Abstract：
:CART peptides are important neurotransmitters, but little is known about their receptors or signaling pathways in cells. In this study we describe the effects of CART 55-102 on the stimulation of extracellular signal-related kinase (ERK) in a pituitary-derived cell line. CART 55-102 treatment resulted in markedly enhanced ERK phosphorylation in AtT20 and GH3 cells, but had no significant effect on ERK phosphorylation levels in a variety of other cell types that were examined. The peptide activated ERK1 and 2 in AtT20 cells in a dose- and time-dependent manner, but an inactive peptide, CART 1-27, had no effect. U0126, an inhibitor of the MEK kinases, blocked the CART-stimulated activation of ERKs. ERK activation was also attenuated by pertussis toxin pre-treatment, but not by genistein, suggesting a Gi/o-dependent mechanism. Overall, these data strongly support the existence of a specific receptor for CART peptide that is a G-protein coupled receptor utilizing a Gi/o mechanism involving MEK1 and 2.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Lakatos A,Prinster S,Vicentic A,Hall RA,Kuhar MJdoi
10.1016/j.neulet.2005.04.072keywords:
subject
Has Abstractpub_date
2005-08-12 00:00:00pages
198-202issue
1-2eissn
0304-3940issn
1872-7972pii
S0304-3940(05)00492-1journal_volume
384pub_type
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
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journal_title：Neuroscience letters
pub_type： 杂志文章
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journal_title：Neuroscience letters
pub_type： 杂志文章
doi：10.1016/j.neulet.2014.03.016
更新日期：2014-05-21 00:00:00
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journal_title：Neuroscience letters
pub_type： 杂志文章
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pub_type： 杂志文章
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更新日期：2009-09-25 00:00:00
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journal_title：Neuroscience letters
pub_type： 杂志文章
doi：10.1016/0304-3940(84)90061-2
更新日期：1984-08-10 00:00:00
