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

Biography & Affiliation

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

Divisions

Pulmonary Medicine

Science Blog

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

Education

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

Publications

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 Delta F508-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.

IL-13–induced intestinal secretory epithelial cell antigen passages are required for IgE-mediated food-induced anaphylaxis. Noah, TK; Knoop, KA; McDonald, KG; Gustafsson, JK; Waggoner, L; Vanoni, S; Batie, M; Arora, K; Naren, AP; Wang, Y; et al. Journal of Allergy and Clinical Immunology. 2019; 144:1058-1073.e3.

CFTR modulator theratyping: Current status, gaps and future directions. Clancy, JP; Cotton, CU; Donaldson, SH; Solomon, GM; VanDevanter, DR; Boyle, MP; Gentzsch, M; Nick, JA; Illek, B; Wallenburg, JC; et al. Journal of Cystic Fibrosis. 2019; 18:22-34.

Solute carrier family 9, subfamily A, member 3 (SLC9A3)/sodium-hydrogen exchanger member 3 (NHE3) dysregulation and dilated intercellular spaces in patients with eosinophilic esophagitis. Zeng, C; Vanoni, S; Wu, D; Caldwell, JM; Wheeler, JC; Arora, K; Noah, TK; Waggoner, L; Besse, JA; Yamani, AN; et al. Journal of Allergy and Clinical Immunology. 2018; 142:1843-1855.

AC6 is the major adenylate cyclase forming a diarrheagenic protein complex with cystic fibrosis transmembrane conductance regulator in cholera. Thomas, A; Ramananda, Y; Mun, K; Naren, AP; Arora, K. The Journal of biological chemistry. 2018; 293:12949-12959.

Personalized medicine in CF: from modulator development to therapy for cystic fibrosis patients with rare CFTR mutations. Harutyunyan, M; Huang, Y; Mun, K; Yang, F; Arora, K; Naren, AP. American Journal of Physiology: Lung Cellular and Molecular Physiology. 2018; 314:L529-L543.

PP-2, a src-kinase inhibitor, is a potential corrector for F508del-CFTR in cystic fibrosis. Wang, Y; Arora, K; Yang, F; Shin, W; Chen, J; Kihara, D; Naren, AP; Jegga, AG. Cold Spring Harbor Laboratory. 2018.

An unexpected protein interaction promotes drug resistance in leukemia. Pitre, A; Ge, Y; Lin, W; Wang, Y; Fukuda, Y; Temirov, J; Phillips, AH; Peters, JL; Fan, Y; Ma, J; et al. Nature Communications. 2017; 8.