Beate Illek

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

If you are interested in making a donation to help further our research, please select UCSF Benioff Children's Hospital Foundation and click on the 'Donate' button above. Select 'other' for the 'I want my funds to support' and type BEATE ILLEK PhD,
Cystic Fibrosis Research, 12.1703.9500.

Alternatively, you may send a check to:

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


CFTR Function in CF Patient-Derived CRC Cells

Cystic fibrosis is a monogenetic disease that is caused by defective
function of the cystic fibrosis conductance regulator (CFTR) gene. More
than 2000 mutations in the CFTR gene are listed in the database and
among those a total of 272 mutations have been identified as
disease-causing ( The goal of my
research project is to develop and refine “a disease in a dish model”
from the pediatric CF population at UCSF Benioff Children’s Hospital
Oakland to tailor pharmacological and cell-based therapies for
correcting the chloride channel defect in individual CF patients.
Approximately 2500 individuals with CF are living in California and the
pediatric CF patient population that receives care at the UCSF Benioff
Children’s Hospitals is characterized by one of the most diverse
ethnic backgrounds in the nation. Patient-specific approaches for CF
treatment are critically important to advance CFTR-directed therapy for
all CF patients. Significant progress in understanding and treating the
underlying CFTR channel defect has been made with the development of
airway epithelial cell culture models over the past 30 years. But only
recent advances by use of conditional reprogramming techniques with a
specific Rho kinase inhibitor and irradiated feeder cells provide a
novel opportunity to generate an abundant amount of “primary-like”
airway epithelial cells to study the cellular physiology and molecular
mechanisms of CF disease in individual patients with CF. The major goal
of my project is to discover CFTR-directed drug effects in carriers with
one or two rare CFTR mutations by examining mutant CFTR chloride
currents in confluent cultures of conditionally reprogrammed nasal and
bronchial epithelial cells (CRC). This project will isolate and generate
CF-CRC cells from individual CF patients to i) monitor drug
responsiveness of CFTR-directed drugs, and ii) to explore the
integration of gene-corrected cells into airway epithelia from the same
patient. This approach presents a long-term source for a personal airway
cell culture model and will advance precision medicine for cystic
fibrosis patients and in particular in patients who are carriers of less
common and rare CFTR mutations.

Revised: Tuesday, June 13, 2017 8:49 AM


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