14-3-3ɛ/ζ Affects the stability of δ-catenin and regulates δ-catenin-induced dendrogenesis
Accumulated evidence suggests that aberrant regulation of δ-catenin leads to pathological consequences such as mental retardation and cognitive dysfunction. This study revealed that 14-3-3ɛ/ζ stabilizes δ-catenin, with different binding regions involved in the interaction. Furthermore, the specific...
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| Veröffentlicht in: | FEBS open bio 2013-01, Vol.3 (1), p.16-21 |
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| description | Accumulated evidence suggests that aberrant regulation of δ-catenin leads to pathological consequences such as mental retardation and cognitive dysfunction. This study revealed that 14-3-3ɛ/ζ stabilizes δ-catenin, with different binding regions involved in the interaction. Furthermore, the specific inhibition of the interaction of 14-3-3 with δ-catenin reduced levels of δ-catenin and significantly impaired the capacity of δ-catenin to induce dendritic branching in both NIH3T3 fibroblasts and primary hippocampal neurons. However, the S1094A δ-catenin mutant, which cannot interact with 14-3-3ζ, still retained the capability of inducing dendrogenesis. Taken together, these results elucidate the underlying events that regulate the stability of δ-catenin and δ-catenin-induced dendrogenesis.
▸ Aberrant regulation of δ-catenin in neurons leads to several pathological consequences. 14-3-3ɛ/ζ Interacts with δ-catenin, increasing its stability. ▸ This interaction significantly affects the induction of dendritic branches in NIH 3T3 fibroblasts. ▸ A similar effect was seen in primary hippocampal neurons. |
| doi_str_mv | 10.1016/j.fob.2012.11.006 |
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▸ Aberrant regulation of δ-catenin in neurons leads to several pathological consequences. 14-3-3ɛ/ζ Interacts with δ-catenin, increasing its stability. ▸ This interaction significantly affects the induction of dendritic branches in NIH 3T3 fibroblasts. ▸ A similar effect was seen in primary hippocampal neurons.</description><identifier>ISSN: 2211-5463</identifier><identifier>EISSN: 2211-5463</identifier><identifier>DOI: 10.1016/j.fob.2012.11.006</identifier><identifier>PMID: 23772369</identifier><language>eng</language><publisher>England: Elsevier B.V</publisher><subject>14-3-3 ; Alzheimer's disease ; Brain research ; Catenin ; Cell cycle ; Cognitive ability ; Data analysis ; Dendritic branching ; Dendrogenesis ; Fibroblasts ; Hippocampus ; Immunoglobulins ; Kinases ; Neuron ; Phosphorylation ; Protein stability ; Proteins ; Software ; δ-Catenin</subject><ispartof>FEBS open bio, 2013-01, Vol.3 (1), p.16-21</ispartof><rights>2013 The Authors</rights><rights>FEBS Open Bio 3 (2013) 2211-5463 ©2015 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.</rights><rights>2013. This work is published under http://creativecommons.org/licenses/by-nc-nd/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 The Authors 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4137-bce2be35bd0488f81e6371a61e53ca20061003c8ddb8a89bd86cf9593728934b3</citedby><cites>FETCH-LOGICAL-c4137-bce2be35bd0488f81e6371a61e53ca20061003c8ddb8a89bd86cf9593728934b3</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/PMC3668525/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3668525/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23772369$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>He, Yongfeng</creatorcontrib><creatorcontrib>Han, Jeong Ran</creatorcontrib><creatorcontrib>Chang, Ockyoung</creatorcontrib><creatorcontrib>Oh, Minsoo</creatorcontrib><creatorcontrib>James, Sarah E.</creatorcontrib><creatorcontrib>Lu, Qun</creatorcontrib><creatorcontrib>Seo, Young-Woo</creatorcontrib><creatorcontrib>Kim, Hangun</creatorcontrib><creatorcontrib>Kim, Kwonseop</creatorcontrib><title>14-3-3ɛ/ζ Affects the stability of δ-catenin and regulates δ-catenin-induced dendrogenesis</title><title>FEBS open bio</title><addtitle>FEBS Open Bio</addtitle><description>Accumulated evidence suggests that aberrant regulation of δ-catenin leads to pathological consequences such as mental retardation and cognitive dysfunction. This study revealed that 14-3-3ɛ/ζ stabilizes δ-catenin, with different binding regions involved in the interaction. Furthermore, the specific inhibition of the interaction of 14-3-3 with δ-catenin reduced levels of δ-catenin and significantly impaired the capacity of δ-catenin to induce dendritic branching in both NIH3T3 fibroblasts and primary hippocampal neurons. However, the S1094A δ-catenin mutant, which cannot interact with 14-3-3ζ, still retained the capability of inducing dendrogenesis. Taken together, these results elucidate the underlying events that regulate the stability of δ-catenin and δ-catenin-induced dendrogenesis.
