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Lisa F Rezende
- Associate Professor of Practice
- Member of the Graduate Faculty
Contact
- (520) 621-9729
- Life Sciences South, Rm. 252
- Tucson, AZ 85721
- lrezende@arizona.edu
Degrees
- Ph.D. Microbiology and Immunology
- Albert Einstein College of Medicine, Bronx, New York, United States
- Studies on the Fidelity and Error Specificity of Human Immunodeficiency Virus Type 1 Reverse Transcriptase.
- B.S. Biochemistry
- California Polytechnic State University- San Luis Obispo, San Luis Obispo, California
Awards
- MCB Teaching Award
- MCB, Fall 2022
- Faculty ACESS Fellow
- University of Arizona, Summer 2022
- Trellis Champion Award
- Student Success and Retention, University of Arizona, Spring 2022
- Galileo Circle Copernicus Award
- Galileo Circle/College of Science, Fall 2021
- Gerald R. Swanson Prize for Teaching Excellence
- University of Arizona Faculty Awards, Spring 2020
Interests
No activities entered.
Courses
2024-25 Courses
-
Critical Reasoning in Biomed
MCB 330 (Fall 2024) -
Intro Biology I Lab
MCB 181L (Fall 2024) -
Introductory Biology I
MCB 181R (Fall 2024) -
Preceptorship
MCB 391 (Fall 2024) -
Special Tutoring Wkshp
MCB 497A (Fall 2024)
2023-24 Courses
-
Cancer Biology for Teachers
MCB 657 (Summer I 2024) -
Molecular Basis of Life
MCB 301 (Summer I 2024) -
Special Tutoring Wkshp
MCB 497A (Summer I 2024) -
Honors Thesis
MCB 498H (Spring 2024) -
Human Gen: Sex,Crime & Disease
MCB 442 (Spring 2024) -
Intro Biology I Lab
MCB 181L (Spring 2024) -
Introductory Biology I
MCB 181R (Spring 2024) -
Molecular Basis of Life
MCB 301 (Spring 2024) -
Preceptorship
MCB 391 (Spring 2024) -
Special Tutoring Wkshp
MCB 497A (Spring 2024) -
Critical Reasoning in Biomed
MCB 330 (Fall 2023) -
Honors Thesis
MCB 498H (Fall 2023) -
Intro Biology I Lab
MCB 181L (Fall 2023) -
Introductory Biology I
MCB 181R (Fall 2023) -
Preceptorship
MCB 391 (Fall 2023) -
Special Tutoring Wkshp
MCB 497A (Fall 2023) -
What is MCB?
MCB 195I (Fall 2023)
2022-23 Courses
-
Apps Cell & Molec Bio Tchers
MCB 570 (Summer I 2023) -
Intro Biology I Lab
MCB 181L (Summer I 2023) -
Preceptorship
MCB 391 (Summer I 2023) -
Special Tutoring Wkshp
MCB 497A (Summer I 2023) -
Honors Thesis
ECOL 498H (Spring 2023) -
Honors Thesis
MCB 498H (Spring 2023) -
Human Gen: Sex,Crime & Disease
MCB 442 (Spring 2023) -
Intro Biology I Lab
MCB 181L (Spring 2023) -
Introductory Biology I
MCB 181R (Spring 2023) -
Preceptorship
MCB 391 (Spring 2023) -
Senior Capstone
MCB 498 (Spring 2023) -
Special Tutoring Wkshp
MCB 497A (Spring 2023) -
Critical Reasoning in Biomed
MCB 330 (Fall 2022) -
Honors Thesis
ECOL 498H (Fall 2022) -
Honors Thesis
MCB 498H (Fall 2022) -
Intro Biology I Lab
MCB 181L (Fall 2022) -
Introductory Biology I
MCB 181R (Fall 2022) -
Preceptorship
MCB 391 (Fall 2022) -
Senior Capstone
MCB 498 (Fall 2022) -
Special Tutoring Wkshp
MCB 497A (Fall 2022)
2021-22 Courses
-
Advanced Genetics for Teachers
MCB 572 (Summer I 2022) -
Cancer Biology for Teachers
MCB 657 (Summer I 2022) -
Intro Biology I Lab
MCB 181L (Summer I 2022) -
Introductory Biology I
MCB 181R (Summer I 2022) -
Preceptorship
MCB 391 (Summer I 2022) -
Honors Thesis
BIOC 498H (Spring 2022) -
Honors Thesis
MCB 498H (Spring 2022) -
