2015
DOI: 10.1007/s00424-015-1762-9
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Oxygen physiology: sensors and ion channels

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Cited by 5 publications
(6 citation statements)
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References 12 publications
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“…PAT1 (SLC36A1) was found to mediate the transportation of amino acids such as proline ( 95 ) and act as an amino acid transceptor for the activation of TOR signaling in several cell lines ( 96 ). In addition, the major neutral amino acid transporter b 0 at1 ( slc6a19 ) ( 97 ) and cationic amino acid transporter b 0,+ at ( slc7a9 ) ( 98 ) were identified in turbot muscle in our previous study ( 99 ) and were found to be upregulated in the present study (Figure 5 D). These data suggested that the intracellular amino acid availabilities, activation of TOR signaling, and downstream anabolic processes were tightly coordinated and regulated.…”
Section: Discussionsupporting
confidence: 70%
“…PAT1 (SLC36A1) was found to mediate the transportation of amino acids such as proline ( 95 ) and act as an amino acid transceptor for the activation of TOR signaling in several cell lines ( 96 ). In addition, the major neutral amino acid transporter b 0 at1 ( slc6a19 ) ( 97 ) and cationic amino acid transporter b 0,+ at ( slc7a9 ) ( 98 ) were identified in turbot muscle in our previous study ( 99 ) and were found to be upregulated in the present study (Figure 5 D). These data suggested that the intracellular amino acid availabilities, activation of TOR signaling, and downstream anabolic processes were tightly coordinated and regulated.…”
Section: Discussionsupporting
confidence: 70%
“…Voltage-induced conformational changes in GPCRs have recently also been confirmed directly by FRET-based reporters [18 •• ]. Through both GIRK and FRET measurements, it has been shown that voltage can have opposite effects on the transmitted signal induced by agonist action on the receptors [11, 18••, 22•]. For example, the GIRK current elicited by acetylcholine binding to M 2 receptors in rabbit or feline atrial myocytes is reduced by depolarisation, while that caused by the agonist pilocarpine is strongly enhanced [11, 22•].…”
Section: Experimental Evidence For Voltage-induced Effects In Gpcrsmentioning
confidence: 99%
“…These channel proteins contain specialised voltage-sensing domains, which are capable of inducing large-scale conformational transitions that gate the channels open or closed, even under small changes of V m [17]. By contrast, voltage-related effects on other membrane proteins such as GPCRs seem less intuitive, although a number of studies have reported compelling evidence for a broad range of V m -induced phenomena in GPCRs [11, 18••, 19, 20, 21, 22•] (for review see Ref [23]). Many important class A GPCR drug targets are expressed in excitable tissue, for instance the aminergic, opioid, adrenergic and purinergic receptors.…”
Section: Introductionmentioning
confidence: 99%
“…Some recent examples underline the unique ability of TRPA1 to sense the redox state of the milieu and, via this mechanism, to signal pain evoked by anticancer treatments. Chemotherapeutic drugs, including bortezomib, oxaliplatin and paclitaxel, elicit cold and mechanical allodynia in mice via oxidative stress‐dependent TRPA1 activation .…”
Section: Introductionmentioning
confidence: 99%
“…[10][11][12][13][14] In addition to exogenous agonists, such as allyl isothiocyanate (AITC, in mustard oil and wasabi), cinnamaldehyde (in cinnamon) and allicin (in garlic), an unprecedented series of endogenous pro-inflammatory substances produced at sites of inflammation or tissue injury, including reactive oxygen, nitrogen and carbonyl species (ROS, RNS and RCS, respectively), directly gate TRPA1. [10][11][12][15][16][17] Some recent examples underline the unique ability of TRPA1 to sense the redox state of the milieu 18 and, via this mechanism, to signal pain evoked by anticancer treatments. Chemotherapeutic drugs, including bortezomib, oxaliplatin and paclitaxel, elicit cold and mechanical allodynia in mice via oxidative stress-dependent TRPA1 activation.…”
Section: Introductionmentioning
confidence: 99%