CRISPR-based identification of N-terminal acetylation in synucleinopathies

A recent study by Kumar et al. identified several biological pathways that regulate the levels of endogenous alpha-synuclein (α-synuclein). They specifically highlighted the N-terminal acetylation (NTA) pathway as an important factor in maintaining the stability of endogenous α-synuclein, suggesting...

Full description

Saved in:
Bibliographic Details
Published in:Trends in neurosciences (Regular ed.) 2024-05, Vol.47 (5), p.324-325
Main Authors: Bae, Eun-Jin, Lee, Seung-Jae
Format: Article
Language:English
Subjects:
Acetylation
alpha-Synuclein - genetics
alpha-Synuclein - metabolism
Animals
Clustered Regularly Interspaced Short Palindromic Repeats - genetics
Humans
NatB
Parkinson’s disease
proteasome
protein aggregation
Protein Processing, Post-Translational - physiology
Synucleinopathies - genetics
Synucleinopathies - metabolism
α-synuclein
Citations: Items that this one cites
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by
cites cdi_FETCH-LOGICAL-c307t-e3d05c27b5d42bcb2956dd872f1c399593e02dafd771fb03259cd090fd627b453
container_end_page 325
container_issue 5
container_start_page 324
container_title Trends in neurosciences (Regular ed.)
container_volume 47
creator Bae, Eun-Jin
Lee, Seung-Jae
description A recent study by Kumar et al. identified several biological pathways that regulate the levels of endogenous alpha-synuclein (α-synuclein). They specifically highlighted the N-terminal acetylation (NTA) pathway as an important factor in maintaining the stability of endogenous α-synuclein, suggesting targeting the NTA pathway as a potential therapeutic approach. A recent study by Kumar et al. identified several biological pathways that regulate the levels of endogenous alpha-synuclein (α-synuclein). They specifically highlighted the N-terminal acetylation (NTA) pathway as an important factor in maintaining the stability of endogenous α-synuclein, suggesting targeting the NTA pathway as a potential therapeutic approach.
doi_str_mv 10.1016/j.tins.2024.03.006
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_3022574527</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0166223624000432</els_id><sourcerecordid>3022574527</sourcerecordid><originalsourceid>FETCH-LOGICAL-c307t-e3d05c27b5d42bcb2956dd872f1c399593e02dafd771fb03259cd090fd627b453</originalsourceid><addsrcrecordid>eNp9kE1LAzEQhoMotlb_gAfZo5ddJ8lmP8CLFD8qRaUqeAvZZBZTttm6SYX-e7ds9ehl5jDP-8I8hJxTSCjQ7GqZBOt8woClCfAEIDsgY1rkRUyh-Dgk4x7KYsZ4NiIn3i8BaFrQ9JiMeCEE78eYPE4Xs9eXRVwpjyayBl2wtdUq2NZFbR09xQG7lXWqiZTGsG2Gi3WR37qNbtC6dq3Cp0V_So5q1Xg82-8Jeb-7fZs-xPPn-9n0Zh5rDnmIkRsQmuWVMCmrdMVKkRlT5KymmpelKDkCM6o2eU7rCjgTpTZQQm2yPpQKPiGXQ--6a7826INcWa-xaZTDduMlB8ZEngqW9ygbUN213ndYy3VnV6rbSgpy51Au5c6h3DmUwGXvsA9d7Ps31QrNX-RXWg9cDwD2X35b7KTXFp1GYzvUQZrW_tf_A1eggu0</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3022574527</pqid></control><display><type>article</type><title>CRISPR-based identification of N-terminal acetylation in synucleinopathies</title><source>Elsevier:Jisc Collections:Elsevier Read and Publish Agreement 2022-2024:Freedom Collection (Reading list)</source><creator>Bae, Eun-Jin ; Lee, Seung-Jae</creator><creatorcontrib>Bae, Eun-Jin ; Lee, Seung-Jae</creatorcontrib><description>A recent study by Kumar et al. identified several biological pathways that regulate the levels of endogenous alpha-synuclein (α-synuclein). They specifically highlighted the N-terminal acetylation (NTA) pathway as an important factor in maintaining the stability of endogenous α-synuclein, suggesting targeting the NTA pathway as a potential therapeutic approach. A recent study by Kumar et al. identified several biological pathways that regulate the levels of endogenous alpha-synuclein (α-synuclein). They specifically highlighted the N-terminal acetylation (NTA) pathway as an important factor in maintaining the stability of endogenous α-synuclein, suggesting targeting the NTA pathway as a potential therapeutic approach.