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You searched for +publisher:"Rutgers University" +contributor:("Bunting, Samuel"). Showing records 1 – 7 of 7 total matches.

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Rutgers University

1. Mendez-Rivera, Letzibeth, 1990-. The Slx5 paradox: expression of a sumo-targeted ubiquitin ligase generates toxic poly-sumo chains in yeast.

Degree: MS, Biochemistry, 2015, Rutgers University

 Defects in DNA repair are associated with a variety of human diseases, but the pathways that regulate DNA repair are poorly understood. Protein modification by… (more)

Subjects/Keywords: Proteins – Synthesis; DNA repair

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APA (6th Edition):

Mendez-Rivera, Letzibeth, 1. (2015). The Slx5 paradox: expression of a sumo-targeted ubiquitin ligase generates toxic poly-sumo chains in yeast. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/46394/

Chicago Manual of Style (16th Edition):

Mendez-Rivera, Letzibeth, 1990-. “The Slx5 paradox: expression of a sumo-targeted ubiquitin ligase generates toxic poly-sumo chains in yeast.” 2015. Masters Thesis, Rutgers University. Accessed April 13, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/46394/.

MLA Handbook (7th Edition):

Mendez-Rivera, Letzibeth, 1990-. “The Slx5 paradox: expression of a sumo-targeted ubiquitin ligase generates toxic poly-sumo chains in yeast.” 2015. Web. 13 Apr 2021.

Vancouver:

Mendez-Rivera, Letzibeth 1. The Slx5 paradox: expression of a sumo-targeted ubiquitin ligase generates toxic poly-sumo chains in yeast. [Internet] [Masters thesis]. Rutgers University; 2015. [cited 2021 Apr 13]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/46394/.

Council of Science Editors:

Mendez-Rivera, Letzibeth 1. The Slx5 paradox: expression of a sumo-targeted ubiquitin ligase generates toxic poly-sumo chains in yeast. [Masters Thesis]. Rutgers University; 2015. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/46394/


Rutgers University

2. Al Hamza, Ali, 1983-. The BRCA1 ring domain is essential for DNA damage repair and G2/M checkpoint activation.

Degree: MS, Physiology and Integrative Biology, 2014, Rutgers University

 The BRCA1 (breast cancer 1, early onset) tumor suppressor gene is involved in a variety of cellular pathways, and is an essential factor for normal… (more)

Subjects/Keywords: BRCA genes; Breast – Cancer – Research; DNA damage

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APA (6th Edition):

Al Hamza, Ali, 1. (2014). The BRCA1 ring domain is essential for DNA damage repair and G2/M checkpoint activation. (Masters Thesis). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/43983/

Chicago Manual of Style (16th Edition):

Al Hamza, Ali, 1983-. “The BRCA1 ring domain is essential for DNA damage repair and G2/M checkpoint activation.” 2014. Masters Thesis, Rutgers University. Accessed April 13, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/43983/.

MLA Handbook (7th Edition):

Al Hamza, Ali, 1983-. “The BRCA1 ring domain is essential for DNA damage repair and G2/M checkpoint activation.” 2014. Web. 13 Apr 2021.

Vancouver:

Al Hamza, Ali 1. The BRCA1 ring domain is essential for DNA damage repair and G2/M checkpoint activation. [Internet] [Masters thesis]. Rutgers University; 2014. [cited 2021 Apr 13]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/43983/.

Council of Science Editors:

Al Hamza, Ali 1. The BRCA1 ring domain is essential for DNA damage repair and G2/M checkpoint activation. [Masters Thesis]. Rutgers University; 2014. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/43983/


Rutgers University

3. Misenko, Sarah Marie, 1990-. 53BP1 regulates dna double-strand break repair in a mouse “BRCA-like” model by a non-resection mechanism.

