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Pediatric Central Nervous System Tumors as Phenotypic Manifestation of Cancer Predisposition Syndromes
Published in David A. Walker, Giorgio Perilongo, Roger E. Taylor, Ian F. Pollack, Brain and Spinal Tumors of Childhood, 2020
Giorgio Perilongo, Irene Toldo, Stefano Sartori
It is well documented that the mitogen activated protein kinase (MAPK) transcription pathway is the crucial downstream pathway activated by RAS for OPG development. The tumorigenesis of OPG in NF1 patients has been extensively investigated. RAS-related MAPK pathway activation is central to tumor development but other “factors” are involved in tumor development and growth. Microenvironmental factors and notably the level of cyclic AMP are also crucial elements favoring tumor growth.41,42
Eicosanoid Binding Sites in Ovarian and Uterine Tissues
Published in Murray D. Mitchell, Eicosanoids in Reproduction, 2020
PGE2 and PGI2 stimulate adenylate cyclase activity.67,68 The cyclic AMP formed plays an intermediary role in increased steroidogenesis by these PGs. As in other cases, cyclic AMP acts by stimulating cyclic AMP-dependent protein kinase, which phosphorylates endogenous protein substrates.
The Role of Relaxin in Uterine Function
Published in Gabor Huszar, The Physiology and Biochemistry of the Uterus in Pregnancy and Labor, 2020
Cyclic AMP has been invoked as a mediator of smooth muscle relaxation in some, but not all, instances.34 Dibutyryl-cAMP and phosphodiesterase inhibitors suppress uterine contractions.34 It has become apparent that relaxin influences the uterine cAMP system under some specialized conditions.
State-of-the-art beta-adrenoreceptor agonists for the treatment of asthma
Published in Expert Opinion on Pharmacotherapy, 2022
W. Tatiana Garzon-Siatoya, Ismael Carrillo-Martin, Sergio E Chiarella, Alexei Gonzalez-Estrada
The human gene that codes for the β2-AR is found on the long arm of chromosome 5. The receptor molecule is a coiled α-helical polypeptide chain that traverses the bilayer cell membrane several times in a serpentine fashion, forming seven transmembrane domains (Figure 3) [8]. The most important target of β2-agonists are β2-AR in smooth muscle. The binding of β2-agonists to the receptor instigates a cascade of intracellular biochemical events that ultimately cause bronchodilation (Figure 3). This occurs through an increment of intracellular cyclic AMP (cAMP) caused by adenylate cyclase activation through the Gs protein subunit α (Gsα), resulting in the activation of protein kinase A. Once activated, protein kinase A prevents phosphorylation of crucial muscle proteins implicated in smooth muscle tone control. Additionally, cAMP inhibits the release of calcium ions from intracellular stores. Altogether, these events lead to an overall relaxation effect of the ASM [28].
Noradrenergic gating of long-lasting synaptic potentiation in the hippocampus: from neurobiology to translational biomedicine
Published in Journal of Neurogenetics, 2018
Peter V. Nguyen, Jennifer N. Gelinas
NE acts through G protein-coupled receptors broadly classified as α1-, α2-, β1-, and β2-adrenergic receptors (reviewed by Gelinas & Nguyen, 2007). Hippocampal pyramidal cells and dentate gyrus granule cells express all four receptor subtypes (Guo & Li, 2007; Hillman, Knudson, Carr, Doze, & Porter, 2005; Nicholas, Pieribone, & Hokfelt, 1993). β-ARs signal through activation of Gs-type G proteins, followed by stimulation of adenylyl cyclase and increased production of intracellular cAMP. Cyclic-AMP activates cAMP-dependent protein kinase (PKA) and, indirectly, extracellular signal-regulated protein kinase (ERK) through Rap1 (a GTPase) and B-Raf (a protein kinase) (Schmitt & Stork, 2000). PKA and ERK both have critical roles in long-term memory formation and long-term synaptic plasticity in numerous species and they putatively have key roles in the memory enhancing effects of β-AR activation (Barros et al., 1999; Kandel, 2001; Nguyen & Woo, 2003; Sweatt, 2004).
Dual regulation of miR-375 and CREM genes in pancreatic beta cells
Published in Islets, 2022
David M. Keller, Isis G. Perez
Cyclic-AMP-mediated transcriptional repression can occur via the protein CREM.12 CREM is in the CREB family of bZIP transcription factors and binds to the CRE sequence and is alternatively spliced. Depending upon the inclusion of a glutamine-rich activation domain, some CREM splice variants activate and some repress transcription.13,14 In addition, usage of an alternate intronic promoter generates an additional repressor called inducible-cAMP-elevated repressor (ICER),15 itself being activated by the cAMP – protein kinase A (PKA) axis. In β-cells there have been several repressing CREM and ICER splice variants identified16,17 which can repress gene transcription by recruiting histone deacetylase 1 to the promoter.18