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You searched for +publisher:"University of New Mexico" +contributor:("Hudson, Laurie"). Showing records 1 – 16 of 16 total matches.

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University of New Mexico

1. Harmon, Molly. Legacy mining metal exposures contribute to circulating oxidized low density lipoprotein and serum inflammatory potential in a native community.

Degree: Biomedical Sciences Graduate Program, 2016, University of New Mexico

  Numerous abandoned uranium mines (AUM) within the Navajo Nation contribute uranium (U), arsenic (As) and other metals to the soil, air and groundwater that… (more)

Subjects/Keywords: Oxidized LDL; Arsenic; Uranium; Inflammation; Atherosclerosis; Inflammatory potential; Mining; Community; Low density lipoprotein; Medicine and Health Sciences

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APA (6th Edition):

Harmon, M. (2016). Legacy mining metal exposures contribute to circulating oxidized low density lipoprotein and serum inflammatory potential in a native community. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/128

Chicago Manual of Style (16th Edition):

Harmon, Molly. “Legacy mining metal exposures contribute to circulating oxidized low density lipoprotein and serum inflammatory potential in a native community.” 2016. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/128.

MLA Handbook (7th Edition):

Harmon, Molly. “Legacy mining metal exposures contribute to circulating oxidized low density lipoprotein and serum inflammatory potential in a native community.” 2016. Web. 18 Jun 2019.

Vancouver:

Harmon M. Legacy mining metal exposures contribute to circulating oxidized low density lipoprotein and serum inflammatory potential in a native community. [Internet] [Doctoral dissertation]. University of New Mexico; 2016. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/128.

Council of Science Editors:

Harmon M. Legacy mining metal exposures contribute to circulating oxidized low density lipoprotein and serum inflammatory potential in a native community. [Doctoral Dissertation]. University of New Mexico; 2016. Available from: https://digitalrepository.unm.edu/biom_etds/128


University of New Mexico

2. Guo, Yuna. R-ketorolac targets Cdc42 and Rac1 and alters ovarian cancer behaviors critical for invasion and metastasis.

Degree: Biomedical Sciences Graduate Program, 2015, University of New Mexico

  Cdc42 (cell division control protein 42) and Rac1 (Ras-related C3 botulinum) are attractive therapeutic targets in ovarian cancer based on their established importance in… (more)

Subjects/Keywords: Rho GTPases; ketorolac; ovarian cancer; NSAIDs; Cdc42; Rac1; Medicine and Health Sciences

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APA (6th Edition):

Guo, Y. (2015). R-ketorolac targets Cdc42 and Rac1 and alters ovarian cancer behaviors critical for invasion and metastasis. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/127

Chicago Manual of Style (16th Edition):

Guo, Yuna. “R-ketorolac targets Cdc42 and Rac1 and alters ovarian cancer behaviors critical for invasion and metastasis.” 2015. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/127.

MLA Handbook (7th Edition):

Guo, Yuna. “R-ketorolac targets Cdc42 and Rac1 and alters ovarian cancer behaviors critical for invasion and metastasis.” 2015. Web. 18 Jun 2019.

Vancouver:

Guo Y. R-ketorolac targets Cdc42 and Rac1 and alters ovarian cancer behaviors critical for invasion and metastasis. [Internet] [Doctoral dissertation]. University of New Mexico; 2015. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/127.

Council of Science Editors:

Guo Y. R-ketorolac targets Cdc42 and Rac1 and alters ovarian cancer behaviors critical for invasion and metastasis. [Doctoral Dissertation]. University of New Mexico; 2015. Available from: https://digitalrepository.unm.edu/biom_etds/127


University of New Mexico

3. Peretti, Amanda. The effects of ketorolac and its enantiomers on breast cancer proliferation and metastasis.

Degree: Biomedical Sciences Graduate Program, 2015, University of New Mexico

  Breast cancer is the second leading cause of cancer related deaths in women. Advanced breast cancer can metastasize to the lungs, liver, bones and… (more)

Subjects/Keywords: breast cancer; cancer; ketorolac; metastasis; NSAID; Medicine and Health Sciences

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APA (6th Edition):

Peretti, A. (2015). The effects of ketorolac and its enantiomers on breast cancer proliferation and metastasis. (Masters Thesis). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/100

Chicago Manual of Style (16th Edition):

Peretti, Amanda. “The effects of ketorolac and its enantiomers on breast cancer proliferation and metastasis.” 2015. Masters Thesis, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/100.

