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Inositol receptor

Another chemoreceptor cell with a sensitivity which cannot be easily explained is the inositol receptor found in many lepidopteran larvae (Schoonhoven, 1972a). Most insects appear to synthesize myo-inositol from glucose, thus having no nutritional requirement for this compound. One known exception is the larva of the moth, Heliothis zea, which is dependent upon dietary inositol (Chippendale, 1978). For some larvae inositol in pure form is a feeding stimulant (Blom, 1978, Stadler and Hanson, 1978) but others such as S. exempta show no behavioral response, despite the fact that inositol occurs in its food plants and that it has a receptor cell for the compound (Ma, 1976a). [Pg.20]

A critical component of the G-protein effector cascade is the hydrolysis of GTP by the activated a-subunit (GTPase). This provides not only a component of the amplification process of the G-protein cascade (63) but also serves to provide further measures of dmg efficacy. Additionally, the scheme of Figure 10 indicates that the coupling process also depends on the stoichiometry of receptors and G-proteins. A reduction in receptor number should diminish the efficacy of coupling and thus reduce dmg efficacy. This is seen in Figure 11, which indicates that the abiUty of the muscarinic dmg carbachol [51 -83-2] to inhibit cAMP formation and to stimulate inositol triphosphate, IP, formation yields different dose—response curves, and that after receptor removal by irreversible alkylation, carbachol becomes a partial agonist (68). [Pg.278]

Indium-111. Kits for labeling using other radionucHdes include two indium-111 compounds. Indium-111 pentetreotide is used for the scintigraphic localization of primary and metastatic neuroendocrine tumors bearing somatostatin receptors. For octreotide DTP A, the active agent is suppHed in a lyopbilized kit with gentisic acid, citrate buffer, and inositol. [Pg.484]

Another mechanism in initiating the contraction is agonist-induced contraction. It results from the hydrolysis of membrane phosphatidylinositol and the formation of inositol triphosphate (IP3)- IP3 in turn triggers the release of intracellular calcium from the sarcoplasmic reticulum and the influx of more extracellular calcium. The third mechanism in triggering the smooth muscle contraction is the increase of calcium influx through the receptor-operated channels. The increased cytosolic calcium enhances the binding to the protein, calmodulin [73298-54-1]. [Pg.141]

Excitation of smooth muscle via alpha-1 receptors (eg, in the utems, vascular smooth muscle) is accompanied by an increase in intraceUular-free calcium, possibly by stimulation of phosphoUpase C which accelerates the breakdown of polyphosphoinositides to form the second messengers inositol triphosphate (IP3) and diacylglycerol (DAG). IP3 releases intracellular calcium, and DAG, by activation of protein kinase C, may also contribute to signal transduction. In addition, it is also thought that alpha-1 adrenergic receptors may be coupled to another second messenger, a pertussis toxin-sensitive G-protein that mediates the translocation of extracellular calcium. [Pg.359]

Local and transient Ca2+ increases that propagate throughout the cytosol of individual cells in the form of waves. Ca2+ waves are generated by a positive feedback activation of Ca2+ release from the intracellular Ca2+ stores through ryanodine receptors or inositol IP3 receptors. [Pg.306]

Inositol 1,4,5-trisphosphate (IP3) receptors are intracellular cation channels. They are expressed in most cells and predominantly within the membranes of the endoplasmic reticulum. They mediate release of Ca2+ from intracellular stores by the many receptors that stimulate IP3 formation. [Pg.661]

Bosanac I et al (2002) Structure of the inositol 1,4,5-trisphosphate receptor binding core in complex with its ligand. Nature 420 696-701... [Pg.664]

Bosanac I et al (2005) Crystal structure of the ligand binding suppressor domain of type 1 inositol 1,4,5-trisphosphate receptor. Mol Cell 17 193-203... [Pg.664]

The NHR contains also the conserved Calcineurin docking site, PxlxIT, required for the physical interaction of NEAT and Calcineurin. Dephosphorylation of at least 13 serines residues in the NHR induces a conformational change that exposes the nuclear localization sequences (NLS), allowing the nuclear translocation of NEAT. Rephosphorylation of these residues unmasks the nuclear export sequences that direct transport back to the cytoplasm. Engagement of receptors such as the antigen receptors in T and B cells is coupled to phospholipase C activation and subsequent production of inositol triphosphate. Increased levels of inositol triphosphate lead to the initial release of intracellular stores of calcium. This early increase of calcium induces opening of the plasma membrane calcium-released-activated-calcium (CRAC) channels,... [Pg.847]