▸ Aberrant regulation of δ-catenin in neurons leads to several pathological consequences. 14-3-3ɛ/ζ Interacts with δ-catenin, increasing its stability. ▸ This interaction significantly affects the induction of dendritic branches in NIH 3T3 fibroblasts. ▸ A similar effect was seen in primary hippocampal neurons.</description><subject>14-3-3</subject><subject>Alzheimer's disease</subject><subject>Brain research</subject><subject>Catenin</subject><subject>Cell cycle</subject><subject>Cognitive ability</subject><subject>Data analysis</subject><subject>Dendritic branching</subject><subject>Dendrogenesis</subject><subject>Fibroblasts</subject><subject>Hippocampus</subject><subject>Immunoglobulins</subject><subject>Kinases</subject><subject>Neuron</subject><subject>Phosphorylation</subject><subject>Protein stability</subject><subject>Proteins</subject><subject>Software</subject><subject>δ-Catenin</subject><issn>2211-5463</issn><issn>2211-5463</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFks9u1DAQxiMEolXpA3BBkbhwSeqx88cRElJb2oJUiQNwxXLsydarrF3spGifhddAvAOXPlNntaVaOIAvtjXffJqZ32TZc2AlMGiOluUQ-pIz4CVAyVjzKNvnHKCoq0Y83nnvZYcpLRmdhvIYe5rtcdG2XDTdfvYFqkIU4tf3o9uf-fEwoJlSPl1hnibdu9FN6zwM-e2PwugJvfO59jaPuJhH-qedQOG8nQ3a3KK3MSzQY3LpWfZk0GPCw_v7IPt8fvbp9F1x-eHi_enxZWEqEG3RG-Q9irq3rJJykICNaEE3gLUwmlPlwJgw0tpeatn1VjZm6OpOtFx2ourFQfZm63s99yu0Bv0U9aiuo1vpuFZBO_VnxLsrtQg3SjSNrHlNBq_uDWL4OmOa1Molg-OoPYY5KaBpcUHTZCR9-Zd0GeboqT3FedcRkZZ1pIKtysSQUsThoRhgagNQLRUBVBuACkBRj5TzYreLh4zfuEjwdiv45kZc_99RnZ-dVB83m7BZBKBBslq2ZPN6a4OE5MZhVMk49ETPRVoAZYP7R5V30f3Aqg</recordid><startdate>20130101</startdate><enddate>20130101</enddate><creator>He, Yongfeng</creator><creator>Han, Jeong Ran</creator><creator>Chang, Ockyoung</creator><creator>Oh, Minsoo</creator><creator>James, Sarah E.</creator><creator>Lu, Qun</creator><creator>Seo, Young-Woo</creator><creator>Kim, Hangun</creator><creator>Kim, Kwonseop</creator><general>Elsevier B.V</general><general>John Wiley & Sons, Inc</general><general>Elsevier</general><scope>6I.</scope><scope>AAFTH</scope><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20130101</creationdate><title>14-3-3ɛ/ζ Affects the stability of δ-catenin and regulates δ-catenin-induced dendrogenesis</title><author>He, Yongfeng ; Han, Jeong Ran ; Chang, Ockyoung ; Oh, Minsoo ; James, Sarah E. ; Lu, Qun ; Seo, Young-Woo ; Kim, Hangun ; Kim, Kwonseop</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4137-bce2be35bd0488f81e6371a61e53ca20061003c8ddb8a89bd86cf9593728934b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>14-3-3</topic><topic>Alzheimer's disease</topic><topic>Brain research</topic><topic>Catenin</topic><topic>Cell cycle</topic><topic>Cognitive ability</topic><topic>Data analysis</topic><topic>Dendritic branching</topic><topic>Dendrogenesis</topic><topic>Fibroblasts</topic><topic>Hippocampus</topic><topic>Immunoglobulins</topic><topic>Kinases</topic><topic>Neuron</topic><topic>Phosphorylation</topic><topic>Protein stability</topic><topic>Proteins</topic><topic>Software</topic><topic>δ-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>He, Yongfeng</creatorcontrib><creatorcontrib>Han, Jeong Ran</creatorcontrib><creatorcontrib>Chang, Ockyoung</creatorcontrib><creatorcontrib>Oh, Minsoo</creatorcontrib><creatorcontrib>James, Sarah E.