Kathryn Oliver

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KathrynE. Oliver

Kathryn E. Oliver

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Biography

University of Alabama Huntsville - Biology

NIH K99/R00 Postdoctoral Fellow at Emory University | President of the Association for Women in Science, Georgia Chapter
Dr. Kathryn E.
Oliver
As a researcher, my objective is to improve our understanding of disease pathogenesis in the context of rare hereditary disorders. My Master’s thesis involved characterizing metabolic strategies by which microbial pathogens chronically persist within the lungs of immunocompromised patients, whereas my pre-doctoral and post-doctoral studies have focused on elucidating novel therapeutic interventions that target the underlying genetic defect in cystic fibrosis (CF). My current work aims to address feasibility of ribosomal perturbation as a means to overcome premature stop mutations, including evaluation of global and transcript-specific effects on translational velocity/fidelity (e.g. ribosome profiling, RNA-seq, tRNA microarrays, mRNA stability assays), in addition to biochemical assessments of protein maturation and function (e.g. pulse-chase, limited proteolysis, cell surface ELISA, patch-clamp, electrophysiology). Through formal collaborations, I have also contributed to investigations concerning nanoparticle-based gene delivery to respiratory basal (progenitor) cells. Overall, I have extensive training in molecular genetics, bacteriology, yeast biology, biochemistry, cellular physiology, mammalian cell culture (including primary human airway epithelia), and mouse models of disease. My ultimate career goal is to leverage these experiences to establish an independent research program that pursues relationships between translational speed, ribosome fidelity, and impact on protein synthesis for cystic fibrosis and other inherited conditions. I am currently funded by an NIH K99/R00 Pathway to Independence Award and open to Assistant Professor roles.

In addition to rigorous research activities, I greatly enjoy educating, equipping, and empowering the next generation of women in science, technology, engineering, and mathematics (STEM). To this end, I currently serve as Founder/President of the Association for Women in Science, Georgia Chapter (https://www.awisga.org).

Transferable skills:
Microsoft Office (PPT, Excel, Word), Data Analytics/Bioinformatics (R, Python, Prism, Tableau), Citation Management (EndNote, Mendeley), Graphic Design (Adobe, Canva, Chimera), Communications (Outlook, G-Suite, Skype, GoToMeeting, Zoom), Website Development (Joomla, Wix), Laboratory Management, Leadership Development, Academic Executive Searches, and University-Wide Advisory Boards. Organized, motivated, fast-paced, collaborative, independent or team-based as appropriate.

Experience

  • Association for Women in Science

    Relevant experience: Recruiting, Applicant Tracking, Talent Acquisition, Talent Management, Executive Search, Leadership Development, Relationship Management, Business Development, Business Strategy, Strategic Partnerships, Advisory Board, Consulting, Customer Service, Marketing, Research, Organization, Communications, Website Development.
    Public press: AWIS Magazine (https://magazine.awis.org/publication/?i=531980&ver=html5&p=44).

Education

  • Auburn University

    Bachelor of Science (BS)

    Zoology (Pre-Med)

  • Auburn University

    Master of Science (MS)

    Microbiology

  • Auburn University

    Laboratory Technician


    Project titles: (1) Impact of human disturbance on freshwater microinvertebrate biodiversity. (2) Effects of dietary calcium on bone mineral mobilization in reproductive Peromyscus.

  • Auburn University

    Graduate Teaching Assistant


    Courses taught: Survey of Life, Principles of Biology, Cell Biology, Immunology, Microbiology. Personal project title: Characterization of the role of dadA in Pseudomonas aeruginosa virulence factor production.

  • University of Alabama at Birmingham

    Doctor of Philosophy (PhD)

    Graduate Biomedical Sciences / Genetics, Genomics & Bioinformatics

  • University of Alabama at Birmingham

    Guest Lecturer


    Course titles: RNA Biology, Histology, Graduate Career Development.

