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You searched for +publisher:"Temple University" +contributor:("Liebermann, Dan A."). Showing records 1 – 16 of 16 total matches.

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Temple University

1. Dasgupta, Yashodhara. NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS.

Degree: PhD, 2014, Temple University

Biology

BCR-ABL1 results from t(9;22)(q34;q11) reciprocal translocation resulting in BCR-ABL1 kinase expression, initiating chronic myeloid leukemia in chronic phase (CML-CP). At the initial stages of… (more)

Subjects/Keywords: Biology

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APA (6th Edition):

Dasgupta, Y. (2014). NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,239008

Chicago Manual of Style (16th Edition):

Dasgupta, Yashodhara. “NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS.” 2014. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,239008.

MLA Handbook (7th Edition):

Dasgupta, Yashodhara. “NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS.” 2014. Web. 18 Nov 2019.

Vancouver:

Dasgupta Y. NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,239008.

Council of Science Editors:

Dasgupta Y. NORMAL ABL1 IS A TUMOR SUPPRESSOR AND THERAPEUTIC TARGET IN BCR-ABL1-POSITIVE LEUKEMIAS. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,239008


Temple University

2. Mukherjee, Kaushiki. Role Of Gadd45a In BCR-ABL and NRASD12 Driven Leukemia.

Degree: PhD, 2015, Temple University

Biochemistry

BCR-ABL is known as the most common translocation in the myeloproliferative (MPD) disorder chronic myelogenous leukemia (CML); it is the first leukemia to be… (more)

Subjects/Keywords: Oncology; Molecular biology; Cellular biology;

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APA (6th Edition):

Mukherjee, K. (2015). Role Of Gadd45a In BCR-ABL and NRASD12 Driven Leukemia. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,322334

Chicago Manual of Style (16th Edition):

Mukherjee, Kaushiki. “Role Of Gadd45a In BCR-ABL and NRASD12 Driven Leukemia.” 2015. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,322334.

MLA Handbook (7th Edition):

Mukherjee, Kaushiki. “Role Of Gadd45a In BCR-ABL and NRASD12 Driven Leukemia.” 2015. Web. 18 Nov 2019.

Vancouver:

Mukherjee K. Role Of Gadd45a In BCR-ABL and NRASD12 Driven Leukemia. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,322334.

Council of Science Editors:

Mukherjee K. Role Of Gadd45a In BCR-ABL and NRASD12 Driven Leukemia. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,322334


Temple University

3. Ramkumar, Poornima. Interaction of JLP with PLK1 recruits FoxK1 to form a ternary complex during mitosis.

Degree: PhD, 2015, Temple University

Molecular Biology and Genetics

JLP (JNK associated Leucine zipper protein) is a scaffolding protein that has been shown to interact with and activate the JNK/p38MAPK… (more)

Subjects/Keywords: Molecular biology; Biochemistry; Cellular biology;

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APA (6th Edition):

Ramkumar, P. (2015). Interaction of JLP with PLK1 recruits FoxK1 to form a ternary complex during mitosis. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,323815

Chicago Manual of Style (16th Edition):

Ramkumar, Poornima. “Interaction of JLP with PLK1 recruits FoxK1 to form a ternary complex during mitosis.” 2015. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,323815.

MLA Handbook (7th Edition):

Ramkumar, Poornima. “Interaction of JLP with PLK1 recruits FoxK1 to form a ternary complex during mitosis.” 2015. Web. 18 Nov 2019.

Vancouver:

Ramkumar P. Interaction of JLP with PLK1 recruits FoxK1 to form a ternary complex during mitosis. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,323815.

Council of Science Editors:

Ramkumar P. Interaction of JLP with PLK1 recruits FoxK1 to form a ternary complex during mitosis. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,323815


Temple University

4. Goldsmith, Zachariah G. Oncogenic Signaling Pathways Activated by Lysophosphatidic Acid (LPA) in Ovarian Carcinoma.

Degree: PhD, 2009, Temple University

Molecular Biology and Genetics

Ovarian cancer is currently the most fatal gynecologic cancer and the fifth leading cause of fatal cancer in women overall. As… (more)

Subjects/Keywords: Biology, Molecular; Health Sciences, Oncology; ERK; G alpha 12; JNK; LPA; lysophosphatidic acid; ovarian cancer

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APA (6th Edition):

Goldsmith, Z. G. (2009). Oncogenic Signaling Pathways Activated by Lysophosphatidic Acid (LPA) in Ovarian Carcinoma. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,34336

Chicago Manual of Style (16th Edition):

Goldsmith, Zachariah G. “Oncogenic Signaling Pathways Activated by Lysophosphatidic Acid (LPA) in Ovarian Carcinoma.” 2009. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,34336.

