FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2017299181> ?p ?o ?g. }

• W2017299181 endingPage "7644" @default.
• W2017299181 startingPage "7640" @default.
• W2017299181 abstract "Alterations in sodium channel expression and function have been suggested as a key molecular event underlying the abnormal processing of pain after peripheral nerve or tissue injury. Although the relative contribution of individual sodium channel subtypes to this process is unclear, the biophysical properties of the tetrodotoxin-resistant current, mediated, at least in part, by the sodium channel PN3 (SNS), suggests that it may play a specialized, pathophysiological role in the sustained, repetitive firing of the peripheral neuron after injury. Moreover, this hypothesis is supported by evidence demonstrating that selective knock-down of PN3 protein in the dorsal root ganglion with specific antisense oligodeoxynucleotides prevents hyperalgesia and allodynia caused by either chronic nerve or tissue injury. In contrast, knock-down of NaN/SNS2 protein, a sodium channel that may be a second possible candidate for the tetrodotoxin-resistant current, appears to have no effect on nerve injury-induced behavioral responses. These data suggest that relief from chronic inflammatory or neuropathic pain might be achieved by selective blockade or inhibition of PN3 expression. In light of the restricted distribution of PN3 to sensory neurons, such an approach might offer effective pain relief without a significant side-effect liability." @default.
• W2017299181 created "2016-06-24" @default.
• W2017299181 creator A5000985336 @default.
• W2017299181 creator A5019058497 @default.
• W2017299181 creator A5036628506 @default.
• W2017299181 creator A5041130733 @default.
• W2017299181 creator A5045741440 @default.
• W2017299181 creator A5055625141 @default.
• W2017299181 creator A5057515173 @default.
• W2017299181 creator A5071744431 @default.
• W2017299181 creator A5072070682 @default.
• W2017299181 creator A5078255099 @default.
• W2017299181 creator A5081384846 @default.
• W2017299181 date "1999-07-06" @default.
• W2017299181 modified "2023-10-14" @default.
• W2017299181 title "A comparison of the potential role of the tetrodotoxin-insensitive sodium channels, PN3/SNS and NaN/SNS2, in rat models of chronic pain" @default.
• W2017299181 cites W1495154814 @default.
• W2017299181 cites W1503163429 @default.
• W2017299181 cites W1583934186 @default.
• W2017299181 cites W1617355594 @default.
• W2017299181 cites W1665224264 @default.
• W2017299181 cites W1759966863 @default.
• W2017299181 cites W1822822588 @default.
• W2017299181 cites W1835398160 @default.
• W2017299181 cites W1844967107 @default.
• W2017299181 cites W1963583009 @default.
• W2017299181 cites W1965866432 @default.
• W2017299181 cites W1974508905 @default.
• W2017299181 cites W1978939719 @default.
• W2017299181 cites W1983382776 @default.
• W2017299181 cites W1985689777 @default.
• W2017299181 cites W1999628618 @default.
• W2017299181 cites W2000702493 @default.
• W2017299181 cites W2003285814 @default.
• W2017299181 cites W2004107882 @default.
• W2017299181 cites W2013947622 @default.
• W2017299181 cites W2018809272 @default.
• W2017299181 cites W2022050392 @default.
• W2017299181 cites W2024920602 @default.
• W2017299181 cites W2033533301 @default.
• W2017299181 cites W2035451747 @default.
• W2017299181 cites W2037361891 @default.
• W2017299181 cites W2045322484 @default.
• W2017299181 cites W2048656464 @default.
• W2017299181 cites W2054514410 @default.
• W2017299181 cites W2057469839 @default.
• W2017299181 cites W2068707948 @default.
• W2017299181 cites W2081533056 @default.
• W2017299181 cites W2086836046 @default.
• W2017299181 cites W2088944306 @default.
• W2017299181 cites W2091746433 @default.
• W2017299181 cites W2134321467 @default.
• W2017299181 cites W2138757225 @default.
• W2017299181 cites W2140695849 @default.
• W2017299181 cites W2162233255 @default.
• W2017299181 doi "https://doi.org/10.1073/pnas.96.14.7640" @default.
• W2017299181 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/33594" @default.
• W2017299181 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10393873" @default.
• W2017299181 hasPublicationYear "1999" @default.
• W2017299181 type Work @default.
• W2017299181 sameAs 2017299181 @default.
• W2017299181 citedByCount "304" @default.
• W2017299181 countsByYear W20172991812012 @default.
• W2017299181 countsByYear W20172991812013 @default.
• W2017299181 countsByYear W20172991812014 @default.
• W2017299181 countsByYear W20172991812015 @default.
• W2017299181 countsByYear W20172991812016 @default.
• W2017299181 countsByYear W20172991812017 @default.
• W2017299181 countsByYear W20172991812018 @default.
• W2017299181 countsByYear W20172991812019 @default.
• W2017299181 countsByYear W20172991812020 @default.
• W2017299181 countsByYear W20172991812021 @default.
• W2017299181 countsByYear W20172991812022 @default.
• W2017299181 countsByYear W20172991812023 @default.
• W2017299181 crossrefType "journal-article" @default.
• W2017299181 hasAuthorship W2017299181A5000985336 @default.
• W2017299181 hasAuthorship W2017299181A5019058497 @default.
• W2017299181 hasAuthorship W2017299181A5036628506 @default.
• W2017299181 hasAuthorship W2017299181A5041130733 @default.
• W2017299181 hasAuthorship W2017299181A5045741440 @default.
• W2017299181 hasAuthorship W2017299181A5055625141 @default.
• W2017299181 hasAuthorship W2017299181A5057515173 @default.
• W2017299181 hasAuthorship W2017299181A5071744431 @default.
• W2017299181 hasAuthorship W2017299181A5072070682 @default.
• W2017299181 hasAuthorship W2017299181A5078255099 @default.
• W2017299181 hasAuthorship W2017299181A5081384846 @default.
• W2017299181 hasBestOaLocation W20172991811 @default.
• W2017299181 hasConcept C126322002 @default.
• W2017299181 hasConcept C15490471 @default.
• W2017299181 hasConcept C169760540 @default.
• W2017299181 hasConcept C170493617 @default.
• W2017299181 hasConcept C178790620 @default.
• W2017299181 hasConcept C185592680 @default.
• W2017299181 hasConcept C2775991916 @default.
• W2017299181 hasConcept C2776281502 @default.
• W2017299181 hasConcept C2776414672 @default.
• W2017299181 hasConcept C2776741303 @default.
• W2017299181 hasConcept C2777107010 @default.

• next