  • University of Alabama at Birmingham


    http://www.uab.edu/gbs/gbso

  • University of Alabama at Birmingham


    UAB Mix feature (lay version): http://www.uab.edu/mix/stories/gobbledygook-to-getting-it-uab-student-shares-science-with-a-lay-audience UAB News feature (technical version): http://www.uab.edu/news/innovation/item/7325-fixing-cystic-fibrosis-in-vitro-studies-show-therapeutically-robust-correction-of-the-most-common-cf-gene-mutation

Publications

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Slowing ribosome velocity restores folding and function of mutant CFTR.

    Journal of Clinical Investigation

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Slowing ribosome velocity restores folding and function of mutant CFTR.

    Journal of Clinical Investigation

  • Transformative therapies for rare CFTR missense alleles.

    Current Opinion in Pharmacology, 34:76-82.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Slowing ribosome velocity restores folding and function of mutant CFTR.

    Journal of Clinical Investigation

  • Transformative therapies for rare CFTR missense alleles.

    Current Opinion in Pharmacology, 34:76-82.

  • Assessing cell-specific effects of genetic variation using tRNA microarrays.

    BMC Genomics

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Slowing ribosome velocity restores folding and function of mutant CFTR.

    Journal of Clinical Investigation

  • Transformative therapies for rare CFTR missense alleles.

    Current Opinion in Pharmacology, 34:76-82.

  • Assessing cell-specific effects of genetic variation using tRNA microarrays.

    BMC Genomics

  • High-throughput yeast phenomics identifies genetic modifiers that partially rescue human W1282X-CFTR.

    American Journal of Respiratory and Critical Care Medicine, 197:A3877.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Slowing ribosome velocity restores folding and function of mutant CFTR.

    Journal of Clinical Investigation

  • Transformative therapies for rare CFTR missense alleles.

    Current Opinion in Pharmacology, 34:76-82.

  • Assessing cell-specific effects of genetic variation using tRNA microarrays.

    BMC Genomics

  • High-throughput yeast phenomics identifies genetic modifiers that partially rescue human W1282X-CFTR.

    American Journal of Respiratory and Critical Care Medicine, 197:A3877.

  • Utilizing yeast phenomics to discover gene interaction networks that influence biogenesis of CFTR nonsense alleles.

    Pediatric Pulmonology 55(S2): 118.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Slowing ribosome velocity restores folding and function of mutant CFTR.

    Journal of Clinical Investigation

  • Transformative therapies for rare CFTR missense alleles.

    Current Opinion in Pharmacology, 34:76-82.

  • Assessing cell-specific effects of genetic variation using tRNA microarrays.

    BMC Genomics

  • High-throughput yeast phenomics identifies genetic modifiers that partially rescue human W1282X-CFTR.

    American Journal of Respiratory and Critical Care Medicine, 197:A3877.

  • Utilizing yeast phenomics to discover gene interaction networks that influence biogenesis of CFTR nonsense alleles.

    Pediatric Pulmonology 55(S2): 118.

  • Ribosomal targeting corrects CFTR class I & II defects.

    Pediatric Pulmonology, 51(S45):209.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Slowing ribosome velocity restores folding and function of mutant CFTR.

    Journal of Clinical Investigation

  • Transformative therapies for rare CFTR missense alleles.

    Current Opinion in Pharmacology, 34:76-82.

  • Assessing cell-specific effects of genetic variation using tRNA microarrays.

    BMC Genomics

  • High-throughput yeast phenomics identifies genetic modifiers that partially rescue human W1282X-CFTR.

    American Journal of Respiratory and Critical Care Medicine, 197:A3877.

  • Utilizing yeast phenomics to discover gene interaction networks that influence biogenesis of CFTR nonsense alleles.

    Pediatric Pulmonology 55(S2): 118.

  • Ribosomal targeting corrects CFTR class I & II defects.

    Pediatric Pulmonology, 51(S45):209.

  • Yeast phenomic models of CF-relevant nonsense mutations reveal gene modifier networks promoting premature termination codon suppression.

    Pediatric Pulmonology, 52(S47):270.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Slowing ribosome velocity restores folding and function of mutant CFTR.

    Journal of Clinical Investigation

  • Transformative therapies for rare CFTR missense alleles.

    Current Opinion in Pharmacology, 34:76-82.