MLA Handbook (7th Edition):

Peretti, Amanda. “The effects of ketorolac and its enantiomers on breast cancer proliferation and metastasis.” 2015. Web. 18 Jun 2019.

Vancouver:

Peretti A. The effects of ketorolac and its enantiomers on breast cancer proliferation and metastasis. [Internet] [Masters thesis]. University of New Mexico; 2015. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/100.

Council of Science Editors:

Peretti A. The effects of ketorolac and its enantiomers on breast cancer proliferation and metastasis. [Masters Thesis]. University of New Mexico; 2015. Available from: https://digitalrepository.unm.edu/biom_etds/100


University of New Mexico

4. Chavez, Miquella. Dynamics of cell-cell junctions in keratinocytes.

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

 Poor wound healing is a serious medical issue of particular concern in the elderly and people with diabetes. One major obstacle for these patients to… (more)

Subjects/Keywords: keratinocytes; wound healing

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APA (6th Edition):

Chavez, M. (2009). Dynamics of cell-cell junctions in keratinocytes. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/28

Chicago Manual of Style (16th Edition):

Chavez, Miquella. “Dynamics of cell-cell junctions in keratinocytes.” 2009. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/28.

MLA Handbook (7th Edition):

Chavez, Miquella. “Dynamics of cell-cell junctions in keratinocytes.” 2009. Web. 18 Jun 2019.

Vancouver:

Chavez M. Dynamics of cell-cell junctions in keratinocytes. [Internet] [Doctoral dissertation]. University of New Mexico; 2009. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/28.

Council of Science Editors:

Chavez M. Dynamics of cell-cell junctions in keratinocytes. [Doctoral Dissertation]. University of New Mexico; 2009. Available from: https://digitalrepository.unm.edu/biom_etds/28


University of New Mexico

5. Kivitz, Michael. Investigation Into The Early Events Of Epithelial Wound Healing and HPV16 Infection.

Degree: Biomedical Sciences Graduate Program, 2014, University of New Mexico

 HPV16 infection evidently occurs within wounded epithelial tissue, but the cellular and molecular events that culminate in infection establishment remain poorly understood. While HPV is… (more)

Subjects/Keywords: HPV16; Wound Healing

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APA (6th Edition):

Kivitz, M. (2014). Investigation Into The Early Events Of Epithelial Wound Healing and HPV16 Infection. (Masters Thesis). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/90

Chicago Manual of Style (16th Edition):

Kivitz, Michael. “Investigation Into The Early Events Of Epithelial Wound Healing and HPV16 Infection.” 2014. Masters Thesis, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/90.

MLA Handbook (7th Edition):

Kivitz, Michael. “Investigation Into The Early Events Of Epithelial Wound Healing and HPV16 Infection.” 2014. Web. 18 Jun 2019.

Vancouver:

Kivitz M. Investigation Into The Early Events Of Epithelial Wound Healing and HPV16 Infection. [Internet] [Masters thesis]. University of New Mexico; 2014. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/90.

Council of Science Editors:

Kivitz M. Investigation Into The Early Events Of Epithelial Wound Healing and HPV16 Infection. [Masters Thesis]. University of New Mexico; 2014. Available from: https://digitalrepository.unm.edu/biom_etds/90


University of New Mexico

6. Alcon, Sara. G-Protein Coupled Estrogen Receptor Regulation of Migration and Metastasis in the Breast.

Degree: Biomedical Sciences Graduate Program, 2014, University of New Mexico

 Proliferation and migration are critical steps within normal mammary development and breast cancer progression. While 17β-estradiol (E2) stimulates proliferation in normal and breast cancer cells… (more)

Subjects/Keywords: Breast Cancer; Fibroblasts; GPER

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APA (6th Edition):

Alcon, S. (2014). G-Protein Coupled Estrogen Receptor Regulation of Migration and Metastasis in the Breast. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/109

Chicago Manual of Style (16th Edition):

Alcon, Sara. “G-Protein Coupled Estrogen Receptor Regulation of Migration and Metastasis in the Breast.” 2014. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/109.

