Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Oct 7;10:16686. doi: 10.1038/s41598-020-73840-4

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Schematic representation of the proposed putative mechanism of action of NESF and NLP in the regulation of GH synthesis in the mammalian somatotrophs. While the GH-secretagogue ghrelin (GRL) activates the cAMP/PKA/CREB pathway to stimulate the synthesis of GH through a GPCR with a Gα-stimulatory subunit (Gαs), NESF and NLP prevent the activation of this signalling pathway by the adenylyl cyclase stimulator forskolin (FK). However, the phosphorylation of CREB is not compromised when the pathway is directly activated at the level of PKA by the cAMP-analog CPT. These results suggest that exogenous nucleobindin encoded peptides likely exert their effects by the inhibition of the adenylyl cyclase, possibly through a GPCR associated with a Gα-inhibitory subunit (Gαi). Figure created with BioRender.com tools.