MLA Handbook (7th Edition):

Goldsmith, Zachariah G. “Oncogenic Signaling Pathways Activated by Lysophosphatidic Acid (LPA) in Ovarian Carcinoma.” 2009. Web. 18 Nov 2019.

Vancouver:

Goldsmith ZG. Oncogenic Signaling Pathways Activated by Lysophosphatidic Acid (LPA) in Ovarian Carcinoma. [Internet] [Doctoral dissertation]. Temple University; 2009. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,34336.

Council of Science Editors:

Goldsmith ZG. Oncogenic Signaling Pathways Activated by Lysophosphatidic Acid (LPA) in Ovarian Carcinoma. [Doctoral Dissertation]. Temple University; 2009. Available from: http://digital.library.temple.edu/u?/p245801coll10,34336


Temple University

5. Magimaidas, Andrew. The Role of the Stress Response Gene Gadd45b in Senescence.

Degree: PhD, 2015, Temple University

Molecular Biology and Genetics

The Gadd45 family of proteins (Gadd45a, Gadd45b, and Gadd45g) has been shown to act as stress sensors in response to various… (more)

Subjects/Keywords: Molecular biology; Genetics;

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APA (6th Edition):

Magimaidas, A. (2015). The Role of the Stress Response Gene Gadd45b in Senescence. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,376546

Chicago Manual of Style (16th Edition):

Magimaidas, Andrew. “The Role of the Stress Response Gene Gadd45b in Senescence.” 2015. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,376546.

MLA Handbook (7th Edition):

Magimaidas, Andrew. “The Role of the Stress Response Gene Gadd45b in Senescence.” 2015. Web. 18 Nov 2019.

Vancouver:

Magimaidas A. The Role of the Stress Response Gene Gadd45b in Senescence. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,376546.

Council of Science Editors:

Magimaidas A. The Role of the Stress Response Gene Gadd45b in Senescence. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,376546


Temple University

6. Mohamed-Hadley, Alisha. THE ROLE OF THE STRESS RESPONSE GENE GADD45A IN MODULATING MYC MEDIATED APOPTOSIS AND DIFFERENTIATION.

Degree: PhD, 2011, Temple University

Molecular Biology and Genetics

The Gadd45 family of proteins is known to play a central role as cellular stress sensors that modulate the response of… (more)

Subjects/Keywords: Molecular Biology; Apoptosis; Cytokine; Gadd45a; Myc; Myeloid cells

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APA (6th Edition):

Mohamed-Hadley, A. (2011). THE ROLE OF THE STRESS RESPONSE GENE GADD45A IN MODULATING MYC MEDIATED APOPTOSIS AND DIFFERENTIATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,126332

Chicago Manual of Style (16th Edition):

Mohamed-Hadley, Alisha. “THE ROLE OF THE STRESS RESPONSE GENE GADD45A IN MODULATING MYC MEDIATED APOPTOSIS AND DIFFERENTIATION.” 2011. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,126332.

MLA Handbook (7th Edition):

Mohamed-Hadley, Alisha. “THE ROLE OF THE STRESS RESPONSE GENE GADD45A IN MODULATING MYC MEDIATED APOPTOSIS AND DIFFERENTIATION.” 2011. Web. 18 Nov 2019.

Vancouver:

Mohamed-Hadley A. THE ROLE OF THE STRESS RESPONSE GENE GADD45A IN MODULATING MYC MEDIATED APOPTOSIS AND DIFFERENTIATION. [Internet] [Doctoral dissertation]. Temple University; 2011. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,126332.

Council of Science Editors:

Mohamed-Hadley A. THE ROLE OF THE STRESS RESPONSE GENE GADD45A IN MODULATING MYC MEDIATED APOPTOSIS AND DIFFERENTIATION. [Doctoral Dissertation]. Temple University; 2011. Available from: http://digital.library.temple.edu/u?/p245801coll10,126332


Temple University

7. Bolton, Elisabeth Spring. Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP.

Degree: PhD, 2013, Temple University

Microbiology and Immunology

In chronic myelogenous leukemia (CML), activation of BCR-ABL, the product of the bcr-abl chimeric gene, leads to constitutive activation of pathways that… (more)

Subjects/Keywords: Biology; Molecular biology; Immunology;

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APA (6th Edition):

Bolton, E. S. (2013). Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,234916

Chicago Manual of Style (16th Edition):

Bolton, Elisabeth Spring. “Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP.” 2013. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,234916.

