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Thomas Boat Chair in Cystic Fibrosis Research, Division of Pulmonary Medicine, Research
Director, Cystic Fibrosis Research Center, Division of Pulmonary Medicine, Research
Professor, UC Department of Pediatrics
Cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP-regulated chloride channel located primarily on the apical surface of epithelial cells that line various organs, including the airways and the gut. CFTR dysfunction is detrimental and may result in life-threatening medical disorders. Dr. Naren's laboratory studies two such disorders; (1) Cystic fibrosis, a lethal genetic disease that affects mostly the Caucasian population (>30,000 in USA), in which the CFTR chloride channel is HYPO-functional and (2) Secretory diarrhea, a disease affecting millions of children worldwide, in which HYPER-function of the CFTR chloride channel can occur due to infectious toxins, such as cholera toxin and E. coli enterotoxin. His lab is interested in identifying interactions between CFTR and its binding partners and defining how spatiotemporal regulation of CFTR-containing macromolecular complexes in the apical compartment of polarized epithelial cells lining the secretory epithelia regulates overall fluid secretion. Our studies will identify new drug targets for cystic fibrosis, secretory diarrhea, and other diseases resulting from CFTR dysfunction and provide insights into the etiology of diseases associated with CFTR-interacting molecules.
Cystic fibrosis; secretory diarrhea.
Cystic Fibrosis Center
Anjaparavanda P. "AP" Naren, PhD8/12/2019
Patient personalized translational tools in cystic fibrosis to transform data from bench to bed-side and back.
Arora, K; Yang, F; Brewington, J; McPhail, G; Cortez, AR; Sundaram, N; Ramananda, Y; Ogden, H; Helmrath, M; Clancy, JP; et al.
American Journal of Physiology - Gastrointestinal and Liver Physiology.
F1099L-CFTR (c.3297C>G) has Impaired Channel Function and Associates with Mild Disease Phenotypes in Two Pediatric Patients.
Zhang, X; Hothi, JS; Zhang, YH; Ren, A; Rock, MJ; Srinivasan, S; Stokes, DC; Naren, AP; Zhang, W.
A SNARE protein Syntaxin 17 captures CFTR to potentiate autophagosomal clearance under stress.
Arora, K; Liyanage, P; Zhong, Q; Naren, AP.
AC6 regulates the microtubule-depolymerizing kinesin KIF19A to control ciliary length in mammals.
Arora, K; Lund, JR; Naren, NA; Zingarelli, B; Naren, AP.
Journal of Biological Chemistry.
Su1243 BENCH TO BED-SIDE AND BACK TRANSLATION IN CF USING PATIENT-DERIVED STEM-CELL BASED MODEL SYSTEMS.
Arora, K; Yang, F; Brewington, J; Cortez, AR; Sundaram, N; Ramananda, Y; Herbert, O; Helmrath, M; Naren, AP.
Mo1373 HUMAN PANCREAS-ON-A-CHIP TO STUDY PRESSURE-INDUCED PANCREATITIS.
Mun, KS; Abu-El-Haija, M; Nathan, JD; Liddle, RA; Naren, AP.
586 ER LUMINAL ERAD AS A NOVEL TARGET TO RESCUE MUTANT CFTR IN THE INTESTINE.
Huang, Y; Arora, K; Mun, KS; Yang, F; Yarlagadda, S; Jegga, A; Weaver, TE; Naren, AP.
Targeting the pregnane X receptor using microbial metabolite mimicry.
Dvorak, Z; Kopp, F; Costello, CM; Kemp, JS; Li, H; Vrzalova, A; Stepankova, M; Bartonkova, I; Jiskrova, E; Poulikova, K; et al.
EMBO Molecular Medicine.
Identification of anoctamin 1 (ANO1) as a key driver of esophageal epithelial proliferation in eosinophilic esophagitis.
Vanoni, S; Zeng, C; Marella, S; Uddin, J; Wu, D; Arora, K; Ptaschinski, C; Que, J; Noah, T; Waggoner, L; et al.
Journal of Allergy and Clinical Immunology.
Targeting DNAJB9, a novel ER luminal co-chaperone, to rescue ΔF508-CFTR.
Huang, Y; Arora, K; Mun, KS; Yang, F; Moon, C; Yarlagadda, S; Jegga, A; Weaver, T; Naren, AP.
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