FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2157278884> ?p ?o ?g. }

• W2157278884 endingPage "2535" @default.
• W2157278884 startingPage "2531" @default.
• W2157278884 abstract "Abstract Familial hemiplegic migraine type 1 (FHM1) is caused by missense mutations in the CACNA1A gene that encodes the α1A pore‐forming subunit of Ca V 2.1 Ca 2+ channels. Knock‐in (KI) transgenic mice expressing Ca V 2.1 Ca 2+ channels with a human pathogenic FHM1 mutation reveal enhanced glutamatergic neurotransmission in the cortex. In this study, we employed an iTRAQ‐based LC‐LC MS/MS approach to identify differentially expressed proteins in cortical synapse proteomes of Cacna1a R192Q KI and wild‐type mice. All expression differences determined were subtle and in the range of 10–30%. Observed upregulated proteins in the mutant mice are involved in processes, such as neurite outgrowth and actin dynamics, vesicle turnover, and glutamate transporters. Our data support the view that in Cacna1a R192Q KI mice, several compensatory mechanisms counterbalancing a dysregulated glutamatergic signaling have come into effect. We propose that such adaptation mechanisms at the synapse level may play a role in the pathophysiology of FHM and possibly in the common forms of migraine." @default.
• W2157278884 created "2016-06-24" @default.
• W2157278884 creator A5012664216 @default.
• W2157278884 creator A5018627313 @default.
• W2157278884 creator A5028794494 @default.
• W2157278884 creator A5037003034 @default.
• W2157278884 creator A5039941295 @default.
• W2157278884 creator A5039947825 @default.
• W2157278884 creator A5046661343 @default.
• W2157278884 creator A5052614408 @default.
• W2157278884 creator A5075095763 @default.
• W2157278884 creator A5075154180 @default.
• W2157278884 creator A5076327499 @default.
• W2157278884 creator A5078566855 @default.
• W2157278884 date "2010-07-01" @default.
• W2157278884 modified "2023-10-18" @default.
• W2157278884 title "Quantitative cortical synapse proteomics of a transgenic migraine mouse model with mutated CaV2.1 calcium channels" @default.
• W2157278884 cites W1603889731 @default.
• W2157278884 cites W1665744388 @default.
• W2157278884 cites W1906779471 @default.
• W2157278884 cites W1966049079 @default.
• W2157278884 cites W1971957784 @default.
• W2157278884 cites W1977228353 @default.
• W2157278884 cites W1978335846 @default.
• W2157278884 cites W1979343320 @default.
• W2157278884 cites W1996691843 @default.
• W2157278884 cites W2024556676 @default.
• W2157278884 cites W2025197615 @default.
• W2157278884 cites W2037879072 @default.
• W2157278884 cites W2046122045 @default.
• W2157278884 cites W2055001048 @default.
• W2157278884 cites W2056512013 @default.
• W2157278884 cites W2057012057 @default.
• W2157278884 cites W2063829584 @default.
• W2157278884 cites W2085677825 @default.
• W2157278884 cites W2091738825 @default.
• W2157278884 cites W2104538689 @default.
• W2157278884 cites W2107611011 @default.
• W2157278884 cites W2128573075 @default.
• W2157278884 cites W2134784646 @default.
• W2157278884 cites W2158247112 @default.
• W2157278884 cites W2320360611 @default.
• W2157278884 cites W2410078883 @default.
• W2157278884 doi "https://doi.org/10.1002/pmic.200900733" @default.
• W2157278884 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20391530" @default.
• W2157278884 hasPublicationYear "2010" @default.
• W2157278884 type Work @default.
• W2157278884 sameAs 2157278884 @default.
• W2157278884 citedByCount "21" @default.
• W2157278884 countsByYear W21572788842012 @default.
• W2157278884 countsByYear W21572788842013 @default.
• W2157278884 countsByYear W21572788842014 @default.
• W2157278884 countsByYear W21572788842015 @default.
• W2157278884 countsByYear W21572788842016 @default.
• W2157278884 countsByYear W21572788842017 @default.
• W2157278884 countsByYear W21572788842019 @default.
• W2157278884 countsByYear W21572788842021 @default.
• W2157278884 crossrefType "journal-article" @default.
• W2157278884 hasAuthorship W2157278884A5012664216 @default.
• W2157278884 hasAuthorship W2157278884A5018627313 @default.
• W2157278884 hasAuthorship W2157278884A5028794494 @default.
• W2157278884 hasAuthorship W2157278884A5037003034 @default.
• W2157278884 hasAuthorship W2157278884A5039941295 @default.
• W2157278884 hasAuthorship W2157278884A5039947825 @default.
• W2157278884 hasAuthorship W2157278884A5046661343 @default.
• W2157278884 hasAuthorship W2157278884A5052614408 @default.
• W2157278884 hasAuthorship W2157278884A5075095763 @default.
• W2157278884 hasAuthorship W2157278884A5075154180 @default.
• W2157278884 hasAuthorship W2157278884A5076327499 @default.
• W2157278884 hasAuthorship W2157278884A5078566855 @default.
• W2157278884 hasConcept C104317684 @default.
• W2157278884 hasConcept C113246987 @default.
• W2157278884 hasConcept C126322002 @default.
• W2157278884 hasConcept C127445978 @default.
• W2157278884 hasConcept C143065580 @default.
• W2157278884 hasConcept C169760540 @default.
• W2157278884 hasConcept C170493617 @default.
• W2157278884 hasConcept C178790620 @default.
• W2157278884 hasConcept C185592680 @default.
• W2157278884 hasConcept C18699975 @default.
• W2157278884 hasConcept C200170125 @default.
• W2157278884 hasConcept C202751555 @default.
• W2157278884 hasConcept C2776497919 @default.
• W2157278884 hasConcept C2777350023 @default.
• W2157278884 hasConcept C2778042195 @default.
• W2157278884 hasConcept C2778541695 @default.
• W2157278884 hasConcept C2780648746 @default.
• W2157278884 hasConcept C46111723 @default.
• W2157278884 hasConcept C501734568 @default.
• W2157278884 hasConcept C519063684 @default.
• W2157278884 hasConcept C54355233 @default.
• W2157278884 hasConcept C61174792 @default.
• W2157278884 hasConcept C71924100 @default.
• W2157278884 hasConcept C75563809 @default.
• W2157278884 hasConcept C86803240 @default.
• W2157278884 hasConcept C95444343 @default.
• W2157278884 hasConceptScore W2157278884C104317684 @default.
• W2157278884 hasConceptScore W2157278884C113246987 @default.

• next