Michael Holtzman On Assignment

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24. Patel AC, Morton JD, Kim EY, Alevy Y, Swanson S, et al. Genetic segregation of airway disease traits despite redundancy of calcium-activated chloride channel family members. Physiol Genomics. 2006;25:502–13. This article demonstrated the activity of Clca family members to regulate mucous cell metaplasia (but not airway hyperreactivity) and to exhibit functional compensation in the mClca3−/− mice. [PubMed]

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27. Fuller CM, Ismailov, Keeton DA, Benos DJ. Phosphorylation and activation of a bovine tracheal anion channel by Ca2+/calmodulin-dependent protein kinase II. J Biol Chem. 1994;269:26642–50. This article provided the first molecular cloning of a Clca gene (bClca1), and provided the first evidence that expression of recombinant Clca protein influenced calcium-dependent chloride flux. [PubMed]

28. Gruber AD, Elble RC, Ji HL, Schreur KD, Fuller CM, Pauli BU. Genomic cloning, molecular characterization, and functional analysis of human CLCA1, the first human member of the family of Ca2+-activated Cl channel proteins. Genomics. 1998;54:200–14. These articles were the first to definitively demonstrate that hCLCA1 and mCLCA3 are not ion channels but instead are secreted soluble proteins. [PubMed]

29. Gibson A, Lewis AP, Affleck K, Aitken AJ, Meldrum E, Thompson N. hCLCA1 and mCLCA3 are secreted non-integral membrane proteins and therefore are not ion channels. J Biol Chem. 2005;280:27205–12. These articles were the first to definitively demonstrate that hCLCA1 and mCLCA3 are not ion channels but instead are secreted soluble proteins. [PubMed]

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