The role of ryanodine receptor type 3 in a mouse model of Alzheimer disease
Dysregulated endoplasmic reticulum (ER) calcium (Ca 2+ ) signaling is reported to play an important role in Alzheimer disease (AD) pathogenesis. The role of ER Ca 2+ release channels, the ryanodine receptors (RyanRs), has been extensively studied in AD models and RyanR expression and activity are up...
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Veröffentlicht in: | Channels (Austin, Tex.) Tex.), 2014-05, Vol.8 (3), p.230-242 |
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creator | Liu, Jie Supnet, Charlene Sun, Suya Zhang, Hua Good, Levi Popugaeva, Elena Bezprozvanny, Ilya |
description | Dysregulated endoplasmic reticulum (ER) calcium (Ca
2+
) signaling is reported to play an important role in Alzheimer disease (AD) pathogenesis. The role of ER Ca
2+
release channels, the ryanodine receptors (RyanRs), has been extensively studied in AD models and RyanR expression and activity are upregulated in the brains of various familial AD (FAD) models. The objective of this study was to utilize a genetic approach to evaluate the importance of RyanR type 3 (RyanR3) in the context of AD pathology. |
doi_str_mv | 10.4161/chan.27471 |
format | Article |
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2+
) signaling is reported to play an important role in Alzheimer disease (AD) pathogenesis. The role of ER Ca
2+
release channels, the ryanodine receptors (RyanRs), has been extensively studied in AD models and RyanR expression and activity are upregulated in the brains of various familial AD (FAD) models. The objective of this study was to utilize a genetic approach to evaluate the importance of RyanR type 3 (RyanR3) in the context of AD pathology.</description><identifier>ISSN: 1933-6950</identifier><identifier>EISSN: 1933-6969</identifier><identifier>DOI: 10.4161/chan.27471</identifier><identifier>PMID: 24476841</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Alzheimer Disease - genetics ; Alzheimer Disease - metabolism ; Amyloid beta-Peptides - metabolism ; amyloid load ; Animals ; Arc ; caffeine ; Disease Models, Animal ; EEG ; Hippocampus - metabolism ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons - metabolism ; Research Paper ; ryanodine receptor ; Ryanodine Receptor Calcium Release Channel - genetics ; Ryanodine Receptor Calcium Release Channel - metabolism ; spine morphology ; spontaneous activity</subject><ispartof>Channels (Austin, Tex.), 2014-05, Vol.8 (3), p.230-242</ispartof><rights>Copyright © 2014 Landes Bioscience 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c490t-27082f67f4491b3c742da73580770eee252609701cd929c21e940600f066ec9d3</citedby><cites>FETCH-LOGICAL-c490t-27082f67f4491b3c742da73580770eee252609701cd929c21e940600f066ec9d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4203752/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4203752/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24476841$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Supnet, Charlene</creatorcontrib><creatorcontrib>Sun, Suya</creatorcontrib><creatorcontrib>Zhang, Hua</creatorcontrib><creatorcontrib>Good, Levi</creatorcontrib><creatorcontrib>Popugaeva, Elena</creatorcontrib><creatorcontrib>Bezprozvanny, Ilya</creatorcontrib><title>The role of ryanodine receptor type 3 in a mouse model of Alzheimer disease</title><title>Channels (Austin, Tex.)</title><addtitle>Channels (Austin)</addtitle><description>Dysregulated endoplasmic reticulum (ER) calcium (Ca
2+
) signaling is reported to play an important role in Alzheimer disease (AD) pathogenesis. The role of ER Ca
2+
release channels, the ryanodine receptors (RyanRs), has been extensively studied in AD models and RyanR expression and activity are upregulated in the brains of various familial AD (FAD) models. The objective of this study was to utilize a genetic approach to evaluate the importance of RyanR type 3 (RyanR3) in the context of AD pathology.</description><subject>Alzheimer Disease - genetics</subject><subject>Alzheimer Disease - metabolism</subject><subject>Amyloid beta-Peptides - metabolism</subject><subject>amyloid load</subject><subject>Animals</subject><subject>Arc</subject><subject>caffeine</subject><subject>Disease Models, Animal</subject><subject>EEG</subject><subject>Hippocampus - metabolism</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Neurons - metabolism</subject><subject>Research Paper</subject><subject>ryanodine receptor</subject><subject>Ryanodine Receptor Calcium Release Channel - genetics</subject><subject>Ryanodine Receptor Calcium Release Channel - metabolism</subject><subject>spine morphology</subject><subject>spontaneous activity</subject><issn>1933-6950</issn><issn>1933-6969</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><recordid>eNptkMtKAzEUhoMoXqobH0CyFKGa2yTNRhDxhoKbug4xc8ZGMklNpkp9eqe2FgU3OSHn4z8nH0KHlJwKKumZm9h4ypRQdAPtUs35UGqpN9f3iuygvVJeCZGcUbqNdpgQSo4E3UX34wngnALg1OA8tzHVPvYv4GDapYy7-RQwxz5ii9s0K9CfNYQFfRE-J-BbyLj2BWyBfbTV2FDgYFUH6On6anx5O3x4vLm7vHgYOqFJN2SKjFgjVSOEps_cKcFqq3g1IkoRAGAVk0QrQl2tmXaMghZEEtIQKcHpmg_Q-TJ3OntuoXYQu2yDmWbf2jw3yXrztxP9xLykdyMY4apifcDxKiCntxmUzrS-OAjBRuj_aKhkWiuqe38DdLJEXU6lZGjWYygxC_tmYd982-_ho9-LrdEf3T1QLQEfm5Rb-5FyqE1n5yHlJtvofDH8n-Av1teR_A</recordid><startdate>20140501</startdate><enddate>20140501</enddate><creator>Liu, Jie</creator><creator>Supnet, Charlene</creator><creator>Sun, Suya</creator><creator>Zhang, Hua</creator><creator>Good, Levi</creator><creator>Popugaeva, Elena</creator><creator>Bezprozvanny, Ilya</creator><general>Taylor & Francis</general><general>Landes Bioscience</general><scope>0YH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140501</creationdate><title>The role of ryanodine receptor type 3 in a mouse model of Alzheimer disease</title><author>Liu, Jie ; 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2+
) signaling is reported to play an important role in Alzheimer disease (AD) pathogenesis. The role of ER Ca
2+
release channels, the ryanodine receptors (RyanRs), has been extensively studied in AD models and RyanR expression and activity are upregulated in the brains of various familial AD (FAD) models. The objective of this study was to utilize a genetic approach to evaluate the importance of RyanR type 3 (RyanR3) in the context of AD pathology.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>24476841</pmid><doi>10.4161/chan.27471</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Alzheimer Disease - genetics Alzheimer Disease - metabolism Amyloid beta-Peptides - metabolism amyloid load Animals Arc caffeine Disease Models, Animal EEG Hippocampus - metabolism Humans Mice Mice, Inbred C57BL Mice, Knockout Neurons - metabolism Research Paper ryanodine receptor Ryanodine Receptor Calcium Release Channel - genetics Ryanodine Receptor Calcium Release Channel - metabolism spine morphology spontaneous activity |
title | The role of ryanodine receptor type 3 in a mouse model of Alzheimer disease |
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