Another type of NR crosstalk, which has only recently been recognized, is the so-called nongenomic actions of several receptors that induce very rapid cellular effects. Effectively, evidence has accumulated over several decades that steroid receptors may have a role that does not require their transcriptional activation, such as modifying the activity of enzymes and ion channels. While the effects of steroids that are mediated by the modulation of gene expression do occur with a time lag of hours, steroids can induce an increase in several second messengers such as inositol triphosphate, cAMP, Ca2+, and the activation of MARK and PI3 kinase within seconds or minutes. Many mechanistic details of these nongenomic phenomena remain poorly understood. Notably, controversy still exists as to the identity of the receptors that initiate the non-genomic steroid actions. However, it now appears that at least some of the reported effects can be attributed to the same steroid receptors that are known as NRs. [Pg.898]

Purinergic System. Figure 2 Schematic of sympathetic cotransmission. ATP and NA released from small granular vesicles (SGV) act on P2X and a-i receptors on smooth muscle, respectively. ATP acting on inotropic P2X receptors evokes excitatory junction potentials (EJPs), increase in intracellular calcium ([Ca2+]j) and fast contraction while occupation of metabotropic ar-adrenoceptors leads to production of inositol triphosphate (IP3), increase in [Ca2+]j and slow contraction. Neuropeptide Y (NPY) stored in large granular vesicles (LGV) acts after release both as a prejunctional inhibitory modulator of release of ATP and NA and as a postjunctional modulatory potentiator of the actions of ATP and NA. Soluble nucleotidases are released from nerve varicosities, and are also present as ectonucleotidases. (Reproduced from Burnstock G (2007) Neurotransmission, neuromodulation cotransmission. In Squire LR (ed) New encyclopaedia of neuroscience. Elsevier, The Netherlands (In Press), with permission from Elsevier). [Pg.1051]

Sarcoplasmic reticulum (SR) is a form of the smoothfaced endoplasmic reticulum (ER) in muscles. It functions as an intracellular Ca2+ store for muscle contraction. Ca2+ is energetically sequestered into the SR by Ca2+-pump/sarcoplasmic endoplasmic reticulum Ca2+-ATPase (SERCA) and released via Ca2+ release channels on stimuli (ryanodine receptor in striated muscles and inositol 1,4,5-trisphosphate receptor in most smooth muscles). Endoplasmic reticulum in non-muscle tissues also functions as an intracellular Ca2+ store. [Pg.1110]

HT2A, 5-HT2Bj and 5-HT2C receptors exhibit 46-50% overall sequence identity and couple preferentially to Gq/n to increase inositol phosphates and cytosolic [Ca2+] (see Tables 1-3). [Pg.1123]

The GABAB-receptors, the muscarinic M2- and IVU-receptors for acetylcholine, the dopamine D2-, D3-and D4-receptors, the a2-adrenoceptors for noradrenaline, the 5-HTiA F-receptors for serotonin, and the opioid p-, 8- and K-receptors couple to G proteins of the Gi/o family and thereby lower [1] the cytoplasmic level of the second messenger cyclic AMP and [2] the open probability ofN- andP/Q-type Ca2+ channels (Table 1). The muscarinic Mr, M3- and M5-receptors for acetylcholine and the ai-adrenoceptors for noradrenaline couple to G proteins of the Gq/11 family and thereby increase the cytoplasmic levels of the second messengers inositol trisphosphate and diacylglycerol (Table 1). The dopamine Dr and D5-receptors and the (3-adrenoceptors for noradrenaline, finally, couple to Gs and thereby increase the cytoplasmic level of cyclic AMP. [Pg.1173]


See other pages where Inositol receptor is mentioned: [Pg.1106]    [Pg.1106]    [Pg.280]    [Pg.280]    [Pg.190]    [Pg.24]    [Pg.83]    [Pg.162]    [Pg.169]    [Pg.473]    [Pg.490]    [Pg.522]    [Pg.568]    [Pg.588]    [Pg.631]    [Pg.661]    [Pg.675]    [Pg.675]    [Pg.760]    [Pg.792]    [Pg.815]    [Pg.817]    [Pg.817]    [Pg.830]    [Pg.857]    [Pg.857]    [Pg.909]    [Pg.916]    [Pg.968]    [Pg.971]    [Pg.1036]    [Pg.1047]    [Pg.1067]    [Pg.1110]    [Pg.1110]    [Pg.1140]    [Pg.1142]   
See also in sourсe #XX -- [ Pg.27 , Pg.28 , Pg.45 ]




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Inositol 1,4,5-trisphosphate (InsP receptors

Inositol 1,4,5-trisphosphate receptor phosphorylation

Inositol 1,4,5-trisphosphate receptor, calcium

Inositol triphosphate diacylglycerol receptor

Inositol triphosphate diacylglycerol receptor system

Inositol triphosphate receptors

Inositol-1,4,5-trisphosphate receptors

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