 Dec 2019.

Vancouver:

Brady K. INVESTIGATION OF THE RESPONSE AND REPAIR OF REPLICATION. [Internet] [Masters thesis]. University of South Carolina; 2014. [cited 2019 Dec 15]. Available from: https://scholarcommons.sc.edu/etd/2776.

Council of Science Editors:

Brady K. INVESTIGATION OF THE RESPONSE AND REPAIR OF REPLICATION. [Masters Thesis]. University of South Carolina; 2014. Available from: https://scholarcommons.sc.edu/etd/2776


University of Pennsylvania

24. Balcerek, Joanna. The Role Of Lnk Adaptor Protein In Hematopoietic Stem Cell Genome Stability And Self-Renewal.

Degree: 2017, University of Pennsylvania

 Hematopoietic stem cells (HSCs) are rare cells that reside in bone marrow. HSCs function to give rise to all blood cells through proliferation and differentiation,… (more)

Subjects/Keywords: cytokine signaling; fanconi anemia; genome stability; hematopoietic stem cell; replication stress; self-renewal; Cell Biology

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APA (6th Edition):

Balcerek, J. (2017). The Role Of Lnk Adaptor Protein In Hematopoietic Stem Cell Genome Stability And Self-Renewal. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/2177

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

Chicago Manual of Style (16th Edition):

Balcerek, Joanna. “The Role Of Lnk Adaptor Protein In Hematopoietic Stem Cell Genome Stability And Self-Renewal.” 2017. Thesis, University of Pennsylvania. Accessed December 15, 2019. https://repository.upenn.edu/edissertations/2177.

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

MLA Handbook (7th Edition):

Balcerek, Joanna. “The Role Of Lnk Adaptor Protein In Hematopoietic Stem Cell Genome Stability And Self-Renewal.” 2017. Web. 15 Dec 2019.

Vancouver:

Balcerek J. The Role Of Lnk Adaptor Protein In Hematopoietic Stem Cell Genome Stability And Self-Renewal. [Internet] [Thesis]. University of Pennsylvania; 2017. [cited 2019 Dec 15]. Available from: https://repository.upenn.edu/edissertations/2177.

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

Council of Science Editors:

Balcerek J. The Role Of Lnk Adaptor Protein In Hematopoietic Stem Cell Genome Stability And Self-Renewal. [Thesis]. University of Pennsylvania; 2017. Available from: https://repository.upenn.edu/edissertations/2177

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


University of Pennsylvania

25. Shastri, Nishita Kalpendu. Defining Sites Of Replication Fork Collapse Caused By Atr Inhibition.

Degree: 2017, University of Pennsylvania

 DEFINING SITES OF REPLICATION FORK COLLAPSE CAUSED BY ATR INHIBITION Nishita K. Shastri Eric J. Brown Replication stress, characterized by stalling of DNA replication and… (more)

Subjects/Keywords: ATR; DNA damage; DNA replication stress; Fork collapse; RPA; Cell Biology; Molecular Biology; Pharmacology

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APA (6th Edition):

Shastri, N. K. (2017). Defining Sites Of Replication Fork Collapse Caused By Atr Inhibition. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/2581

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

Chicago Manual of Style (16th Edition):

Shastri, Nishita Kalpendu. “Defining Sites Of Replication Fork Collapse Caused By Atr Inhibition.” 2017. Thesis, University of Pennsylvania. Accessed December 15, 2019. https://repository.upenn.edu/edissertations/2581.

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

MLA Handbook (7th Edition):

Shastri, Nishita Kalpendu. “Defining Sites Of Replication Fork Collapse Caused By Atr Inhibition.” 2017. Web. 15 Dec 2019.

Vancouver:

Shastri NK. Defining Sites Of Replication Fork Collapse Caused By Atr Inhibition. [Internet] [Thesis]. University of Pennsylvania; 2017. [cited 2019 Dec 15]. Available from: https://repository.upenn.edu/edissertations/2581.