MLA Handbook (7th Edition):

Bolton, Elisabeth Spring. “Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP.” 2013. Web. 18 Nov 2019.

Vancouver:

Bolton ES. Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP. [Internet] [Doctoral dissertation]. Temple University; 2013. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,234916.

Council of Science Editors:

Bolton ES. Genomic Instability Originates From Leukemia Stem Cells In a Mouse Model of CML-CP. [Doctoral Dissertation]. Temple University; 2013. Available from: http://digital.library.temple.edu/u?/p245801coll10,234916


Temple University

8. Padgaonkar, Amol. Discovery, Biological and Structural Characterization of ON108600, a Novel Kinase Inhibitor in Triple Negative Breast Cancer.

Degree: PhD, 2014, Temple University

Molecular Biology and Genetics

Selective killing of tumor cells requires the identification of drug targets critical to pathways that drive or support cancer progression. Protein… (more)

Subjects/Keywords: Molecular biology; Cellular biology; Oncology;

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APA (6th Edition):

Padgaonkar, A. (2014). Discovery, Biological and Structural Characterization of ON108600, a Novel Kinase Inhibitor in Triple Negative Breast Cancer. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,269327

Chicago Manual of Style (16th Edition):

Padgaonkar, Amol. “Discovery, Biological and Structural Characterization of ON108600, a Novel Kinase Inhibitor in Triple Negative Breast Cancer.” 2014. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,269327.

MLA Handbook (7th Edition):

Padgaonkar, Amol. “Discovery, Biological and Structural Characterization of ON108600, a Novel Kinase Inhibitor in Triple Negative Breast Cancer.” 2014. Web. 18 Nov 2019.

Vancouver:

Padgaonkar A. Discovery, Biological and Structural Characterization of ON108600, a Novel Kinase Inhibitor in Triple Negative Breast Cancer. [Internet] [Doctoral dissertation]. Temple University; 2014. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,269327.

Council of Science Editors:

Padgaonkar A. Discovery, Biological and Structural Characterization of ON108600, a Novel Kinase Inhibitor in Triple Negative Breast Cancer. [Doctoral Dissertation]. Temple University; 2014. Available from: http://digital.library.temple.edu/u?/p245801coll10,269327


Temple University

9. Maifrede, Silvia. EGR-1 TUMOR SUPPRESSOR IN BCR-ABL DRIVEN LEUKEMIA.

Degree: PhD, 2015, Temple University

Molecular Biology and Genetics

Chronic Myelogenous Leukemia (CML) is a hematological disease originated with a chromosomal translocation t(9;22)(q34;q11) in a pluripotent hematopoietic stem cell. CML… (more)

Subjects/Keywords: Molecular biology;

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APA (6th Edition):

Maifrede, S. (2015). EGR-1 TUMOR SUPPRESSOR IN BCR-ABL DRIVEN LEUKEMIA. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,321048

Chicago Manual of Style (16th Edition):

Maifrede, Silvia. “EGR-1 TUMOR SUPPRESSOR IN BCR-ABL DRIVEN LEUKEMIA.” 2015. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,321048.

MLA Handbook (7th Edition):

Maifrede, Silvia. “EGR-1 TUMOR SUPPRESSOR IN BCR-ABL DRIVEN LEUKEMIA.” 2015. Web. 18 Nov 2019.

Vancouver:

Maifrede S. EGR-1 TUMOR SUPPRESSOR IN BCR-ABL DRIVEN LEUKEMIA. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,321048.

Council of Science Editors:

Maifrede S. EGR-1 TUMOR SUPPRESSOR IN BCR-ABL DRIVEN LEUKEMIA. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,321048


Temple University

10. Madireddi, Priyanka. THE ROLE OF CIS- AND TRANS-ACTING FACTORS IN REGULATION OF DNA METHYLATION.

Degree: PhD, 2015, Temple University

Molecular Biology and Genetics

High level DNA methylation of promoter CpG islands (CGIs) represses gene expression. However, low-level CGI methylation is currently not distinguished from… (more)

Subjects/Keywords: Molecular biology; Genetics

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APA (6th Edition):

Madireddi, P. (2015). THE ROLE OF CIS- AND TRANS-ACTING FACTORS IN REGULATION OF DNA METHYLATION. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,376391

Chicago Manual of Style (16th Edition):

Madireddi, Priyanka. “THE ROLE OF CIS- AND TRANS-ACTING FACTORS IN REGULATION OF DNA METHYLATION.” 2015. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,376391.