Human Gen: Sex,Crime & Disease
MCB 442 (Spring 2022) -
Intro Biology I Lab
MCB 181L (Spring 2022) -
Introductory Biology I
MCB 181R (Spring 2022) -
Preceptorship
MCB 391 (Spring 2022) -
STEM Outreach and Recruitment
MCB 397C (Spring 2022) -
Special Tutoring Wkshp
MCB 497A (Spring 2022) -
Critical Reasoning in Biomed
MCB 330 (Fall 2021) -
Honors Thesis
BIOC 498H (Fall 2021) -
Honors Thesis
MCB 498H (Fall 2021) -
Preceptorship
MCB 391 (Fall 2021) -
The Biology of Cancer
MCB 325 (Fall 2021)
2020-21 Courses
-
Intro Biology I Lab
MCB 181L (Summer I 2021) -
Introductory Biology I
MCB 181R (Summer I 2021) -
Molecular Biology
MCB 411 (Summer I 2021) -
Preceptorship
MCB 391 (Summer I 2021) -
Intro Biology I Lab
MCB 181L (Spring 2021) -
Introductory Biology I
MCB 181R (Spring 2021) -
Preceptorship
MCB 391 (Spring 2021) -
STEM Outreach and Recruitment
MCB 397C (Spring 2021) -
Critical Reasoning in Biomed
MCB 330 (Fall 2020) -
Human Gen: Sex,Crime & Disease
MCB 442 (Fall 2020) -
Intro Biology I Lab
MCB 181L (Fall 2020) -
Introductory Biology I
MCB 181R (Fall 2020) -
Preceptorship
MCB 391 (Fall 2020)
2019-20 Courses
-
Advanced Genetics for Teachers
MCB 572 (Summer I 2020) -
Cell Biology
MCB 410 (Summer I 2020) -
Intro Biology I Lab
MCB 181L (Summer I 2020) -
Introductory Biology I
MCB 181R (Summer I 2020) -
Intro Biology I Lab
MCB 181L (Spring 2020) -
Introductory Biology I
MCB 181R (Spring 2020) -
STEM Outreach and Recruitment
MCB 397C (Spring 2020) -
What is MCB?
MCB 195I (Spring 2020) -
Intro Biology I Lab
MCB 181L (Fall 2019) -
Introductory Biology I
MCB 181R (Fall 2019)
2018-19 Courses
-
Cancer Biology for Teachers
MCB 657 (Summer I 2019) -
Intro Biology I Lab
MCB 181L (Summer I 2019) -
Introductory Biology I
MCB 181R (Summer I 2019) -
Intro Biology I Lab
MCB 181L (Spring 2019) -
Introductory Biology I
MCB 181R (Spring 2019) -
STEM Outreach and Recruitment
MCB 397C (Spring 2019) -
Intro Biology I Lab
MCB 181L (Fall 2018) -
Introductory Biology I
MCB 181R (Fall 2018) -
MCB Boot Camp
MCB 195I (Fall 2018) -
Molecular Genetics
MCB 304 (Fall 2018) -
STEM Outreach and Recruitment
MCB 397C (Fall 2018)
2017-18 Courses
-
Apps Cell & Molec Bio Tchers
MCB 570 (Summer I 2018) -
Cancer Biology for Teachers
MCB 657 (Summer I 2018) -
Intro Biology I Lab
MCB 181L (Summer I 2018) -
Introductory Biology I
MCB 181R (Summer I 2018) -
Intro Biology I Lab
MCB 181L (Spring 2018) -
Introductory Biology I
MCB 181R (Spring 2018) -
STEM Outreach and Recruitment
MCB 397C (Spring 2018) -
Intro Biology I Lab
MCB 181L (Fall 2017) -
Intro Biology II Lab
ECOL 182L (Fall 2017) -
Introductory Biology I
MCB 181R (Fall 2017) -
Molecular Genetics
MCB 304 (Fall 2017) -
STEM Outreach and Recruitment
MCB 397C (Fall 2017)
2016-17 Courses
-
Intro Biology I Lab
MCB 181L (Spring 2017) -
Introductory Biology I
MCB 181R (Spring 2017)
2015-16 Courses
-
Microbiology for Teachers
BIOC 697A (Summer I 2016) -
Cancer Biology for Teachers
BIOC 657 (Spring 2016)
Scholarly Contributions
Chapters
- Dean, M., Friedman, S. J., Sutphen, R., Bourquardez Clark, E., Duquette, D., & Rezende, L. F. (2020). Partners, not participants: Engaging patients in the American BRCA outcomes and utilization of testing (ABOUT) network. In Patient and stakeholder involvement in health research. Sage.
