Beate Illek

beate Illek, phd
Summer Student Program
Phone: 510-450-7699

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Cystic Fibrosis Research, 12.1703.9500.

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UCSF Benioff Children's Hospitals Foundation
2201 Broadway, Suite 600,
Oakland, CA 94612

Clearly mark your check or cover letter to Dr. Illek's so that your gift will be directed to support this work. To make a gift of securities in support of research, please telephone the Foundation at (510) 428-3814.


CHORI Staff Directory


Beate Illek, Ph.D., is Assistant Scientist and Director of the Cystic Fibrosis Research Laboratory at Children’s Hospital Oakland Research Institute. Her laboratory provides a research arm to the Pediatric Pulmonology by studying salt and water transport across epithelial tissues. This physiological process is highly relevant for the pathology of cystic fibrosis and diarrheal diseases in children. Dr. Illek received her doctoral degree in Germany with honors (summa cum laude) and performed postdoctoral research in the Department of Molecular and Cell Biology at UC Berkeley and in the Department of Cell Biology and Physiology at the University of Pittsburgh. Dr. Illek and her team identified a number of small molecules that target the CFTR chloride ion channel including genistein and other flavonoids which paved the way for CFTR-based drug development. Their work provided the first proof-of-principal for the treatment of the underlying chloride ion channel defect in carriers with the G551D-CFTR mutation. Since then, genistein and other flavonoids have been used worldwide as a gold standard to probe CFTR channel activity in a variety of tissues and cell culture models.

Cystic fibrosis belongs to one of the most common genetic disease occurring in childhood in the United States. Approximately 70,000 people suffer from cystic fibrosis worldwide and more than 10 million Americans are unknowing, symptomless carriers of the defective gene. Cystic fibrosis is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, which encodes a chloride channel protein that mediates the secretion of chloride and bicarbonate ions across epithelial tissues. The genetic defect affects mostly the lungs, pancreas, liver, intestines, sinuses and reproductive organs. For example, the lungs of children with cystic fibrosis are not properly flushed when CFTR function is impaired and get clogged with sticky mucus which makes it hard to breathe and predisposes them to repeated bacterial infections.  As of today there are a total of 2009 mutations listed in the CF mutation database ( and about 272 mutations have been identified to cause cystic fibrosis. The goal of Dr. Illek’s current research is to find new therapies that restore the functional activity of disease-causing CFTR mutations. In particular, Dr. Illek and her colleagues at UCSF have generated a patient-in-a-dish model that can be used to test patient-specific responses to a variety of CFTR-based drug treatments. By performing personalized CFTR chloride transport measurements in the laboratory, Dr. Illek hopes to facilitate the outcome for precision medicine in the clinic.

Gruenert Cell Line Distribution Program

Revised: Thursday, December 19, 2019 11:13 AM


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