MLA Handbook (7th Edition):

Madireddi, Priyanka. “THE ROLE OF CIS- AND TRANS-ACTING FACTORS IN REGULATION OF DNA METHYLATION.” 2015. Web. 18 Nov 2019.

Vancouver:

Madireddi P. THE ROLE OF CIS- AND TRANS-ACTING FACTORS IN REGULATION OF DNA METHYLATION. [Internet] [Doctoral dissertation]. Temple University; 2015. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,376391.

Council of Science Editors:

Madireddi P. THE ROLE OF CIS- AND TRANS-ACTING FACTORS IN REGULATION OF DNA METHYLATION. [Doctoral Dissertation]. Temple University; 2015. Available from: http://digital.library.temple.edu/u?/p245801coll10,376391


Temple University

11. Chawla, Rachna. Role of CDK4 in Development and Cancer.

Degree: PhD, 2008, Temple University

Molecular Biology and Genetics

The mammalian cell cycle is divided into four distinct phases: G1, S, G2, and M. The transition from G1 to S… (more)

Subjects/Keywords: Biology; Molecular

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APA (6th Edition):

Chawla, R. (2008). Role of CDK4 in Development and Cancer. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,7450

Chicago Manual of Style (16th Edition):

Chawla, Rachna. “Role of CDK4 in Development and Cancer.” 2008. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,7450.

MLA Handbook (7th Edition):

Chawla, Rachna. “Role of CDK4 in Development and Cancer.” 2008. Web. 18 Nov 2019.

Vancouver:

Chawla R. Role of CDK4 in Development and Cancer. [Internet] [Doctoral dissertation]. Temple University; 2008. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,7450.

Council of Science Editors:

Chawla R. Role of CDK4 in Development and Cancer. [Doctoral Dissertation]. Temple University; 2008. Available from: http://digital.library.temple.edu/u?/p245801coll10,7450


Temple University

12. Zumbrun, Steven David. Distinct Mechanisms Regulate Induction of Stress Effector, gadd45b.

Degree: PhD, 2008, Temple University

Molecular Biology and Genetics

The GADD45 family of proteins consists of three small nuclear proteins, GADD45A, GADD45B, and GADD45G, which are implicated in modulating the… (more)

Subjects/Keywords: Biology, Molecular; gadd45b; MMS; post-transcriptional regulation; Sorbitol; stress response; transcriptional regulation

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APA (6th Edition):

Zumbrun, S. D. (2008). Distinct Mechanisms Regulate Induction of Stress Effector, gadd45b. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,23355

Chicago Manual of Style (16th Edition):

Zumbrun, Steven David. “Distinct Mechanisms Regulate Induction of Stress Effector, gadd45b.” 2008. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,23355.

MLA Handbook (7th Edition):

Zumbrun, Steven David. “Distinct Mechanisms Regulate Induction of Stress Effector, gadd45b.” 2008. Web. 18 Nov 2019.

Vancouver:

Zumbrun SD. Distinct Mechanisms Regulate Induction of Stress Effector, gadd45b. [Internet] [Doctoral dissertation]. Temple University; 2008. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,23355.

Council of Science Editors:

Zumbrun SD. Distinct Mechanisms Regulate Induction of Stress Effector, gadd45b. [Doctoral Dissertation]. Temple University; 2008. Available from: http://digital.library.temple.edu/u?/p245801coll10,23355


Temple University

13. Happel, Christine. Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression.

Degree: PhD, 2009, Temple University

Molecular Biology and Genetics

Opioid receptor modulation of pro-inflammatory cytokine production is vital for host defense and the inflammatory response. Previous results have shown the… (more)

Subjects/Keywords: Biology, Microbiology; Chemokines; NF-kappaB; Opioid; Opioid receptor; PKC

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APA (6th Edition):

Happel, C. (2009). Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,28438

Chicago Manual of Style (16th Edition):

Happel, Christine. “Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression.” 2009. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,28438.