Journals/Publications
- Rezende, L., Yi, R. H., Welcsh, P., Dearfield, C. T., Owens, K., & Friedman, S. J. (2022). Effectiveness of a tool to increase understanding of breast cancer media articles. Health Education Journal, 001789692211458. doi:10.1177/00178969221145802
- Blowers, P., Elfring, L. K., Talanquer, V. A., Rezende, L. F., Eadie, E. C., Maximillian, J., Kim, Y. A., Southard, K. M., Southard, K. M., Kim, Y. A., Maximillian, J., Eadie, E. C., Rezende, L. F., Talanquer, V. A., Elfring, L. K., & Blowers, P. (2021). Responsive Teaching in Online Learning Environments: Using an Instructional Team to Promote Formative Assessment and Sense of Community. Journal of College Science Teaching, 50(4).
- Pugh Yi, R. H., Rezende, L. F., Deerfield, C. T., Welcsh, P. L., & Friedman, S. J. (2019). Results of a Pilot Test of Effects of an Online Resource on Lay Audience Understanding of Media Reports on Breast Cancer Research. Health Education Journal, 78(5), 607-617.
- Rezende, L., Yi, R. H., Dearfield, C. T., Welcsh, P., & Friedman, S. J. (2019). Results of a pilot test of effects of an online resource on lay audience understanding of media reports on breast cancer research. Health Education Journal, 78(5), 607-617. doi:10.1177/0017896919841406
- Bolger, M. S., Rezende, L. F., Dykstra, E. M., Elfring, L. K., Katcher, J., Nadler, M., & Hester, S. D. (2018). Authentic Inquiry through Modeling in Biology (AIM-Bio): An Introductory Laboratory Curriculum that Increases Undergraduates' Scientific Agency and Skills.. CBE: Life Science Education, 17(4), ar63.
- Hester, S. D., Nadler, M., Katcher, J., Elfring, L. K., Dykstra, E., Rezende, L. F., & Bolger, M. S. (2018). Authentic Inquiry through Modeling in Biology (AIM-Bio): An Introductory Laboratory Curriculum That Increases Undergraduates' Scientific Agency and Skills. CBE life sciences education, 17(4), ar63.More infoProviding opportunities for science, technology, engineering, and mathematics undergraduates to engage in authentic scientific practices is likely to influence their view of science and may impact their decision to persist through graduation. Laboratory courses provide a natural place to introduce students to scientific practices, but existing curricula often miss this opportunity by focusing on confirming science content rather than exploring authentic questions. Integrating authentic science within laboratory courses is particularly challenging at high-enrollment institutions and community colleges, where access to research-active faculty may be limiting. The Authentic Inquiry through Modeling in Biology (AIM-Bio) curriculum presented here engages students in authentic scientific practices through iterative cycles of model generation, testing, and revision. AIM-Bio university and community college students demonstrated their ability to propose diverse models for biological phenomena, formulate and address hypotheses by designing and conducting experiments, and collaborate with classmates to revise models based on experimental data. Assessments demonstrated that AIM-Bio students had an enhanced sense of project ownership and greater identification as scientists compared with students in existing laboratory courses. AIM-Bio students also experienced measurable gains in their nature of science understanding and skills for doing science. Our results suggest AIM-Bio as a potential alternative to more resource-intensive curricula with similar outcomes.
