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Effect of thyroid deficiency on Go α-subunit isoforms in developing rat cerebral cortex

Neurochemical Research, ISSN: 0364-3190, Vol: 20, Issue: 10, Page: 1249-1255
1995
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Article Description

Postnatal development of Gα isoforms in rat cerebral cortex was studied by SDS-PAGE and immunoblotting. When rat cerebral cortical membranes were resolved on separating gels containing 9% acrylamide and 8 M urea, three electrophoretically distinct Gα-immunoreactive proteins were evident. Comparison of their electrophoretic mobilities and partial tryptic digest pattern with recombinant Gα or Gα-specific antibody revealed that the slowest and intermediate-migrating bands represent unmodified and fatty acylated forms of Gα protein, respectively. The fastestmigrating band corresponds to Gα. While the fatty acylated form of Gα is the predominant species, its appearance paralleled that observed for Gα in developing rat cortex. Perinatal hypothyroidism induced by methimazole treatment did not significantly alter the appearance of cerebral cortical Gα and Gα between days 1 and 22 postpartum. Our findings support the earlier idea that heterogeneity of Gα proteins in mammalian brain is likely the result of different co- or post-translational processings of each splice variant of Gα. While the appearance of Gα isoforms is developmentally regulated, they likely do not play an obligatory role in neonatal brain development. Alternatively, the expression of Gα isoforms in developing rat cortex may be controlled by an intrinsic signal(s) that is independent of the thyroid status. © 1995 Plenum Publishing Corporation.

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