MLA Handbook (7th Edition):

Happel, Christine. “Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression.” 2009. Web. 18 Nov 2019.

Vancouver:

Happel C. Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression. [Internet] [Doctoral dissertation]. Temple University; 2009. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,28438.

Council of Science Editors:

Happel C. Molecular Basis for Mu-Opioid Regulation of Chemokine Gene Expression. [Doctoral Dissertation]. Temple University; 2009. Available from: http://digital.library.temple.edu/u?/p245801coll10,28438


Temple University

14. Finley, Matthew James. Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function.

Degree: PhD, 2009, Temple University

Molecular Biology and Genetics

Opioid receptor-mediated regulation of chemokine receptors is vital for the host immune response, development, and neurological function. Previous studies have demonstrated… (more)

Subjects/Keywords: Biology, Molecular; Biology, Genetics; Biology, Neuroscience; Chemokine; Expression; Interferon Regulatory Factor; Opioid, Regulation; STAT3

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APA (6th Edition):

Finley, M. J. (2009). Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,62878

Chicago Manual of Style (16th Edition):

Finley, Matthew James. “Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function.” 2009. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,62878.

MLA Handbook (7th Edition):

Finley, Matthew James. “Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function.” 2009. Web. 18 Nov 2019.

Vancouver:

Finley MJ. Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function. [Internet] [Doctoral dissertation]. Temple University; 2009. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,62878.

Council of Science Editors:

Finley MJ. Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function. [Doctoral Dissertation]. Temple University; 2009. Available from: http://digital.library.temple.edu/u?/p245801coll10,62878


Temple University

15. Samakai, Elsie. TRANSCRIPTIONAL CONTROL OF Ca2+ SIGNALING IN T CELLS.

Degree: PhD, 2017, Temple University

Biochemistry

Antigen presentation to T cells results in their activation through T Cell Receptor (TCR) stimulation, resulting in sustained elevation of cytosolic Ca2+ concentration critical… (more)

Subjects/Keywords: Biochemistry; Immunology;

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APA (6th Edition):

Samakai, E. (2017). TRANSCRIPTIONAL CONTROL OF Ca2+ SIGNALING IN T CELLS. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,466164

Chicago Manual of Style (16th Edition):

Samakai, Elsie. “TRANSCRIPTIONAL CONTROL OF Ca2+ SIGNALING IN T CELLS.” 2017. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,466164.

MLA Handbook (7th Edition):

Samakai, Elsie. “TRANSCRIPTIONAL CONTROL OF Ca2+ SIGNALING IN T CELLS.” 2017. Web. 18 Nov 2019.

Vancouver:

Samakai E. TRANSCRIPTIONAL CONTROL OF Ca2+ SIGNALING IN T CELLS. [Internet] [Doctoral dissertation]. Temple University; 2017. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,466164.

Council of Science Editors:

Samakai E. TRANSCRIPTIONAL CONTROL OF Ca2+ SIGNALING IN T CELLS. [Doctoral Dissertation]. Temple University; 2017. Available from: http://digital.library.temple.edu/u?/p245801coll10,466164


Temple University

16. Reed, Katherine Sullivan. Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Cancers.

Degree: PhD, 2018, Temple University

Biomedical Sciences

PARP inhibitors (PARPi) have been used to induce synthetic lethality in BRCA-deficient tumors in clinical trials with limited success due to the development… (more)

Subjects/Keywords: Oncology; Cellular biology;

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

APA (6th Edition):

Reed, K. S. (2018). Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Cancers. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,507327

Chicago Manual of Style (16th Edition):

Reed, Katherine Sullivan. “Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Cancers.” 2018. Doctoral Dissertation, Temple University. Accessed November 18, 2019. http://digital.library.temple.edu/u?/p245801coll10,507327.

MLA Handbook (7th Edition):

Reed, Katherine Sullivan. “Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Cancers.” 2018. Web. 18 Nov 2019.

Vancouver:

Reed KS. Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Cancers. [Internet] [Doctoral dissertation]. Temple University; 2018. [cited 2019 Nov 18]. Available from: http://digital.library.temple.edu/u?/p245801coll10,507327.

Council of Science Editors:

Reed KS. Simultaneous Targeting of PARP1 and RAD52 Triggers Dual Synthetic Lethality in BRCA-Deficient Cancers. [Doctoral Dissertation]. Temple University; 2018. Available from: http://digital.library.temple.edu/u?/p245801coll10,507327

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