- Rezende, L. F., Elfring, L. K., Hester, S. D., Nadler, M., Katcher, J., Dykstra, E., & Bolger, M. S. (2018). Authentic Inquiry through Modeling in Biology (AIM-Bio): An Introductory Laboratory Curriculum That Increases Undergraduates’ Scientific Agency and Skills. CBE—Life Sciences Education, 17(4), ar63. doi:10.1187/cbe.18-06-0090
- Samimi, G., Bernardini, M. Q., Brody, L. C., Caga-Anan, C. F., Campbell, I. G., Chenevix-Trench, G., Couch, F. J., Dean, M., de Hullu, J. A., Domchek, S. M., Drapkin, R., Spencer Feigelson, H., Friedlander, M., Gaudet, M. M., Harmsen, M. G., Hurley, K., James, P. A., Kwon, J. S., Lacbawan, F., , Lheureux, S., et al. (2017). Traceback: A Proposed Framework to Increase Identification and Genetic Counseling of BRCA1 and BRCA2 Mutation Carriers Through Family-Based Outreach. Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 35(20), 2329-2337.More infoIn May 2016, the Division of Cancer Prevention and the Division of Cancer Control and Population Sciences, National Cancer Institute, convened a workshop to discuss a conceptual framework for identifying and genetically testing previously diagnosed but unreferred patients with ovarian cancer and other unrecognized BRCA1 or BRCA2 mutation carriers to improve the detection of families at risk for breast or ovarian cancer. The concept, designated Traceback, was prompted by the recognition that although BRCA1 and BRCA2 mutations are frequent in women with ovarian cancer, many such women have not been tested, especially if their diagnosis predated changes in testing guidelines. The failure to identify mutation carriers among probands represents a lost opportunity to prevent cancer in unsuspecting relatives through risk-reduction intervention in mutation carriers and to provide appropriate reassurances to noncarriers. The Traceback program could provide an important opportunity to reach families from racial, ethnic, and socioeconomic groups who historically have not sought or been offered genetic counseling and testing and thereby contribute to a reduction in health disparities in women with germline BRCA mutations. To achieve an interdisciplinary perspective, the workshop assembled international experts in genetics, medical and gynecologic oncology, clinical psychology, epidemiology, genomics, cost-effectiveness modeling, pathology, bioethics, and patient advocacy to identify factors to consider when undertaking a Traceback program. This report highlights the workshop deliberations with the goal of stimulating research and providing a framework for pilot studies to assess the feasibility and ethical and logistical considerations related to the development of best practices for implementation of Traceback studies.
- Yi, R. H., Rezende, L. F., Huynh, J., Kramer, K., Cranmer, M., Schlager, L., Dearfield, C. T., & Friedman, S. J. (2017). XRAYS (eXamining Relevance of Articles to Young Survivors) Program Survey of Information Needs and Media Use by Young Breast Cancer Survivors and Young Women at High-Risk for Breast Cancer. Health communication, 1-6.More infoWomen age 45 years or younger with breast cancer, or who are at high-risk for breast cancer due to previously having the disease or to genetic risk, have distinct health risks and needs from their older counterparts. Young women frequently seek health information through the Internet and mainstream media, but often find it does not address their particular concerns, that it is difficult to evaluate or interpret, or even misleading. To help women better understand media coverage about new research, Facing Our Risk of Cancer Empowered (FORCE) developed the CDC-funded XRAYS (eXamining Relevance of Articles to Young Survivors) program. To assure that the XRAYS program is responsive to the community's needs, FORCE launched a web-based survey to assess where young women seek information about breast cancer, and to learn their unmet information needs. A total of 1,178 eligible women responded to the survey. In general, the breast cancer survivors and high-risk women between ages 18-45 years who responded to this survey, are using multiple media sources to seek information about breast cancer risk, prevention, screening, and treatment. They place trust in several media sources and use them to inform their medical decisions. Only about one-third of respondents to this survey report discussing media sources with their health care providers. Current survey results indicate that, by providing credible information on the quality of evidence and reporting in media reports on cancer, XRAYS is addressing a key need for health information. Results suggest that it will be useful for XRAYS to offer reviews of articles on a broad range of topics that can inform decisions at each stage of risk assessment and treatment.