  • Assessing cell-specific effects of genetic variation using tRNA microarrays.

    BMC Genomics

  • High-throughput yeast phenomics identifies genetic modifiers that partially rescue human W1282X-CFTR.

    American Journal of Respiratory and Critical Care Medicine, 197:A3877.

  • Utilizing yeast phenomics to discover gene interaction networks that influence biogenesis of CFTR nonsense alleles.

    Pediatric Pulmonology 55(S2): 118.

  • Ribosomal targeting corrects CFTR class I & II defects.

    Pediatric Pulmonology, 51(S45):209.

  • Yeast phenomic models of CF-relevant nonsense mutations reveal gene modifier networks promoting premature termination codon suppression.

    Pediatric Pulmonology, 52(S47):270.

  • Partial rescue of G542X- and W1282X-CFTR is achieved following suppression of specific ribosomal components.

    Pediatric Pulmonology, 54(S2): 199.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Slowing ribosome velocity restores folding and function of mutant CFTR.

    Journal of Clinical Investigation

  • Transformative therapies for rare CFTR missense alleles.

    Current Opinion in Pharmacology, 34:76-82.

  • Assessing cell-specific effects of genetic variation using tRNA microarrays.

    BMC Genomics

  • High-throughput yeast phenomics identifies genetic modifiers that partially rescue human W1282X-CFTR.

    American Journal of Respiratory and Critical Care Medicine, 197:A3877.

  • Utilizing yeast phenomics to discover gene interaction networks that influence biogenesis of CFTR nonsense alleles.

    Pediatric Pulmonology 55(S2): 118.

  • Ribosomal targeting corrects CFTR class I & II defects.

    Pediatric Pulmonology, 51(S45):209.

  • Yeast phenomic models of CF-relevant nonsense mutations reveal gene modifier networks promoting premature termination codon suppression.

    Pediatric Pulmonology, 52(S47):270.

  • Partial rescue of G542X- and W1282X-CFTR is achieved following suppression of specific ribosomal components.

    Pediatric Pulmonology, 54(S2): 199.

  • Positive epistatic interactions between CF-causing variants and a silent polymorphism are elicited through effects on ribosome velocity.

    Pediatric Pulmonology 55(S2): 71.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Slowing ribosome velocity restores folding and function of mutant CFTR.

    Journal of Clinical Investigation

  • Transformative therapies for rare CFTR missense alleles.

    Current Opinion in Pharmacology, 34:76-82.

  • Assessing cell-specific effects of genetic variation using tRNA microarrays.

    BMC Genomics

  • High-throughput yeast phenomics identifies genetic modifiers that partially rescue human W1282X-CFTR.

    American Journal of Respiratory and Critical Care Medicine, 197:A3877.

  • Utilizing yeast phenomics to discover gene interaction networks that influence biogenesis of CFTR nonsense alleles.

    Pediatric Pulmonology 55(S2): 118.

  • Ribosomal targeting corrects CFTR class I & II defects.

    Pediatric Pulmonology, 51(S45):209.

  • Yeast phenomic models of CF-relevant nonsense mutations reveal gene modifier networks promoting premature termination codon suppression.

    Pediatric Pulmonology, 52(S47):270.

  • Partial rescue of G542X- and W1282X-CFTR is achieved following suppression of specific ribosomal components.

    Pediatric Pulmonology, 54(S2): 199.

  • Positive epistatic interactions between CF-causing variants and a silent polymorphism are elicited through effects on ribosome velocity.

    Pediatric Pulmonology 55(S2): 71.

  • The P67L CFTR biogenesis defect and role of N-terminal lasso helices that impact CFTR folding and maturation.

    Pediatric Pulmonology, 52(S47):232.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Slowing ribosome velocity restores folding and function of mutant CFTR.

    Journal of Clinical Investigation

  • Transformative therapies for rare CFTR missense alleles.

    Current Opinion in Pharmacology, 34:76-82.

  • Assessing cell-specific effects of genetic variation using tRNA microarrays.

    BMC Genomics

  • High-throughput yeast phenomics identifies genetic modifiers that partially rescue human W1282X-CFTR.

