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Disruption of type 5 adenylyl cyclase negates the developmental increase in Gαolf expression in the striatum
Author(s) -
Iwamoto Tamio,
Iwatsubo Kousaku,
Okumura Satoshi,
Hashimoto Yoko,
Tsunematsu Takashi,
Toya Yoshiyuki,
Hervé Denis,
Umemura Satoshi,
Ishikawa Yoshihiro
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(04)00333-3
Subject(s) - adenylyl cyclase , gs alpha subunit , adcy9 , adcy10 , camp dependent pathway , striatum , adcy3 , adcy6 , medicine , endocrinology , gene knockout , gene isoform , biology , chemistry , biochemistry , dopamine , gene , stimulation
The two stimulatory G protein α subunits, Gαs and Gαolf, activate adenylyl cyclase in a similar way. We examined whether type 5 adenylyl cyclase knockout, the major striatal isoform, can differentially and/or developmentally change the expression of these G proteins in the striatum. Gαs and Gαolf expressions at birth were unaffected in knockouts, which, however, demonstrated a blunted developmental increase in Gαolf, but not Gαs. Adenylyl cyclase activity was unaffected at birth, but subsequently became lower in knockouts. These findings suggest that type 5 adenylyl cyclase does not contribute to striatal cAMP signaling at birth. However, it may play an important role in developmental changes in the expression of Gαolf, but not Gαs.