- Tran, N. Q., Rezende, L. F., Qimron, U., Richardson, C. C., & Tabor, S. (2008). Gene 1.7 of bacteriophage T7 confers sensitivity of phage growth to dideoxythymidine. Proceedings of the National Academy of Sciences of the United States of America, 105(27), 9373-8.More infoBacteriophage T7 DNA polymerase efficiently incorporates dideoxynucleotides into DNA, resulting in chain termination. Dideoxythymidine (ddT) present in the medium at levels not toxic to Escherichia coli inhibits phage T7. We isolated 95 T7 phage mutants that were resistant to ddT. All contained a mutation in T7 gene 1.7, a nonessential gene of unknown function. When gene 1.7 was expressed from a plasmid, T7 phage resistant to ddT still arose; analysis of 36 of these mutants revealed that all had a single mutation in gene 5, which encodes T7 DNA polymerase. This mutation changes tyrosine-526 to phenylalanine, which is known to increase dramatically the ability of T7 DNA polymerase to discriminate against dideoxynucleotides. DNA synthesis in cells infected with wild-type T7 phage was inhibited by ddT, suggesting that it resulted in chain termination of DNA synthesis in the presence of gene 1.7 protein. Overexpression of gene 1.7 from a plasmid rendered E. coli cells sensitive to ddT, indicating that no other T7 proteins are required to confer sensitivity to ddT.
- Rezende, L. F., & Prasad, V. R. (2004). Nucleoside-analog resistance mutations in HIV-1 reverse transcriptase and their influence on polymerase fidelity and viral mutation rates. The international journal of biochemistry & cell biology, 36(9), 1716-34.More infoNucleoside-analog inhibitors of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) were the first drugs used against the virus. It is long known that monotherapy with these and other drugs leads to the rapid development of viral resistance and it is being increasingly appreciated that a significant percentage of individuals receiving highly active antiretroviral therapy (HAART) also develop resistance. Considering the fact that RT is responsible both for optimal rate of replication and an accurate copying of the viral genome, the consequence of drug-resistance mutations in RT to the biochemistry of this enzyme and to the biology of the virus are critically important. The biochemistry of HIV-1 reverse transcriptase variants harboring nucleoside-analog resistance mutations has been studied extensively. In this review, we describe a number of studies into the polymerase fidelity of nucleoside-analog resistant HIV-1 reverse transcriptase as well as the mutation rate of HIV-1 harboring these mutations.
- He, Z. G., Rezende, L. F., Willcox, S., Griffith, J. D., & Richardson, C. C. (2003). The carboxyl-terminal domain of bacteriophage T7 single-stranded DNA-binding protein modulates DNA binding and interaction with T7 DNA polymerase. The Journal of biological chemistry, 278(32), 29538-45.More infoGene 2.5 of bacteriophage T7 is an essential gene that encodes a single-stranded DNA-binding protein (gp2.5). Previous studies have demonstrated that the acidic carboxyl terminus of the protein is essential and that it mediates multiple protein-protein interactions. A screen for lethal mutations in gene 2.5 uncovered a variety of essential amino acids, among which was a single amino acid substitution, F232L, at the carboxyl-terminal residue. gp2.5-F232L exhibits a 3-fold increase in binding affinity for single-stranded DNA and a slightly lower affinity for T7 DNA polymerase when compared with wild type gp2.5. gp2.5-F232L stimulates the activity of T7 DNA polymerase and, in contrast to wild-type gp2.5, promotes strand displacement DNA synthesis by T7 DNA polymerase. A carboxyl-terminal truncation of gene 2.5 protein, gp2.5-Delta 26C, binds single-stranded DNA 40-fold more tightly than the wild-type protein and cannot physically interact with T7 DNA polymerase. gp2.5-Delta 26C is inhibitory for DNA synthesis catalyzed by T7 DNA polymerase on single-stranded DNA, and it does not stimulate strand displacement DNA synthesis at high concentration. The biochemical and genetic data support a model in which the carboxyl-terminal tail modulates DNA binding and mediates essential interactions with T7 DNA polymerase.
