Publisher Correction: Internalized TSH receptors en route to the TGN induce local Gs-protein signaling and gene transcription

Abstract

The original version of this Article contained errors in the three equations reported in the Methods section entitled ‘Statistics’, as described in the accompanying Publisher Correction. These errors have been corrected in both the PDF and HTML versions of the article.

A cellular perspective of bias at G protein‐coupled receptors

“…A second type of intracellular signaling occurs at endosomes following agonist‐induced endocytosis 9,10 . Importantly, intracellular GPCR activation can drive distinct signaling events compared to agonists which restrict receptor activity to the cell surface 34–40 . Kinetic bias (also called temporal bias or kinetic context) highlights the interplay of ligand binding rates and the duration of GPCR signaling and regulatory pathways 7,8,41 .…”

Calcitonin gene‑related peptide: A promising bridge between cancer development and cancer‑associated pain in oral squamous cell carcinoma (Review)

“…A similar result was obtained in a study on substance P, which is frequently regarded as coexisting with CGRP ( 77 , 78 ). A number of studies agree that endosomal signaling is more efficient compared with the traditional plasma membrane signaling and may result in tumorigenesis ( 76 , 79 ). Godbole et al ( 79 ) demonstrated that the TSH receptor co-internalizes with TSH and traffics retrogradely to the trans-Golgi network, where it activates an endogenous pool of G s proteins; this leads to a delayed phase of local cAMP production and protein kinase A activation at a critical position near the nucleus, which appears to be required for efficient phosphorylation and gene transcription of the cAMP response element-binding protein.…”