Cholera toxin treatment produces down-regulation of the alpha-subunit of the stimulatory guanine-nucleotide-binding protein (Gs).
about
Regulation of amyloid precursor protein processing by serotonin signalingPeriplakin interferes with G protein activation by the melanin-concentrating hormone receptor-1 by binding to the proximal segment of the receptor C-terminal tail.Type 1 cannabinoid receptor ligands display functional selectivity in a cell culture model of striatal medium spiny projection neurons.Gonadotrophin-releasing hormone receptor agonist-mediated down-regulation of Gq alpha/G11 alpha (pertussis toxin-insensitive) G proteins in alpha T3-1 gonadotroph cells reflects increased G protein turnover but not alterations in mRNA levels.Stimulation of beta(3)-adrenoceptors causes phosphorylation of p38 mitogen-activated protein kinase via a stimulatory G protein-dependent pathway in 3T3-L1 adipocytes.Modification of heterotrimeric G-proteins in Swiss 3T3 cells stimulated with Pasteurella multocida toxin.Biased Type 1 Cannabinoid Receptor Signaling Influences Neuronal Viability in a Cell Culture Model of Huntington Disease.beta-Adrenergic-responsive activation of extracellular signal-regulated protein kinases in salivary cells: role of epidermal growth factor receptor and cAMP.Mechanisms of regulation of G(11)alpha protein by dexamethasone in osteoblastic UMR 106-01 cells.A novel N-terminal motif for palmitoylation of G-protein alpha subunits.Gi3 does not contribute to the inhibition of adenylate cyclase when stimulation of an alpha 2-adrenergic receptor causes activation of both Gi2 and Gi3.Spatial intensity distribution analysis quantifies the extent and regulation of homodimerization of the secretin receptor.Gs alpha is a substrate for mono(ADP-ribosyl)transferase of NG108-15 cells. ADP-ribosylation regulates Gs alpha activity and abundance.Enhanced degradation of the phosphoinositidase C-linked guanine-nucleotide-binding protein Gq alpha/G11 alpha following activation of the human M1 muscarinic acetylcholine receptor expressed in CHO cells.Cholera toxin impairment of opioid-mediated inhibition of adenylate cyclase in neuroblastoma x glioma hybrid cells is due to a toxin-induced decrease in opioid receptor levels.Stimulus deprivation increases pineal Gs alpha and G beta.Pertussis toxin activates L-arginine uptake in pulmonary endothelial cells through downregulation of PKC-alpha activity.Widespread distribution of Gq alpha/G11 alpha detected immunologically by an antipeptide antiserum directed against the predicted C-terminal decapeptide.Reduction of adenylyl cyclase activity by cholera toxin in myeloid cells. Long-term down-regulation of Gs alpha subunits by cholera toxin treatment.Bioluminescence resonance energy transfer-based biosensors allow monitoring of ligand- and transducer-mediated GPCR conformational changes
P2860
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P2860
Cholera toxin treatment produces down-regulation of the alpha-subunit of the stimulatory guanine-nucleotide-binding protein (Gs).
description
1989 nî lūn-bûn
@nan
1989年の論文
@ja
1989年論文
@yue
1989年論文
@zh-hant
1989年論文
@zh-hk
1989年論文
@zh-mo
1989年論文
@zh-tw
1989年论文
@wuu
1989年论文
@zh
1989年论文
@zh-cn
name
Cholera toxin treatment produc ...... cleotide-binding protein (Gs).
@en
Cholera toxin treatment produc ...... ine-nucleotide-binding protein
@nl
type
label
Cholera toxin treatment produc ...... cleotide-binding protein (Gs).
@en
Cholera toxin treatment produc ...... ine-nucleotide-binding protein
@nl
prefLabel
Cholera toxin treatment produc ...... cleotide-binding protein (Gs).
@en
Cholera toxin treatment produc ...... ine-nucleotide-binding protein
@nl
P2093
P2860
P356
P1433
P1476
Cholera toxin treatment produc ...... cleotide-binding protein (Gs).
@en
P2093
P2860
P304
P356
10.1042/BJ2620643
P407
P577
1989-09-01T00:00:00Z