    American Journal of Respiratory and Critical Care Medicine, 197:A3877.

  • Utilizing yeast phenomics to discover gene interaction networks that influence biogenesis of CFTR nonsense alleles.

    Pediatric Pulmonology 55(S2): 118.

  • Ribosomal targeting corrects CFTR class I & II defects.

    Pediatric Pulmonology, 51(S45):209.

  • Yeast phenomic models of CF-relevant nonsense mutations reveal gene modifier networks promoting premature termination codon suppression.

    Pediatric Pulmonology, 52(S47):270.

  • Partial rescue of G542X- and W1282X-CFTR is achieved following suppression of specific ribosomal components.

    Pediatric Pulmonology, 54(S2): 199.

  • Positive epistatic interactions between CF-causing variants and a silent polymorphism are elicited through effects on ribosome velocity.

    Pediatric Pulmonology 55(S2): 71.

  • The P67L CFTR biogenesis defect and role of N-terminal lasso helices that impact CFTR folding and maturation.

    Pediatric Pulmonology, 52(S47):232.

  • Ribosomal protein L12 (Rpl12/uL11) is a molecular target suitable for rescue of CFTR defects with multiple disease subcategories.

    Pediatric Pulmonology, 53(S2):148.

  • Epistatic effects of complex alleles on cystic fibrosis phenotype – a protein translational perspective.

    Pediatric Pulmonology, 54(S2): 198.

  • Examples of CFTR “super-responders”, as well as variants with negligible activity and minimal pharmacologic correction.

    Pediatric Pulmonology, 53(S2):168.

  • Positive epistasis between disease-causing missense mutations and silent polymorphism with effect on mRNA translation velocity.

    Proceedings of the National Academy of Sciences (USA)

  • Optimizing the FRT model for studies of cystic fibrosis disease mechanism and drug discovery.

    Pediatric Pulmonology, 52(S47):221.

  • Global assessment of the integrated stress response in CF patient-derived airway and intestinal tissues.

    Journal of Cystic Fibrosis

  • Suppression of peroxisome and ribosomal constituents partially restores plasma membrane localization and function of W1282X-CFTR.

    Pediatric Pulmonology, 53(S2):209.

  • Ribosomal stalk protein silencing partially corrects the ΔF508-CFTR functional expression defect.

    PLoS Biology, 14(5):e1002462.

  • Slowing translation stabilizes CFTR transmembrane domains, increases open channel probability & enhances folding in vivo.

    Pediatric Pulmonology, 52(S47):220.

  • Integration of yeast gene interaction network models to predict modifiers of CFTR molecular phenotype.

    Pediatric Pulmonology, 53(S2):207.

  • Slowing ribosome velocity restores folding and function of mutant CFTR.

    Journal of Clinical Investigation

  • Transformative therapies for rare CFTR missense alleles.

    Current Opinion in Pharmacology, 34:76-82.

  • Assessing cell-specific effects of genetic variation using tRNA microarrays.

    BMC Genomics

  • High-throughput yeast phenomics identifies genetic modifiers that partially rescue human W1282X-CFTR.

    American Journal of Respiratory and Critical Care Medicine, 197:A3877.

  • Utilizing yeast phenomics to discover gene interaction networks that influence biogenesis of CFTR nonsense alleles.

    Pediatric Pulmonology 55(S2): 118.

  • Ribosomal targeting corrects CFTR class I & II defects.

    Pediatric Pulmonology, 51(S45):209.

  • Yeast phenomic models of CF-relevant nonsense mutations reveal gene modifier networks promoting premature termination codon suppression.

    Pediatric Pulmonology, 52(S47):270.

  • Partial rescue of G542X- and W1282X-CFTR is achieved following suppression of specific ribosomal components.

    Pediatric Pulmonology, 54(S2): 199.

  • Positive epistatic interactions between CF-causing variants and a silent polymorphism are elicited through effects on ribosome velocity.

    Pediatric Pulmonology 55(S2): 71.

  • The P67L CFTR biogenesis defect and role of N-terminal lasso helices that impact CFTR folding and maturation.

    Pediatric Pulmonology, 52(S47):232.

BYS 219

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