- Hyland, E. M., Rezende, L. F., & Richardson, C. C. (2003). The DNA binding domain of the gene 2.5 single-stranded DNA-binding protein of bacteriophage T7. The Journal of biological chemistry, 278(9), 7247-56.More infoGene 2.5 of bacteriophage T7 encodes a single-stranded DNA-binding protein that is essential for viral survival. Its crystal structure reveals a conserved oligosaccharide/oligonucleotide binding fold predicted to interact with single-stranded DNA. However, there is no experimental evidence to support this hypothesis. Recently, we reported a genetic screen for lethal mutations in gene 2.5 that we are using to identify functional domains of the gene 2.5 protein. This screen uncovered a number of mutations that led to amino acid substitutions in the proposed DNA binding domain. Three variant proteins, gp2.5-Y158C, gp2.5-K152E, and gp2.5-Y111C/Y158C, exhibit a decrease in binding affinity for oligonucleotides. A fourth, gp2.5-K109I, exhibits an altered mode of binding single-stranded DNA. A carboxyl-terminal truncation of gene 2.5 protein, gp2.5-Delta26C, binds single-stranded DNA 10-fold more tightly than the wild-type protein. The three altered proteins defective in single-stranded DNA binding cannot mediate the annealing of homologous DNA, whereas gp2.5-Delta26C mediates the reaction more effectively than does wild-type. Gp2.5-K109I retains this annealing ability, albeit slightly less efficiently. With the exception of gp2.5-Delta26C, all variant proteins form dimers in solution and physically interact with T7 DNA polymerase.
- Rezende, L. F., Willcox, S., Griffith, J. D., & Richardson, C. C. (2003). A single-stranded DNA-binding protein of bacteriophage T7 defective in DNA annealing. The Journal of biological chemistry, 278(31), 29098-105.More infoThe annealing of complementary strands of DNA is a vital step during the process of DNA replication, recombination, and repair. In bacteriophage T7-infected cells, the product of viral gene 2.5, a single-stranded DNA-binding protein, performs this function. We have identified a single amino acid residue in gene 2.5 protein, arginine 82, that is critical for its DNA annealing activity. Expression of gene 2.5 harboring this mutation does not complement the growth of a T7 bacteriophage lacking gene 2.5. Purified gene 2.5 protein-R82C binds single-stranded DNA with a greater affinity than the wild-type protein but does not mediate annealing of complementary strands of DNA. A carboxyl-terminal-deleted protein, gene 2.5 protein-Delta26C, binds even more tightly to single-stranded DNA than does gene 2.5 protein-R82C, but it anneals homologous strands of DNA as well as does the wild-type protein. The altered protein forms dimers and interacts with T7 DNA polymerase comparable with the wild-type protein. Gene 2.5 protein-R82C condenses single-stranded M13 DNA in a manner similar to wild-type protein when viewed by electron microscopy.
- Rezende, L. F., Hollis, T., Ellenberger, T., & Richardson, C. C. (2002). Essential amino acid residues in the single-stranded DNA-binding protein of bacteriophage T7. Identification of the dimer interface. The Journal of biological chemistry, 277(52), 50643-53.More infoGene 2.5 of bacteriophage T7 is an essential gene that encodes a single-stranded DNA-binding protein. T7 phage with gene 2.5 deleted can grow only on Escherichia coli cells that express gene 2.5 from a plasmid. This complementation assay was used to screen for lethal mutations in gene 2.5. By screening a library of randomly mutated plasmids encoding gene 2.5, we identified 20 different single amino acid alterations in gene 2.5 protein that are lethal in vivo. The location of these essential residues within the three-dimensional structure of gene 2.5 protein assists in the identification of motifs in the protein. In this study we show that a subset of these alterations defines the dimer interface of gene 2.5 protein predicted by the crystal structure. Recombinantly expressed and purified gene 2.5 protein-P22L, gene 2.5 protein-F31S, and gene 2.5 protein-G36S do not form dimers at salt concentrations where the wild-type gene 2.5 protein exists as a dimer. The basis of the lethality of these mutations in vivo is not known because altered proteins retain the ability to bind single-stranded DNA, anneal complementary strands of DNA, and interact with T7 DNA polymerase.
- Rezende, L. F., Kew, Y., & Prasad, V. R. (2001). Forward mutation rate of human immunodeficiency virus type 1 reverse transcriptase in vitro: Effect of increased processivity on overall fidelity and error specificity,". Journal of Biomedical Science, 8(2), 197-205.