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

Council of Science Editors:

Shastri NK. Defining Sites Of Replication Fork Collapse Caused By Atr Inhibition. [Thesis]. University of Pennsylvania; 2017. Available from: https://repository.upenn.edu/edissertations/2581

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


University of California – San Francisco

26. Jay, Kyle Aaron. Phenotypes Occuring in Saccharomyces cerevisiae Early after Telomerase Inactivation.

Degree: Biochemistry and Molecular Biology, 2015, University of California – San Francisco

 Telomeres are DNA and protein complexes that cap the ends of linear chromosomes. These caps serve two primary functions: to buffer against the loss of… (more)

Subjects/Keywords: Biology; Molecular biology; Genetics; DNA Damage Response; Mother Cell Aging; Replication Stress; Telomerase; Telomere; TOR

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APA (6th Edition):

Jay, K. A. (2015). Phenotypes Occuring in Saccharomyces cerevisiae Early after Telomerase Inactivation. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/68q699zq

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

Chicago Manual of Style (16th Edition):

Jay, Kyle Aaron. “Phenotypes Occuring in Saccharomyces cerevisiae Early after Telomerase Inactivation.” 2015. Thesis, University of California – San Francisco. Accessed December 15, 2019. http://www.escholarship.org/uc/item/68q699zq.

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

MLA Handbook (7th Edition):

Jay, Kyle Aaron. “Phenotypes Occuring in Saccharomyces cerevisiae Early after Telomerase Inactivation.” 2015. Web. 15 Dec 2019.

Vancouver:

Jay KA. Phenotypes Occuring in Saccharomyces cerevisiae Early after Telomerase Inactivation. [Internet] [Thesis]. University of California – San Francisco; 2015. [cited 2019 Dec 15]. Available from: http://www.escholarship.org/uc/item/68q699zq.

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

Council of Science Editors:

Jay KA. Phenotypes Occuring in Saccharomyces cerevisiae Early after Telomerase Inactivation. [Thesis]. University of California – San Francisco; 2015. Available from: http://www.escholarship.org/uc/item/68q699zq

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


University of Michigan

27. Smak, Jordann. Cell Cycle-Specific Functions and Regulation of the DNA Nuclease SNM1B.

Degree: PhD, Cellular & Molecular Biology, 2019, University of Michigan

 DNA replication is a fundamental cellular process that ensures the accurate duplication and transmission of genetic information. The replication machinery is frequently challenged by endogenous… (more)

Subjects/Keywords: DNA Repair; DNA Replication Stress; SNM1B Nuclease; Molecular, Cellular and Developmental Biology; Science

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APA (6th Edition):

Smak, J. (2019). Cell Cycle-Specific Functions and Regulation of the DNA Nuclease SNM1B. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/149866

Chicago Manual of Style (16th Edition):

Smak, Jordann. “Cell Cycle-Specific Functions and Regulation of the DNA Nuclease SNM1B.” 2019. Doctoral Dissertation, University of Michigan. Accessed December 15, 2019. http://hdl.handle.net/2027.42/149866.

MLA Handbook (7th Edition):

Smak, Jordann. “Cell Cycle-Specific Functions and Regulation of the DNA Nuclease SNM1B.” 2019. Web. 15 Dec 2019.

Vancouver:

Smak J. Cell Cycle-Specific Functions and Regulation of the DNA Nuclease SNM1B. [Internet] [Doctoral dissertation]. University of Michigan; 2019. [cited 2019 Dec 15]. Available from: http://hdl.handle.net/2027.42/149866.

Council of Science Editors:

Smak J. Cell Cycle-Specific Functions and Regulation of the DNA Nuclease SNM1B. [Doctoral Dissertation]. University of Michigan; 2019. Available from: http://hdl.handle.net/2027.42/149866

28. Kalogeropoulou, Argyro. Διερεύνηση του μοριακού μηχανισμού δράσης της Geminin στα πρώιμα εμβρυϊκά βλαστικά νευρικά κύτταρα.

Degree: 2019, University of Patras; Πανεπιστήμιο Πατρών

 The cerebral cortex consists the outer layer of the mammalian brain and is one of the most complicated regions, characterised by excessive cell diversity. The… (more)

Subjects/Keywords: Geminin; Νευροεπιθηλιακά κύτταρα; Μικροκεφαλία; Αντιγραφικό στρες; Γονιδιωματική αστάθεια; Geminin; Neuroepithelium; Microcephaly; Replication stress; Genomic instability

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

APA (6th Edition):

Kalogeropoulou, A. (2019). Διερεύνηση του μοριακού μηχανισμού δράσης της Geminin στα πρώιμα εμβρυϊκά βλαστικά νευρικά κύτταρα. (Thesis). University of Patras; Πανεπιστήμιο Πατρών. Retrieved from http://hdl.handle.net/10442/hedi/46503

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

Chicago Manual of Style (16th Edition):

Kalogeropoulou, Argyro. “Διερεύνηση του μοριακού μηχανισμού δράσης της Geminin στα πρώιμα εμβρυϊκά βλαστικά νευρικά κύτταρα.” 2019. Thesis, University of Patras; Πανεπιστήμιο Πατρών. Accessed December 15, 2019. http://hdl.handle.net/10442/hedi/46503.

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

MLA Handbook (7th Edition):

Kalogeropoulou, Argyro. “Διερεύνηση του μοριακού μηχανισμού δράσης της Geminin στα πρώιμα εμβρυϊκά βλαστικά νευρικά κύτταρα.” 2019. Web. 15 Dec 2019.

Vancouver:

Kalogeropoulou A. Διερεύνηση του μοριακού μηχανισμού δράσης της Geminin στα πρώιμα εμβρυϊκά βλαστικά νευρικά κύτταρα. [Internet] [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2019. [cited 2019 Dec 15]. Available from: http://hdl.handle.net/10442/hedi/46503.

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

Council of Science Editors:

Kalogeropoulou A. Διερεύνηση του μοριακού μηχανισμού δράσης της Geminin στα πρώιμα εμβρυϊκά βλαστικά νευρικά κύτταρα. [Thesis]. University of Patras; Πανεπιστήμιο Πατρών; 2019. Available from: http://hdl.handle.net/10442/hedi/46503

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


Université Montpellier II

29. Hodroj, Dana. Du pore nucléaire à l'endommagement de l'ADN : l'aller et retour de Ddx19 médié par ATR pour résoudre des conflits entre la transcription et la réplication : From the nuclear pore to DNA damage : the ATR-mediated shuttling of Ddx19 to resolve transcription-replication conflicts.

Degree: Docteur es, Biologie Santé, 2014, Université Montpellier II

 Les cellules sont constamment exposées à des agents endommageant de l'ADN d'origine exogène, notamment les rayons ultraviolets, les irradiations γ, et l'exposition aux agents chimiques… (more)

Subjects/Keywords: Instabilité génomique; Stress réplicatif; Atr; ARN hélicase; Nucléopore; R-Loops; Genome instability; Replication stress; Atr; RNA helicase; Nucleopore; R-Loops

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

APA (6th Edition):

Hodroj, D. (2014). Du pore nucléaire à l'endommagement de l'ADN : l'aller et retour de Ddx19 médié par ATR pour résoudre des conflits entre la transcription et la réplication : From the nuclear pore to DNA damage : the ATR-mediated shuttling of Ddx19 to resolve transcription-replication conflicts. (Doctoral Dissertation). Université Montpellier II. Retrieved from http://www.theses.fr/2014MON20121

Chicago Manual of Style (16th Edition):

Hodroj, Dana. “Du pore nucléaire à l'endommagement de l'ADN : l'aller et retour de Ddx19 médié par ATR pour résoudre des conflits entre la transcription et la réplication : From the nuclear pore to DNA damage : the ATR-mediated shuttling of Ddx19 to resolve transcription-replication conflicts.” 2014. Doctoral Dissertation, Université Montpellier II. Accessed December 15, 2019. http://www.theses.fr/2014MON20121.

