A photo of AP Naren.

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

513-636-3796

My Biography & Research

Biography

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.

Research Interests

Cystic fibrosis; secretory diarrhea.

Academic Affiliation

Professor, UC Department of Pediatrics

Clinical Divisions

Cystic Fibrosis Center

Research Divisions

Pulmonary Medicine



Blog Posts

Pancreas-On-A-Chip May Advance Cystic Fibrosis Research

Tools for Science

Pancreas-On-A-Chip May Advance Cystic Fibrosis Research

Anjaparavanda P. "AP" Naren, PhD8/12/2019

My Education

PhD: Biochemistry, Indian Institute of Science, Bangalore, India, 1993.

My Publications

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. Life. 2021; 11.

A SNARE protein Syntaxin 17 captures CFTR to potentiate autophagosomal clearance under stress. Arora, K; Liyanage, P; Zhong, Q; Naren, AP. FASEB Journal. 2021; 35.

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. 2020; 295:14250-14259.

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. Gastroenterology. 2020; 158:s-555.

Mo1373 HUMAN PANCREAS-ON-A-CHIP TO STUDY PRESSURE-INDUCED PANCREATITIS. Mun, KS; Abu-El-Haija, M; Nathan, JD; Liddle, RA; Naren, AP. Gastroenterology. 2020; 158:s-868.

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. Gastroenterology. 2020; 158:s-125.

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. 2020; 12.

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. 2020; 145:239-254.e2.

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. Scientific Reports. 2019; 9.

Patient-derived pancreas-on-a-chip to model cystic fibrosis-related disorders. Mun, KS; Arora, K; Huang, Y; Yang, F; Yarlagadda, S; Ramananda, Y; Abu-El-Haija, M; Palermo, JJ; Appakalai, BN; Nathan, JD; et al. Nature Communications. 2019; 10.