</creatorcontrib><creatorcontrib>Lu, Qun</creatorcontrib><creatorcontrib>Seo, Young-Woo</creatorcontrib><creatorcontrib>Kim, Hangun</creatorcontrib><creatorcontrib>Kim, Kwonseop</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library Free Content</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>FEBS open bio</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>He, Yongfeng</au><au>Han, Jeong Ran</au><au>Chang, Ockyoung</au><au>Oh, Minsoo</au><au>James, Sarah E.</au><au>Lu, Qun</au><au>Seo, Young-Woo</au><au>Kim, Hangun</au><au>Kim, Kwonseop</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>14-3-3ɛ/ζ Affects the stability of δ-catenin and regulates δ-catenin-induced dendrogenesis</atitle><jtitle>FEBS open bio</jtitle><addtitle>FEBS Open Bio</addtitle><date>2013-01-01</date><risdate>2013</risdate><volume>3</volume><issue>1</issue><spage>16</spage><epage>21</epage><pages>16-21</pages><issn>2211-5463</issn><eissn>2211-5463</eissn><abstract>Accumulated evidence suggests that aberrant regulation of δ-catenin leads to pathological consequences such as mental retardation and cognitive dysfunction. This study revealed that 14-3-3ɛ/ζ stabilizes δ-catenin, with different binding regions involved in the interaction. Furthermore, the specific inhibition of the interaction of 14-3-3 with δ-catenin reduced levels of δ-catenin and significantly impaired the capacity of δ-catenin to induce dendritic branching in both NIH3T3 fibroblasts and primary hippocampal neurons. However, the S1094A δ-catenin mutant, which cannot interact with 14-3-3ζ, still retained the capability of inducing dendrogenesis. Taken together, these results elucidate the underlying events that regulate the stability of δ-catenin and δ-catenin-induced dendrogenesis.
▸ Aberrant regulation of δ-catenin in neurons leads to several pathological consequences. 14-3-3ɛ/ζ Interacts with δ-catenin, increasing its stability. ▸ This interaction significantly affects the induction of dendritic branches in NIH 3T3 fibroblasts. ▸ A similar effect was seen in primary hippocampal neurons.</abstract><cop>England</cop><pub>Elsevier B.V</pub><pmid>23772369</pmid><doi>10.1016/j.fob.2012.11.006</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 14-3-3 Alzheimer's disease Brain research Catenin Cell cycle Cognitive ability Data analysis Dendritic branching Dendrogenesis Fibroblasts Hippocampus Immunoglobulins Kinases Neuron Phosphorylation Protein stability Proteins Software δ-Catenin |
| title | 14-3-3ɛ/ζ Affects the stability of δ-catenin and regulates δ-catenin-induced dendrogenesis |
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