MLA Handbook (7th Edition):

Alcon, Sara. “G-Protein Coupled Estrogen Receptor Regulation of Migration and Metastasis in the Breast.” 2014. Web. 18 Jun 2019.

Vancouver:

Alcon S. G-Protein Coupled Estrogen Receptor Regulation of Migration and Metastasis in the Breast. [Internet] [Doctoral dissertation]. University of New Mexico; 2014. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/109.

Council of Science Editors:

Alcon S. G-Protein Coupled Estrogen Receptor Regulation of Migration and Metastasis in the Breast. [Doctoral Dissertation]. University of New Mexico; 2014. Available from: https://digitalrepository.unm.edu/biom_etds/109


University of New Mexico

7. Lilyquist, Jenna. The Differential Contribution of Behavior and Biology to Breslow Thickness and Melanoma Survival in Males Compared to Females.

Degree: Biomedical Sciences Graduate Program, 2015, University of New Mexico

 There are many well-documented differences between males and females regarding melanoma including incidence rates, presentation, markers of progression, and survival. A common hypothesis to explain… (more)

Subjects/Keywords: Melanoma; Breslow thickness; Sex; Skin awareness; UV exposure; SNPs; Molecular epidmiology; Immune response; DNA repair

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APA (6th Edition):

Lilyquist, J. (2015). The Differential Contribution of Behavior and Biology to Breslow Thickness and Melanoma Survival in Males Compared to Females. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/134

Chicago Manual of Style (16th Edition):

Lilyquist, Jenna. “The Differential Contribution of Behavior and Biology to Breslow Thickness and Melanoma Survival in Males Compared to Females.” 2015. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/134.

MLA Handbook (7th Edition):

Lilyquist, Jenna. “The Differential Contribution of Behavior and Biology to Breslow Thickness and Melanoma Survival in Males Compared to Females.” 2015. Web. 18 Jun 2019.

Vancouver:

Lilyquist J. The Differential Contribution of Behavior and Biology to Breslow Thickness and Melanoma Survival in Males Compared to Females. [Internet] [Doctoral dissertation]. University of New Mexico; 2015. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/134.

Council of Science Editors:

Lilyquist J. The Differential Contribution of Behavior and Biology to Breslow Thickness and Melanoma Survival in Males Compared to Females. [Doctoral Dissertation]. University of New Mexico; 2015. Available from: https://digitalrepository.unm.edu/biom_etds/134


University of New Mexico

8. Quan, Krystle K. The Role of Snai2/Slug in Diabetes-impaired Wound Healing.

Degree: Biomedical Sciences Graduate Program, 2013, University of New Mexico

 Impaired wound healing is a common complication of diabetes mellitus. Advanced glycation end products (AGEs) are a consequence of diabetes and are formed from non-enzymatic… (more)

Subjects/Keywords: EGFR; Diabetes; Glyoxal; Snai2; Wound Healing; Advanced Glycation End Products

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APA (6th Edition):

Quan, K. K. (2013). The Role of Snai2/Slug in Diabetes-impaired Wound Healing. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/141

Chicago Manual of Style (16th Edition):

Quan, Krystle K. “The Role of Snai2/Slug in Diabetes-impaired Wound Healing.” 2013. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/141.

MLA Handbook (7th Edition):

Quan, Krystle K. “The Role of Snai2/Slug in Diabetes-impaired Wound Healing.” 2013. Web. 18 Jun 2019.

Vancouver:

Quan KK. The Role of Snai2/Slug in Diabetes-impaired Wound Healing. [Internet] [Doctoral dissertation]. University of New Mexico; 2013. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/141.

Council of Science Editors:

Quan KK. The Role of Snai2/Slug in Diabetes-impaired Wound Healing. [Doctoral Dissertation]. University of New Mexico; 2013. Available from: https://digitalrepository.unm.edu/biom_etds/141


University of New Mexico

9. Griego, Anastacia. Evaluation of the Epidermal Growth Factor Receptor Signaling Pathway as a Therapeutic Target in Human Papillomavirus-Associated Disease.

