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.
Anjaparavanda P. (AP) Naren, PhD8/12/2019
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.
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.
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.
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.
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.
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.
Guanylate cyclase 2C agonism corrects CFTR mutants.
Arora, K; Huang, Y; Mun, K; Yarlagadda, S; Sundaram, N; Kessler, MM; Hannig, G; Kurtz, CB; Silos-Santiago, I; Helmrath, M; et al.
CFTR-NHERF2-LPA(2) Complex in the Airway and Gut Epithelia.
Zhang, W; Zhang, Z; Zhang, Y; Naren, AP.
International Journal of Molecular Sciences.
Epithelial Gpr116 regulates pulmonary alveolar homeostasis via G(q/11) signaling.
Brown, K; Filuta, A; Ludwig, M; Seuwen, K; Jaros, J; Vidal, S; Arora, K; Naren, AP; Kandasamy, K; Parthasarathi, K; et al.
Hsp90 regulation of fibroblast activation in pulmonary fibrosis.
Sontake, V; Wang, Y; Kasam, RK; Sinner, D; Reddy, GB; Naren, AP; McCormack, FX; White, ES; Jegga, AG; Madala, SK.
3333 Burnet Avenue, Cincinnati, Ohio 45229-3026
© 1999-2019 Cincinnati Children's Hospital Medical Center. All rights reserved.