J
Jamie L. Sundsbak
Researcher at Mayo Clinic
Publications - 16
Citations - 1874
Jamie L. Sundsbak is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Autosomal dominant polycystic kidney disease & PKD1. The author has an hindex of 14, co-authored 16 publications receiving 1541 citations. Previous affiliations of Jamie L. Sundsbak include University of Utah.
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Journal ArticleDOI
Imaging Classification of Autosomal Dominant Polycystic Kidney Disease: A Simple Model for Selecting Patients for Clinical Trials
Maria V. Irazabal,Laureano J. Rangel,Eric J. Bergstralh,Sara L. Osborn,Amber J. Harmon,Jamie L. Sundsbak,Kyongtae T. Bae,Arlene B. Chapman,Jared J. Grantham,Michal Mrug,Marie C. Hogan,Ziad M. El-Zoghby,Peter C. Harris,Bradley J. Erickson,Bernard F. King,Vicente E. Torres +15 more
TL;DR: A longitudinal mixed regression model to predict eGFR decline showed that log2HtTKV and age significantly interacted with time in typical patients, but not in atypical patients.
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Integrin-Mediated Host Cell Invasion by Type 1–Piliated Uropathogenic Escherichia coli
TL;DR: Results indicate that β1 and α3 integrins are functionally important receptors for type 1 pili–expressing bacteria within the urinary tract and possibly at other sites within the host.
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Identification of Gene Mutations in Autosomal Dominant Polycystic Kidney Disease through Targeted Resequencing
Sandro Rossetti,Katharina Hopp,Robert A. Sikkink,Jamie L. Sundsbak,Yean Kit Lee,Vickie J. Kubly,Bruce W. Eckloff,Christopher J. Ward,Christopher G. Winearls,Vicente E. Torres,Peter C. Harris +10 more
TL;DR: A strategy to analyze both the PKD1 and PKD2 genes using next-generation sequencing by pooling long-range PCR amplicons and multiplexing bar-coded libraries is developed and validated and is a model for future genetic characterization of large ADPKD populations.
Journal ArticleDOI
Actin-gated intracellular growth and resurgence of uropathogenic Escherichia coli.
TL;DR: An aetiological basis for recurrent urinary tract infections is suggested, linking bladder cell differentiation and the accompanying redistribution of actin microfilaments with the resurgence of UPEC from quiescent intravacuolar reservoirs within the bladder epithelium.
Journal ArticleDOI
Predicted Mutation Strength of Nontruncating PKD1 Mutations Aids Genotype-Phenotype Correlations in Autosomal Dominant Polycystic Kidney Disease
Christina M. Heyer,Jamie L. Sundsbak,Kaleab Z. Abebe,Arlene B. Chapman,Vicente E. Torres,Jared J. Grantham,Kyongtae T. Bae,Robert W. Schrier,Ronald D. Perrone,William E. Braun,Theodore I. Steinman,Michal Mrug,Alan S.L. Yu,Godela Brosnahan,Katharina Hopp,Maria V. Irazabal,William M. Bennett,Michael F. Flessner,Charity G. Moore,Douglas Landsittel,Peter C. Harris +20 more
TL;DR: Overall, the contribution of genic and PKD1 allelic effects and sex to the ADPKD phenotype is quantified and it is shown that other factors shared by families influence htTKV, with these additional genetic/environmental factors significantly affecting the AD PKD phenotype.