Includes bibliographical references and index.
|Statement||edited by Masaatsu K. Uchida.|
|Contributions||Uchida, Masaatsu K.|
|LC Classifications||QP517.C45 R43 1996|
|The Physical Object|
|Pagination||viii, 213 p. :|
|Number of Pages||213|
|LC Control Number||96160989|
Handbook of Cell Signaling. Book • Edited by: Ralph A. Bradshaw and Edward A. Dennis. Browse book content. Agonist-Induced Desensitization and Endocytosis of G-Protein-Coupled Receptors. Book chapter Full text access. Receptor–Ligand Recognition in the TGFβ Family as Suggested by the Crystal Structures of BMP-2–BR-IA ec and. Abstract. Extracellular stimuli modify [Ca 2+] i through a variety of signaling systems. The most widespread of these is a system that signals Ca 2+ mobilization through the formation of Ca 2+-mobilizing messengers, the inositol inositol polyphosphate—Ca 2+ signaling system is associated with many growth factor, hormone, and neurotransmitter receptor Cited by: 7. Publisher Summary. Signaling by G-protein-coupled receptors (GPCR) can be achieved through receptor phosphorylation and desensitization by the G-protein-coupled receptor kinases (GRKs), a family of serine/threonine kinases, which rapidly phosphorylates agonist-bound receptors and uncouples them from their cognate G protein. Downregulation of the TSH Receptor. Desensitization of some G protein–coupled receptors has been shown to involve phosphorylation of specific residues by G protein receptor kinases (homologous desensitization) or PKA (heterologous desensitization) enzymes When compared with other G protein–coupled receptors.
Desensitization describes the rapid signal attenuation in response to stimulation of cells by receptor agonists. Changes in the coupling efficiency of receptors to signal transduction pathways and receptor internalization can account for desensitization and the development of pharmacodynamic tolerance. The results show that desensitization is heterologous and may involve the guanine nucleotide-binding (G) protein. The differential desensitization to the effects on I K,ACh and I Ca suggests the involvement of two different signalling pathways in the Cited by: 9. For many GPCRs, receptor ubiquitination promotes degradation of agonist-activated receptors in the lysosomes. Other proteins also play important roles in desensitization, including phosphodiesterases, RGS family proteins and A-kinase-anchoring proteins. Together, this intricate network of kinases, ubiquitin ligases, Cited by: -heterologous desensitization is more sensitive to agonist concentration because it separates receptor occupancy from activation of PKA and subsequent phosphorylation of the receptor. serves as an amplification step-because GRK phosphorylates only agonist occupied receptors, homologous desensitization is relatively insensitive to agonist.
In the case of the μ-opioid receptor (MOPr), we have shown that two agonists, morphine and the peptide agonist DAMGO, can induce MOPr desensitization by different mechanisms involving largely protein kinase C (PKC) and G protein-coupled receptor kinase/arrestin : Chris P. Bailey, Eamonn Kelly. Homologous desensitization. Homologous desensitization occurs when a receptor decreases its response to an agonist at high concentration. It is a process through which, after prolonged agonist exposure, the receptor is uncoupled from its signaling cascade and thus the cellular effect of receptor activation is attenuated. desensitization in LC cells was unaffected by the activation of PKC with phorbol esters; however, desensitization induced by ME and morphine was increased (Bailey et al., , ). The present study examined the difference between ME-and morphine-induced MOP receptor desensitization in the presence of PKC activators. Measures included the acuteCited by: Desensitization is a phenomenon that is common to many ligand-gated ion channels but has been demonstrated only rarely with physiological stimulation. Numerous studies describe desensitization of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor by exogenous agonists, but whether synaptic stimulation causes desensitization has been Cited by: