3 edition of Receptor desensitization and Ca²⁺-signaling found in the catalog.
Receptor desensitization and Ca²⁺-signaling
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|
The beta 2 receptor gene has binding sites for the steroid receptor complex; might offset one of the mechanisms for desensitization, the most serious adverse effect of long-acting beta 2 agonists. Long-acting beta 2 agonists can facilitate the translocation of the glucocorticoid receptor across the nuclear membrane when no ligand is present and. Signal regulation of protease-activated receptor-2 and structural determinants of G[alpha]q-dependent activation and deactivation of phospholipase C-[beta] Last Modified Ma Author: Tiffany K. Ricks. Bottom Line: Changes in receptor levels, receptor desensitization, and locally produced oxytocin are factors that influence the effect of oxytocin on uterine contractility in of these oxytocin receptor antagonists are used only as pharmacological tools, while others have tocolytic this paper, we summarize the action of oxytocin and its receptor and we .
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Receptor desensitization and Ca²-signaling: cellular aspects of possible molecular dynamics. Receptor desensitization is a reduced response to a neurotransmitter or agonist drug due to a decrease in number of receptors Receptor desensitization and Ca²⁺-signaling book, or decreased activity of intracellular signaling pathways and ion channels, after prolonged exposure to the neurotransmitter or drug.
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 Receptor desensitization and Ca²⁺-signaling book 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: A Pharmacology Primer Theory, Applications, and Methods.
Book • 2nd Edition • Authors: such as its affinity for receptors. Drugs must interact with receptors to produce an effect and the affinity is a chemical term used to quantify the strength of that interaction.
The receptor desensitization and tachyphylaxis are also. In book: Glucose-sensing Receptor in Pancreatic Beta-cells, pp m to Ca2+ influx and the desensitization-resensitization effects can be. Abstract. The secretin receptor is prototypic of a recently described family of G protein-coupled receptors.
We recently demonstrated its phosphorylation in response to agonist stimulation and elimination of this covalent modification by C-terminal truncation (F. Ozcelebi et al. () Mol. Pharmacol. 48, ). In contrast, desensitization usually refers to molecular changes at the level of receptor signaling and can be homologous (reduced effects restricted to agonists acting through a specific receptor) or heterologous (reduced effects of agonists acting at other receptors that share a component of the signaling cascade, Lefkowitz et al., ).
However, common use of the Cited by: Background: Desensitization is a serious side effect of many drugs and is also a fundamental problem for modeling drug-receptor gh there has been very little theoretical or experimental work to describe the pharmacological effects of agonist/antagonist combinations, this study was designed to test both a theoretical model and a specific method to prevent rapid receptor.
The nonselective S1P receptor agonist FTY also led to reduced ERK activation in response to subsequent S1P stimulation, but desensitization persisted after overnight S1P exposure. For the first time, we demonstrate that the S1P/S1P 1 –Gi–MEK 1/2–ERK 1/2 cascade is an important signaling pathway that mediates cell survival during Cited by: Receptor inactivation.
As with all signalling components, receptors need to be switched off as well as on. Receptor inactivation can operate in several ways including removal of the ligand by degradation or sequestration, and desensitization of the target cell. Abstract.
TRPV1 receptor agonists such as the vanilloid capsaicin and the potent analog resiniferatoxin are well known potent analgesics. Depending on the vanilloid, dose, and administration site, nociceptor refractoriness may last from minutes up to months, suggesting the contribution of different cellular mechanisms ranging from channel receptor desensitization.
Opioid receptors (OR) are part of the class A of G-protein coupled receptors and the target of the opiates, the most powerful analgesic molecules used in clinic. During a protracted use, a tolerance to analgesic effect develops resulting in a Cited by: RECEPTOR DESENSITIZATION Varun m.
mehta Department of pharmacology -I (). TRPV1 activation by capsaicin is followed by nociceptor desensitization, a state characterized by the inability of the receptor to respond to the vanilloid capsaicin or other noxious stimuli. TRPV1 desensitization is a process markedly depending on Ca 2+ and involves various intracellular signaling pathways (6).Cited by: a, The rapid and nearly complete desensitization of the wild-type (WT) GluR2 receptor is blocked by either the LY mutation or by the bottom right panel, black columns show percentage Cited by: Morphine tolerance is associated with enhanced MOR desensitization.
Desensitization induced by met-enkephalin, DAMGO and morphine (and methadone; Quillinan et al., ) are all more pronounced in LC (Dang and Williams, ; ), as well as PAG neurons (Ingram et al., ) after chronic exposure to by: In this video we discuss desensitization of receptors, specifically looking at the beta 2 receptor.
Epithelial Ca2+ Model Prediction: Suramin Enhances P2Y2 Receptor Desensitization by Accelerating their Phosphorylation Rate Article in Biophysical Journal (2)a. Another form of Ca2+ signaling by G protein-coupled receptors involves activation of Gi to release Gβγ, which activates PLCβ1 .
Whether Gβγ has additional roles in. The interaction between sodium-calcium-exchanger (NCX) and the endoplasmic reticulum (ER) with respect to Ca²⁺ signaling was studied using fura-2 fluorescence imaging microscopy in human endothelial cells.
The inflammatory agonist histamine was used to increase the intracellular Ca²⁺ concentration. Under resting conditions, the endothelial NCX serves to. Although the mechanism of desensitization is well characterized in other receptor systems such as opioid receptors and adrenergic receptors (Marie.
1. Loss of Receptor Function Rapid Due to change in receptor conformation Eg; phosphorylation of specific amino acids in GPCRs blocks coupling to G- proteins 9. Reduction of Receptor Number slower, long-term desensitization E.g: phosphorylation of specific amino acids in GPCRs causes removal from cell surface 3.
This desensitization of 5-HT 1A autoreceptors seems to occur at the level of receptor-G protein interactions rather than their simple downregulation. In fact, an autoradiographic study showed that the 5-HT 1A agonist-stimulated [ 35 S]-GTPγS binding is reduced in rats treated for 21 days with clorgyline [ 36 ].Author: Ouissame Mnie-Filali, Erika Abrial, Laura Lambás-Señas, Nasser Haddjeri.
Ionotropic glutamate receptors are ligand-gated ion channels that mediate excitatory synaptic transmission in the vertebrate brain. To gain a better understanding of how structural changes gate Cited by: An autoreceptor is a type of receptor located in the membranes of presynaptic nerve serves as part of a negative feedback loop in signal is only sensitive to the neurotransmitters or hormones released by the neuron on which the autoreceptor sits.
Similarly, a heteroreceptor is sensitive to neurotransmitters and hormones that are not released by the cell. The various functional states of glutamate receptors control much of the brain's neuronal activity. Our understanding of how one of those states — desensitization Cited by: 4.
Typically, desensitization is a receptor (biochemistry) -based phenomenon in which one receptor type, when bound to its ligand, becomes unable to further influence the signalling pathways by which it regulates cells and, in the case of cell surface membrane receptors, may thereafter be.
Get this from a library. Signal transduction by a recombinant mP2Y2 nucleotide receptor: signaling, desensitization, and relevance to therapeutical. Ensembl ENSG ENSMUSG UniProt P Q8VEB1 RefSeq (mRNA) NM_ NM_ RefSeq (protein) NP_ NP_ Location (UCSC) Chr – Mb Chr – Mb PubMed search Wikidata View/Edit Human View/Edit Mouse G protein-coupled receptor kinase 5 is a member of the G protein-coupled receptor Aliases: GRK5, GPRK5, G protein-coupled.
Gainetdinov, R. R. et al. Muscarinic supersensitivity and impaired receptor desensitization in G protein-coupled receptor kinase 5-deficient mice. Neu Cited by: Request PDF | Measurement of receptor desensitization and internalization in intact cells | Epitope tagged a2-AR subtypes have been used to address a variety of.
Downregulation (i.e., decrease in number) is the inverse of upregulation. It occurs due to repeated or long-term administration of an agonist.
Along with downregulation, desensitization of the receptor to the drug may also occur. This is a physicochemical alteration in the receptor which makes it unresponsive to the drug; this is also called.