MLA Handbook (7th Edition):

Hodroj, Dana. “Du pore nucléaire à l'endommagement de l'ADN : l'aller et retour de Ddx19 médié par ATR pour résoudre des conflits entre la transcription et la réplication : From the nuclear pore to DNA damage : the ATR-mediated shuttling of Ddx19 to resolve transcription-replication conflicts.” 2014. Web. 15 Dec 2019.

Vancouver:

Hodroj D. Du pore nucléaire à l'endommagement de l'ADN : l'aller et retour de Ddx19 médié par ATR pour résoudre des conflits entre la transcription et la réplication : From the nuclear pore to DNA damage : the ATR-mediated shuttling of Ddx19 to resolve transcription-replication conflicts. [Internet] [Doctoral dissertation]. Université Montpellier II; 2014. [cited 2019 Dec 15]. Available from: http://www.theses.fr/2014MON20121.

Council of Science Editors:

Hodroj D. Du pore nucléaire à l'endommagement de l'ADN : l'aller et retour de Ddx19 médié par ATR pour résoudre des conflits entre la transcription et la réplication : From the nuclear pore to DNA damage : the ATR-mediated shuttling of Ddx19 to resolve transcription-replication conflicts. [Doctoral Dissertation]. Université Montpellier II; 2014. Available from: http://www.theses.fr/2014MON20121


Université Montpellier II

30. Poli, Jérôme. Dynamique de la réplication du génome et réponses cellulaires au stress réplicatif : Dynamics of DNA replication and cellular responses to replicative stress.

Degree: Docteur es, Biologie Santé, 2013, Université Montpellier II

L'environnement des organismes vivants est par définition fluctuant, toutes variations aléatoires du milieu de vie constituent un stress pour les cellules. Au fil de l'évolution,… (more)

Subjects/Keywords: Réplication; Dntp; Stress réplicatif; Dommage de l'ADN; ARN non codants; Mrn; Replication; Dntp; Replicative stress; DNA damage; Non coding RNA; Mrn

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

APA (6th Edition):

Poli, J. (2013). Dynamique de la réplication du génome et réponses cellulaires au stress réplicatif : Dynamics of DNA replication and cellular responses to replicative stress. (Doctoral Dissertation). Université Montpellier II. Retrieved from http://www.theses.fr/2013MON20233

Chicago Manual of Style (16th Edition):

Poli, Jérôme. “Dynamique de la réplication du génome et réponses cellulaires au stress réplicatif : Dynamics of DNA replication and cellular responses to replicative stress.” 2013. Doctoral Dissertation, Université Montpellier II. Accessed December 15, 2019. http://www.theses.fr/2013MON20233.

MLA Handbook (7th Edition):

Poli, Jérôme. “Dynamique de la réplication du génome et réponses cellulaires au stress réplicatif : Dynamics of DNA replication and cellular responses to replicative stress.” 2013. Web. 15 Dec 2019.

Vancouver:

Poli J. Dynamique de la réplication du génome et réponses cellulaires au stress réplicatif : Dynamics of DNA replication and cellular responses to replicative stress. [Internet] [Doctoral dissertation]. Université Montpellier II; 2013. [cited 2019 Dec 15]. Available from: http://www.theses.fr/2013MON20233.

Council of Science Editors:

Poli J. Dynamique de la réplication du génome et réponses cellulaires au stress réplicatif : Dynamics of DNA replication and cellular responses to replicative stress. [Doctoral Dissertation]. Université Montpellier II; 2013. Available from: http://www.theses.fr/2013MON20233

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