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10.1177/0748730414540453 http://scihub22266oqcxt.onion/10.1177/0748730414540453 C4608047!4608047 !25238857     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25238857 &cmd=llinks): Failed to open stream: HTTP request failed! 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A specific role for the REV-ERB?-controlled L-Type Voltage-Gated Calcium Channel CaV1 2 in resetting the circadian clock in the late night |pdf=|usr=}}{{25238857 }} gab.com Text A specific role for the REV-ERB -controlled L-Type Voltage-Gated Calcium Channel CaV1 2 in resetting the circadian clock in the late night JO: J Biol Rhythms http://www.kidney.de/pget.php?&tw=1&pmid=25238857 #FOAvip Within the suprachiasmatic nucleus (SCN) of the hypothalamus, circadian timekeeping and resetting have been shown to be largely dependent on both membrane depolarization and intracellular second-messenger signaling. In both of these processes, voltage-gated calcium channels (VGCCs) mediate voltage-dependent calcium influx, which propagates neural impulses by stimulating vesicle fusion and instigates intracellular pathways resulting in clock gene expression. Through the cumulative actions of these processes, the phase of the internal clock is modified to match the light cycle of the external environment. To parse out the distinct roles of the L-type VGCCs, we analyzed mice deficient in Cav1.2 (Cacna1c) in brain tissue. We found that mice deficient in the Cav1.2 channel exhibited a significant reduction in their ability to phase-advance circadian behavior when subjected to a light pulse in the late night. Furthermore, the study revealed that the expression of Cav1.2 mRNA was rhythmic (peaking during the late night) and was regulated by the circadian clock component REV-ERB?. Finally, the induction of clock genes in both the early and late subjective night was affected by the loss of Cav1.2, with reductions in Per2 and Per1 in the early and late night, respectively. In sum, these results reveal a role of the L-type VGCC Cav1.2 in mediating both clock gene expression and phase advances in response to a light pulse in the late night. Twit Text FOAVip A specific role for the REV-ERB -controlled L-Type Voltage-Gated Calcium Channel CaV1 2 in resetting the circadian clock in the late night ????J Biol Rhythms http://www.kidney.de/pget.php?&tw=1&pmid=25238857 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25238857 #FOAvip English Wikipedia <ref>{{Cite pmid|25238857 }}</ref> A specific role for the REV-ERB?-controlled L-Type Voltage-Gated Calcium Channel CaV1 2 in resetting the circadian clock in the late night #MMPMID25238857 Schmutz I ; Chavan R ; Ripperger JA ; Maywood ES ; Langwieser N ; Jurik A ; Stauffer A ; Delorme JE ; Moosmang S ; Hastings MH ; Hofmann F ; Albrecht U J Biol Rhythms 2014[Aug]; 29 (4 ): 288-98 PMID25238857 show ga Within the suprachiasmatic nucleus (SCN) of the hypothalamus, circadian timekeeping and resetting have been shown to be largely dependent on both membrane depolarization and intracellular second-messenger signaling. In both of these processes, voltage-gated calcium channels (VGCCs) mediate voltage-dependent calcium influx, which propagates neural impulses by stimulating vesicle fusion and instigates intracellular pathways resulting in clock gene expression. Through the cumulative actions of these processes, the phase of the internal clock is modified to match the light cycle of the external environment. To parse out the distinct roles of the L-type VGCCs, we analyzed mice deficient in Cav1.2 (Cacna1c) in brain tissue. We found that mice deficient in the Cav1.2 channel exhibited a significant reduction in their ability to phase-advance circadian behavior when subjected to a light pulse in the late night. Furthermore, the study revealed that the expression of Cav1.2 mRNA was rhythmic (peaking during the late night) and was regulated by the circadian clock component REV-ERB?. Finally, the induction of clock genes in both the early and late subjective night was affected by the loss of Cav1.2, with reductions in Per2 and Per1 in the early and late night, respectively. In sum, these results reveal a role of the L-type VGCC Cav1.2 in mediating both clock gene expression and phase advances in response to a light pulse in the late night. |Animals [MESH] |Calcium Channels, L-Type/*genetics [MESH] |Calcium/metabolism [MESH] |Circadian Clocks/*genetics [MESH] |Circadian Rhythm/*genetics [MESH] |Gene Expression/genetics [MESH] |Light [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Nuclear Proteins/genetics [MESH] |Nuclear Receptor Subfamily 1, Group D, Member 1/*genetics [MESH] |Period Circadian Proteins/genetics [MESH] |Photoperiod [MESH] |RNA, Messenger/genetics [MESH]A specific role for the REV-ERB?-controlled L-Type Voltage-Gated Calci(epmc).pdf DeepDyve Pubget Overpricing