- Drosopoulos, W. C., Rezende, L. F., Wainberg, M. A., & Prasad, V. R. (1998). Virtues of being faithful: Can we limit genetic variation in human immunodeficiency virus?. Journal of Molecular Medicine, 76(9), 604-612.
- Rezende, L. F., Drosopoulos, W. C., & Prasad, V. R. (1998). The influence of 3TC-resistance mutation M184I on the fidelity and error specificity of human immunodeficiency virus type 1 reverse transcriptase. Nucleic Acids Research, 26(12), 3066-3072.
- Rezende, L. F., Ueno, T., Mitsuya, H., & Prasad, V. R. (1998). The impact of multi-dideoxynucleoside resistance-conferring mutations in human immunodeficiency virus type 1 on fidelity and error specificity of reverse transcriptase. Journal of Virology, 72(4), 2890-2895.
- Hsu, M., Inouye, P., Rezende, L. F., Richard, N., Li, Z., Prasad, V., & Wainberg, M. A. (1997). Higher fidelity of RNA-dependent DNA mispair extension by M184V drug-resistant than wild-type reverse transcriptase of human immunodeficiency virus type 1. Nucleic Acids Research, 25(22), 4532-4536.
Presentations
- Marsteller, P., Beaulieu, E., Bill, B., Flaherty, D., Gass, S., Rezende, L. F., & Zwich, M. (2022, July). Applying Universal Design for Learning Principles to Case Studies. BIOME Annual Conference. Online: BIOME.
- Rezende, L. F., & Romanoski, S. (2022, May). Changing Patient Advocates Attitudes and Practice: Lessons from Escape to Thrive. Escape to Thrive. Tucson, Arizona: BagIt.
- Elfring, L. K., Rezende, L. F., Lattimore, K. L., & Hester, S. D. (2021). An Instructional-Teams Project for supporting instructional reform. 2021 ASCN Transforming Institutions Conference.
- Rezende, L. F. (2019, February). Communicating Complex Science to the Public: Lessons from the XRAYS Program. NIH CSER Consortium Engagement Work Group Meeting. Webinar: NIH CSER Consortium.
- Rezende, L. F. (2016, November). Experiences Talking to Family Members About Inherited Mutations That Increase Cancer Risk: Results from the ABOUT Network Family Communication Survey. Michigan Department of Health and Human Services Cancer Genomics Webinar Series. Webinar: Michigan Department of Health and Human Services.
- Rezende, L. F. (2015, March). Finding the gaps between national guidelines and patient decisions in the hereditary cancer community. NIH Collaboratory Grand Rounds. Webinar: NIH Collabatory.
- Rezende, L. F., & Schlager, L. (2014, November). BRCA Positive: Now What?”. International Society of Nurses in Genetics World ConferenceInternational Society of Nurses in Genetics.
Poster Presentations
- Pugh Yi, R. H., Welcsh, P., Rezende, L., Dearfiled, C., Owens, K., & Friedman, S. J. (2019, December). Effectiveness of an online educational resource in increasing lay users' understanding of information in media reports on breast cancer research. San Antonio Breast Cancer Symposium.
- Pugh Yi, R. H., Welscsh, P., Rezende, L., Dearfield, C., Owens, K., & Friedman, S. J. (2019, December). Effects of an online educational resource on lay audience understanding of limitations of quality in media reports and research methods. San Antonio Breast Cancer Symposium. San Antonio, TX.
- Pugh Yi, R. H., Rezende, L. F., Dearfield, C. T., Welcsh, P. L., & Friedman, S. J. (2018, December). Effects of Online Resource to Support Laypersons’ Understanding of Media Reports on Breast Cancer Research. San Antonio Breast Cancer Symposium. San Antonio.
- Lisa, S., Rezende, L. F., Friedman, S., Cohen, S., & Rose, D. (2017, November 3). Peer Navigation Benefits People Affected by Hereditary Cancers. International Society of Nurses in Genetics World Congress. Reston, VA: International Society of Nurses in Genetics.
- Schlager, L., Rezende, L. F., Friedman, S., Huynh, J., & Pugh Yi, R. (2017, November 3). XRAYS: Unconfuse the News for Young Breast Cancer Survivors and Those at High Risk of Breast Cancer. International Society of Nurses in Genetics World Congress. Reston, VA: International Society of Nurses in Genetics.