Degree: Biomedical Sciences Graduate Program, 2016, University of New Mexico

  Human papillomaviruses (HPVs) are the most common sexually transmitted infectious agents. They are responsible for >99% of all cervical cancers as well as subsets… (more)

Subjects/Keywords: HPV; EGFR; growth factor receptor; human papillomavirus; cetuximab; cancer; Medicine and Health Sciences

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APA (6th Edition):

Griego, A. (2016). Evaluation of the Epidermal Growth Factor Receptor Signaling Pathway as a Therapeutic Target in Human Papillomavirus-Associated Disease. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/155

Chicago Manual of Style (16th Edition):

Griego, Anastacia. “Evaluation of the Epidermal Growth Factor Receptor Signaling Pathway as a Therapeutic Target in Human Papillomavirus-Associated Disease.” 2016. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/155.

MLA Handbook (7th Edition):

Griego, Anastacia. “Evaluation of the Epidermal Growth Factor Receptor Signaling Pathway as a Therapeutic Target in Human Papillomavirus-Associated Disease.” 2016. Web. 18 Jun 2019.

Vancouver:

Griego A. Evaluation of the Epidermal Growth Factor Receptor Signaling Pathway as a Therapeutic Target in Human Papillomavirus-Associated Disease. [Internet] [Doctoral dissertation]. University of New Mexico; 2016. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/155.

Council of Science Editors:

Griego A. Evaluation of the Epidermal Growth Factor Receptor Signaling Pathway as a Therapeutic Target in Human Papillomavirus-Associated Disease. [Doctoral Dissertation]. University of New Mexico; 2016. Available from: https://digitalrepository.unm.edu/biom_etds/155


University of New Mexico

10. Ezeh, Peace Chinyere. MECHANISMS OF LOW DOSE ARSENIC LYMPHOID STEM CELL IMMUNOTOXICITY AND POTENTIAL INTERACTIONS WITH DIBENZO[def, p]CHRYSENE (DBC).

Degree: Biomedical Sciences Graduate Program, 2015, University of New Mexico

  In vivo assessment of the effects of inorganic arsenic, arsenite (As+3), on the bone marrow (BM) immune progenitor cells in mice showed that 300… (more)

Subjects/Keywords: Arsenic; Immunosuppression; Lymphoid progenitors; Stem cells; Monomethylarsounous acid; Dibenzo[def; p]chrysene; Immunotoxicity; Low dose arsenite interactions; Medicine and Health Sciences

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APA (6th Edition):

Ezeh, P. C. (2015). MECHANISMS OF LOW DOSE ARSENIC LYMPHOID STEM CELL IMMUNOTOXICITY AND POTENTIAL INTERACTIONS WITH DIBENZO[def, p]CHRYSENE (DBC). (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/123

Chicago Manual of Style (16th Edition):

Ezeh, Peace Chinyere. “MECHANISMS OF LOW DOSE ARSENIC LYMPHOID STEM CELL IMMUNOTOXICITY AND POTENTIAL INTERACTIONS WITH DIBENZO[def, p]CHRYSENE (DBC).” 2015. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/123.

MLA Handbook (7th Edition):

Ezeh, Peace Chinyere. “MECHANISMS OF LOW DOSE ARSENIC LYMPHOID STEM CELL IMMUNOTOXICITY AND POTENTIAL INTERACTIONS WITH DIBENZO[def, p]CHRYSENE (DBC).” 2015. Web. 18 Jun 2019.

Vancouver:

Ezeh PC. MECHANISMS OF LOW DOSE ARSENIC LYMPHOID STEM CELL IMMUNOTOXICITY AND POTENTIAL INTERACTIONS WITH DIBENZO[def, p]CHRYSENE (DBC). [Internet] [Doctoral dissertation]. University of New Mexico; 2015. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/123.

Council of Science Editors:

Ezeh PC. MECHANISMS OF LOW DOSE ARSENIC LYMPHOID STEM CELL IMMUNOTOXICITY AND POTENTIAL INTERACTIONS WITH DIBENZO[def, p]CHRYSENE (DBC). [Doctoral Dissertation]. University of New Mexico; 2015. Available from: https://digitalrepository.unm.edu/biom_etds/123


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 June 18, 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. 18 Jun 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 Jun 18]. 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


University of New Mexico

12. Martinez-Finley, Ebany. Perinatal arsenic exposure inhibits binding ability of glucocorticoid receptors to nuclear response elements altering gene expression and affecting learning behavior.

