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March 29, 2006Physiological GenomicsOpen Access

Genetic segregation of airway disease traits despite redundancy of calcium-activated chloride channel family members

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Population

Mouse model for virus-induced long-term expression of airway disease traits (F2 intercross population…

Comparison

mClca3 and mClca5 gene transfer; mClca3 knockout vs Wild-type mice

Design

Preclinical

Authors

APAnand C. PatelRoche (Switzerland)JMJeffrey D. MortonChristchurch Clinical Studies TrustEKEdy Y. KimBrigham and Women's Hospital

Discussion

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Implication

CLCA redundancy in murine metaplasia cautions against single-gene targeting for airway disease; leaves open whether shared homologies merit therapeutic pursuit in humans.

Structured PICO

P
Population
Mouse model for virus-induced long-term expression of airway disease traits (F2 intercross population derived from susceptible and nonsusceptible strains, mClca3(-/-) mice, wild-type mice)
I
Intervention
mClca3 and mClca5 gene transfer; mClca3 knockout
C
Comparator
Wild-type mice
O
Outcome
Mucous cell metaplasia and airway hyperreactivitysurrogate

CLCA family members exhibit functional redundancy in mediating mucous cell metaplasia, suggesting shared homologies could be targets for hypersecretory airway disease.

Cite This Study

Patel et al. (2006) studied this question.

synapsesocial.com/papers/6a896429f8670bac6e33403dhttps://doi.org/10.1152/physiolgenomics.00321.2005
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