</description><identifier>ISSN: 0166-2236</identifier><identifier>EISSN: 1878-108X</identifier><identifier>DOI: 10.1016/j.tins.2024.03.006</identifier><identifier>PMID: 38553385</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Acetylation ; alpha-Synuclein - genetics ; alpha-Synuclein - metabolism ; Animals ; Clustered Regularly Interspaced Short Palindromic Repeats - genetics ; Humans ; NatB ; Parkinson’s disease ; proteasome ; protein aggregation ; Protein Processing, Post-Translational - physiology ; Synucleinopathies - genetics ; Synucleinopathies - metabolism ; α-synuclein</subject><ispartof>Trends in neurosciences (Regular ed.), 2024-05, Vol.47 (5), p.324-325</ispartof><rights>2024 Elsevier Ltd</rights><rights>Copyright © 2024 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c307t-e3d05c27b5d42bcb2956dd872f1c399593e02dafd771fb03259cd090fd627b453</cites><orcidid>0000-0002-5155-5335</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38553385$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bae, Eun-Jin</creatorcontrib><creatorcontrib>Lee, Seung-Jae</creatorcontrib><title>CRISPR-based identification of N-terminal acetylation in synucleinopathies</title><title>Trends in neurosciences (Regular ed.)</title><addtitle>Trends Neurosci</addtitle><description>A recent study by Kumar et al. identified several biological pathways that regulate the levels of endogenous alpha-synuclein (α-synuclein). They specifically highlighted the N-terminal acetylation (NTA) pathway as an important factor in maintaining the stability of endogenous α-synuclein, suggesting targeting the NTA pathway as a potential therapeutic approach. A recent study by Kumar et al. identified several biological pathways that regulate the levels of endogenous alpha-synuclein (α-synuclein). They specifically highlighted the N-terminal acetylation (NTA) pathway as an important factor in maintaining the stability of endogenous α-synuclein, suggesting targeting the NTA pathway as a potential therapeutic approach.</description><subject>Acetylation</subject><subject>alpha-Synuclein - genetics</subject><subject>alpha-Synuclein - metabolism</subject><subject>Animals</subject><subject>Clustered Regularly Interspaced Short Palindromic Repeats - genetics</subject><subject>Humans</subject><subject>NatB</subject><subject>Parkinson’s disease</subject><subject>proteasome</subject><subject>protein aggregation</subject><subject>Protein Processing, Post-Translational - physiology</subject><subject>Synucleinopathies - genetics</subject><subject>Synucleinopathies - metabolism</subject><subject>α-synuclein</subject><issn>0166-2236</issn><issn>1878-108X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kE1LAzEQhoMotlb_gAfZo5ddJ8lmP8CLFD8qRaUqeAvZZBZTttm6SYX-e7ds9ehl5jDP-8I8hJxTSCjQ7GqZBOt8woClCfAEIDsgY1rkRUyh-Dgk4x7KYsZ4NiIn3i8BaFrQ9JiMeCEE78eYPE4Xs9eXRVwpjyayBl2wtdUq2NZFbR09xQG7lXWqiZTGsG2Gi3WR37qNbtC6dq3Cp0V_So5q1Xg82-8Jeb-7fZs-xPPn-9n0Zh5rDnmIkRsQmuWVMCmrdMVKkRlT5KymmpelKDkCM6o2eU7rCjgTpTZQQm2yPpQKPiGXQ--6a7826INcWa-xaZTDduMlB8ZEngqW9ygbUN213ndYy3VnV6rbSgpy51Au5c6h3DmUwGXvsA9d7Ps31QrNX-RXWg9cDwD2X35b7KTXFp1GYzvUQZrW_tf_A1eggu0</recordid><startdate>202405</startdate><enddate>202405</enddate><creator>Bae, Eun-Jin</creator><creator>Lee, Seung-Jae</creator><general>Elsevier Ltd</general><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><orcidid>https://orcid.org/0000-0002-5155-5335</orcidid></search><sort><creationdate>202405</creationdate><title>CRISPR-based identification of N-terminal acetylation in synucleinopathies</title><author>Bae, Eun-Jin ; Lee, Seung-Jae</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c307t-e3d05c27b5d42bcb2956dd872f1c399593e02dafd771fb03259cd090fd627b453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acetylation</topic><topic>alpha-Synuclein - genetics</topic><topic>alpha-Synuclein - metabolism</topic><topic>Animals</topic><topic>Clustered Regularly Interspaced Short Palindromic Repeats - genetics</topic><topic>Humans</topic><topic>NatB</topic><topic>Parkinson’s disease</topic><topic>proteasome</topic><topic>protein aggregation</topic><topic>Protein Processing, Post-Translational - physiology</topic><topic>Synucleinopathies - genetics</topic><topic>Synucleinopathies - metabolism</topic><topic>α-synuclein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bae, Eun-Jin</creatorcontrib><creatorcontrib>Lee, Seung-Jae</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Trends in neurosciences (Regular ed.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bae, Eun-Jin</au><au>Lee, Seung-Jae</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CRISPR-based identification of N-terminal acetylation in synucleinopathies</atitle><jtitle>Trends in neurosciences (Regular ed.)</jtitle><addtitle>Trends Neurosci</addtitle><date>2024-05</date><risdate>2024</risdate><volume>47</volume><issue>5</issue><spage>324</spage><epage>325</epage><pages>324-325</pages><issn>0166-2236</issn><eissn>1878-108X</eissn><abstract>A recent study by Kumar et al. identified several biological pathways that regulate the levels of endogenous alpha-synuclein (α-synuclein). They specifically highlighted the N-terminal acetylation (NTA) pathway as an important factor in maintaining the stability of endogenous α-synuclein, suggesting targeting the NTA pathway as a potential therapeutic approach. A recent study by Kumar et al. identified several biological pathways that regulate the levels of endogenous alpha-synuclein (α-synuclein). They specifically highlighted the N-terminal acetylation (NTA) pathway as an important factor in maintaining the stability of endogenous α-synuclein, suggesting targeting the NTA pathway as a potential therapeutic approach.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>38553385</pmid><doi>10.1016/j.tins.2024.03.006</doi><tpages>2</tpages><orcidid>https://orcid.org/0000-0002-5155-5335</orcidid></addata></record>
fulltext fulltext
identifier ISSN: 0166-2236
ispartof Trends in neurosciences (Regular ed.), 2024-05, Vol.47 (5), p.324-325
issn 0166-2236
1878-108X
language eng
recordid cdi_proquest_miscellaneous_3022574527
source Elsevier:Jisc Collections:Elsevier Read and Publish Agreement 2022-2024:Freedom Collection (Reading list)
subjects Acetylation
alpha-Synuclein - genetics
alpha-Synuclein - metabolism
Animals
Clustered Regularly Interspaced Short Palindromic Repeats - genetics
Humans
NatB
Parkinson’s disease
proteasome
protein aggregation
Protein Processing, Post-Translational - physiology
Synucleinopathies - genetics
Synucleinopathies - metabolism
α-synuclein
title CRISPR-based identification of N-terminal acetylation in synucleinopathies
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-24T22%3A54%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=CRISPR-based%20identification%20of%20N-terminal%20acetylation%20in%20synucleinopathies&rft.jtitle=Trends%20in%20neurosciences%20(Regular%20ed.)&rft.au=Bae,%20Eun-Jin&rft.date=2024-05&rft.volume=47&rft.issue=5&rft.spage=324&rft.epage=325&rft.pages=324-325&rft.issn=0166-2236&rft.eissn=1878-108X&rft_id=info:doi/10.1016/j.tins.2024.03.006&rft_dat=%3Cproquest_cross%3E3022574527%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c307t-e3d05c27b5d42bcb2956dd872f1c399593e02dafd771fb03259cd090fd627b453%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=3022574527&rft_id=info:pmid/38553385&rfr_iscdi=true