Degree: Biomedical Sciences Graduate Program, 2010, University of New Mexico

 Learning deficits in children following arsenic (As) exposure via drinking water have been epidemiologically described in the last decade. Arsenic is a persistent environmental toxin… (more)

Subjects/Keywords: arsenic; glucocorticoid receptors; MAPK pathway; learning and memory

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APA (6th Edition):

Martinez-Finley, E. (2010). Perinatal arsenic exposure inhibits binding ability of glucocorticoid receptors to nuclear response elements altering gene expression and affecting learning behavior. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/15

Chicago Manual of Style (16th Edition):

Martinez-Finley, Ebany. “Perinatal arsenic exposure inhibits binding ability of glucocorticoid receptors to nuclear response elements altering gene expression and affecting learning behavior.” 2010. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/15.

MLA Handbook (7th Edition):

Martinez-Finley, Ebany. “Perinatal arsenic exposure inhibits binding ability of glucocorticoid receptors to nuclear response elements altering gene expression and affecting learning behavior.” 2010. Web. 18 Jun 2019.

Vancouver:

Martinez-Finley E. Perinatal arsenic exposure inhibits binding ability of glucocorticoid receptors to nuclear response elements altering gene expression and affecting learning behavior. [Internet] [Doctoral dissertation]. University of New Mexico; 2010. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/15.

Council of Science Editors:

Martinez-Finley E. Perinatal arsenic exposure inhibits binding ability of glucocorticoid receptors to nuclear response elements altering gene expression and affecting learning behavior. [Doctoral Dissertation]. University of New Mexico; 2010. Available from: https://digitalrepository.unm.edu/biom_etds/15


University of New Mexico

13. Unione, Amelia H.T. The role of Bcl-2 modifying factor (Bmf) in airway epithelial cell death.

Degree: Biomedical Sciences Graduate Program, 2010, University of New Mexico

 One of the components that obstruct the airway in asthma is the sudden and increased secretion of mucus from metaplastic mucous cells in small airways.… (more)

Subjects/Keywords: airway epithelial cells; Bmf

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APA (6th Edition):

Unione, A. H. T. (2010). The role of Bcl-2 modifying factor (Bmf) in airway epithelial cell death. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/22

Chicago Manual of Style (16th Edition):

Unione, Amelia H T. “The role of Bcl-2 modifying factor (Bmf) in airway epithelial cell death.” 2010. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/22.

MLA Handbook (7th Edition):

Unione, Amelia H T. “The role of Bcl-2 modifying factor (Bmf) in airway epithelial cell death.” 2010. Web. 18 Jun 2019.

Vancouver:

Unione AHT. The role of Bcl-2 modifying factor (Bmf) in airway epithelial cell death. [Internet] [Doctoral dissertation]. University of New Mexico; 2010. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/22.

Council of Science Editors:

Unione AHT. The role of Bcl-2 modifying factor (Bmf) in airway epithelial cell death. [Doctoral Dissertation]. University of New Mexico; 2010. Available from: https://digitalrepository.unm.edu/biom_etds/22


University of New Mexico

14. Agola, Jacob. Assessment of functional characteristics of small GTPases using small molecules.

Degree: Biomedical Sciences Graduate Program, 2011, University of New Mexico

 Rab and Rho subfamilies of GTPases are functionally linked to intracellular trafficking and organization of the cytoskeleton respectively. Despite their roles, use of small molecule… (more)

Subjects/Keywords: Rab; Rho; Rac; Cdc42 and Ras GTPases; drug discovery; fluorescent GTP and GDP; enzyme kinetics; GEF; flow cytometry; ovarian cancer; competitive and allosteric inhibitors

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APA (6th Edition):

Agola, J. (2011). Assessment of functional characteristics of small GTPases using small molecules. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/108

Chicago Manual of Style (16th Edition):

Agola, Jacob. “Assessment of functional characteristics of small GTPases using small molecules.” 2011. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/108.

MLA Handbook (7th Edition):

Agola, Jacob. “Assessment of functional characteristics of small GTPases using small molecules.” 2011. Web. 18 Jun 2019.