Degree: PhD, Biochemistry, 2017, Rutgers University

DNA end resection is believed to be a step that influences the choice between the two major DNA double-strand break (DSB) repair pathways: homologous recombination… (more)

Subjects/Keywords: DNA damage; DNA repair

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APA (6th Edition):

Misenko, Sarah Marie, 1. (2017). 53BP1 regulates dna double-strand break repair in a mouse “BRCA-like” model by a non-resection mechanism. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/55597/

Chicago Manual of Style (16th Edition):

Misenko, Sarah Marie, 1990-. “53BP1 regulates dna double-strand break repair in a mouse “BRCA-like” model by a non-resection mechanism.” 2017. Doctoral Dissertation, Rutgers University. Accessed April 13, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/55597/.

MLA Handbook (7th Edition):

Misenko, Sarah Marie, 1990-. “53BP1 regulates dna double-strand break repair in a mouse “BRCA-like” model by a non-resection mechanism.” 2017. Web. 13 Apr 2021.

Vancouver:

Misenko, Sarah Marie 1. 53BP1 regulates dna double-strand break repair in a mouse “BRCA-like” model by a non-resection mechanism. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Apr 13]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55597/.

Council of Science Editors:

Misenko, Sarah Marie 1. 53BP1 regulates dna double-strand break repair in a mouse “BRCA-like” model by a non-resection mechanism. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55597/


Rutgers University

4. Patel, Dharm S., 1989-. The bloom syndrome protein, BLM, inhibits homologous recombination by disrupting RAD51 nucleoprotein filaments.

Degree: PhD, Biochemistry, 2017, Rutgers University

BRCA1-deficient cells exhibit increased genomic instability following DNA damaging treatments due to a defect in the homologous recombination (HR) DNA repair pathway. Here, we show… (more)

Subjects/Keywords: DNA repair; BRCA genes

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APA (6th Edition):

Patel, Dharm S., 1. (2017). The bloom syndrome protein, BLM, inhibits homologous recombination by disrupting RAD51 nucleoprotein filaments. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/55608/

Chicago Manual of Style (16th Edition):

Patel, Dharm S., 1989-. “The bloom syndrome protein, BLM, inhibits homologous recombination by disrupting RAD51 nucleoprotein filaments.” 2017. Doctoral Dissertation, Rutgers University. Accessed April 13, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/55608/.

MLA Handbook (7th Edition):

Patel, Dharm S., 1989-. “The bloom syndrome protein, BLM, inhibits homologous recombination by disrupting RAD51 nucleoprotein filaments.” 2017. Web. 13 Apr 2021.

Vancouver:

Patel, Dharm S. 1. The bloom syndrome protein, BLM, inhibits homologous recombination by disrupting RAD51 nucleoprotein filaments. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Apr 13]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55608/.

Council of Science Editors:

Patel, Dharm S. 1. The bloom syndrome protein, BLM, inhibits homologous recombination by disrupting RAD51 nucleoprotein filaments. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/55608/


Rutgers University

5. FENG, XING, 1987-. Roles of SETD4 in radiation sensitivity and tumorigenesis.

Degree: PhD, Pharmacology, Cellular and Molecular, 2018, Rutgers University

The SET domain protein methyltransferases play a critical role in histone modifications and global epigenetic regulations. Recent evidence suggests that some SET domain proteins may… (more)

Subjects/Keywords: Cancer – Gene therapy

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APA (6th Edition):

FENG, XING, 1. (2018). Roles of SETD4 in radiation sensitivity and tumorigenesis. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/59084/

Chicago Manual of Style (16th Edition):

FENG, XING, 1987-. “Roles of SETD4 in radiation sensitivity and tumorigenesis.” 2018. Doctoral Dissertation, Rutgers University. Accessed April 13, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/59084/.

MLA Handbook (7th Edition):

FENG, XING, 1987-. “Roles of SETD4 in radiation sensitivity and tumorigenesis.” 2018. Web. 13 Apr 2021.