Vancouver:

Agola J. Assessment of functional characteristics of small GTPases using small molecules. [Internet] [Doctoral dissertation]. University of New Mexico; 2011. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/108.

Council of Science Editors:

Agola J. Assessment of functional characteristics of small GTPases using small molecules. [Doctoral Dissertation]. University of New Mexico; 2011. Available from: https://digitalrepository.unm.edu/biom_etds/108


University of New Mexico

15. Kenney, Shelby. Characterization of R-ketorolac as a single enantiomer selective inhibitor of Cdc42 and Rac1 in ovarian cancer.

Degree: Biomedical Sciences Graduate Program, 2015, University of New Mexico

 Ovarian cancer is the 5th leading cause of cancer death for women in the United States and is frequently diagnosed at an advanced stage with… (more)

Subjects/Keywords: Cdc42; Rac1; ovarian cancer; ketorolac; migration; adhesion; Rho GTPases

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APA (6th Edition):

Kenney, S. (2015). Characterization of R-ketorolac as a single enantiomer selective inhibitor of Cdc42 and Rac1 in ovarian cancer. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/132

Chicago Manual of Style (16th Edition):

Kenney, Shelby. “Characterization of R-ketorolac as a single enantiomer selective inhibitor of Cdc42 and Rac1 in ovarian cancer.” 2015. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/132.

MLA Handbook (7th Edition):

Kenney, Shelby. “Characterization of R-ketorolac as a single enantiomer selective inhibitor of Cdc42 and Rac1 in ovarian cancer.” 2015. Web. 18 Jun 2019.

Vancouver:

Kenney S. Characterization of R-ketorolac as a single enantiomer selective inhibitor of Cdc42 and Rac1 in ovarian cancer. [Internet] [Doctoral dissertation]. University of New Mexico; 2015. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/132.

Council of Science Editors:

Kenney S. Characterization of R-ketorolac as a single enantiomer selective inhibitor of Cdc42 and Rac1 in ovarian cancer. [Doctoral Dissertation]. University of New Mexico; 2015. Available from: https://digitalrepository.unm.edu/biom_etds/132


University of New Mexico

16. King, Brenee S. The Contribution of Poly(ADP-ribose)polymerase-1 Activity in the Nucleotide Excision Repair Pathway.

Degree: Biomedical Sciences Graduate Program, 2012, University of New Mexico

  Exposure to ultraviolet radiation (UVR) promotes the formation of UVR-induced, DNA helix distorting photolesions such as (6-4) pyrimidine-pyrimidone photoproducts (6-4 PPs) and cyclobutane pyrimidine… (more)

Subjects/Keywords: "NER; PARP; DNA repair; ultraviolet radiation; XPA; XPC"; Medicine and Health Sciences

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

APA (6th Edition):

King, B. S. (2012). The Contribution of Poly(ADP-ribose)polymerase-1 Activity in the Nucleotide Excision Repair Pathway. (Doctoral Dissertation). University of New Mexico. Retrieved from https://digitalrepository.unm.edu/biom_etds/66

Chicago Manual of Style (16th Edition):

King, Brenee S. “The Contribution of Poly(ADP-ribose)polymerase-1 Activity in the Nucleotide Excision Repair Pathway.” 2012. Doctoral Dissertation, University of New Mexico. Accessed June 18, 2019. https://digitalrepository.unm.edu/biom_etds/66.

MLA Handbook (7th Edition):

King, Brenee S. “The Contribution of Poly(ADP-ribose)polymerase-1 Activity in the Nucleotide Excision Repair Pathway.” 2012. Web. 18 Jun 2019.

Vancouver:

King BS. The Contribution of Poly(ADP-ribose)polymerase-1 Activity in the Nucleotide Excision Repair Pathway. [Internet] [Doctoral dissertation]. University of New Mexico; 2012. [cited 2019 Jun 18]. Available from: https://digitalrepository.unm.edu/biom_etds/66.

Council of Science Editors:

King BS. The Contribution of Poly(ADP-ribose)polymerase-1 Activity in the Nucleotide Excision Repair Pathway. [Doctoral Dissertation]. University of New Mexico; 2012. Available from: https://digitalrepository.unm.edu/biom_etds/66

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