Vancouver:

FENG, XING 1. Roles of SETD4 in radiation sensitivity and tumorigenesis. [Internet] [Doctoral dissertation]. Rutgers University; 2018. [cited 2021 Apr 13]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/59084/.

Council of Science Editors:

FENG, XING 1. Roles of SETD4 in radiation sensitivity and tumorigenesis. [Doctoral Dissertation]. Rutgers University; 2018. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/59084/


Rutgers University

6. Foo, Tzeh Keong, 1989-. BRCA1-PALB2 interaction and its roles in maintenance of genome stability and suppression of cancer development.

Degree: PhD, Pharmacology, Cellular and Molecular, 2019, Rutgers University

 DDR is often considered as a critical barrier during tumor initiation with most pre-malignant cells accumulate endogenous DNA damage before acquiring additional genetic alterations that… (more)

Subjects/Keywords: BRCA genes

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APA (6th Edition):

Foo, Tzeh Keong, 1. (2019). BRCA1-PALB2 interaction and its roles in maintenance of genome stability and suppression of cancer development. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/60154/

Chicago Manual of Style (16th Edition):

Foo, Tzeh Keong, 1989-. “BRCA1-PALB2 interaction and its roles in maintenance of genome stability and suppression of cancer development.” 2019. Doctoral Dissertation, Rutgers University. Accessed April 13, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/60154/.

MLA Handbook (7th Edition):

Foo, Tzeh Keong, 1989-. “BRCA1-PALB2 interaction and its roles in maintenance of genome stability and suppression of cancer development.” 2019. Web. 13 Apr 2021.

Vancouver:

Foo, Tzeh Keong 1. BRCA1-PALB2 interaction and its roles in maintenance of genome stability and suppression of cancer development. [Internet] [Doctoral dissertation]. Rutgers University; 2019. [cited 2021 Apr 13]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60154/.

Council of Science Editors:

Foo, Tzeh Keong 1. BRCA1-PALB2 interaction and its roles in maintenance of genome stability and suppression of cancer development. [Doctoral Dissertation]. Rutgers University; 2019. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/60154/

7. Mahdi, Amar Hekmat, 1977-. Understanding the role of the PALB2-BRCA1 interaction in tumor suppression.

Degree: PhD, Physiology and Integrative Biology, 2017, Rutgers University

 Homologous recombination (HR) is the only error-free pathway for the repair of DNA double strand breaks (DSBs). BRCA1 and BRCA2, the two major breast cancer… (more)

Subjects/Keywords: Cancer – Prevention; Breast – Cancer

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APA (6th Edition):

Mahdi, Amar Hekmat, 1. (2017). Understanding the role of the PALB2-BRCA1 interaction in tumor suppression. (Doctoral Dissertation). Rutgers University. Retrieved from https://rucore.libraries.rutgers.edu/rutgers-lib/53735/

Chicago Manual of Style (16th Edition):

Mahdi, Amar Hekmat, 1977-. “Understanding the role of the PALB2-BRCA1 interaction in tumor suppression.” 2017. Doctoral Dissertation, Rutgers University. Accessed April 13, 2021. https://rucore.libraries.rutgers.edu/rutgers-lib/53735/.

MLA Handbook (7th Edition):

Mahdi, Amar Hekmat, 1977-. “Understanding the role of the PALB2-BRCA1 interaction in tumor suppression.” 2017. Web. 13 Apr 2021.

Vancouver:

Mahdi, Amar Hekmat 1. Understanding the role of the PALB2-BRCA1 interaction in tumor suppression. [Internet] [Doctoral dissertation]. Rutgers University; 2017. [cited 2021 Apr 13]. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/53735/.

Council of Science Editors:

Mahdi, Amar Hekmat 1. Understanding the role of the PALB2-BRCA1 interaction in tumor suppression. [Doctoral Dissertation]. Rutgers University; 2017. Available from: https://rucore.libraries.rutgers.edu/rutgers-lib/53735/

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