A ONECUT1 regulatory, non-coding region in pancreatic development and diabetes
In a patient with permanent neonatal syndromic diabetes clinically similar to cases with ONECUT1 biallelic mutations, we identified a disease-causing deletion located upstream of ONECUT1. Through genetic, genomic, and functional studies, we identified a crucial regulatory region acting as an enhance...
Gespeichert in:
| Veröffentlicht in: | Cell reports (Cambridge) 2024-11, Vol.43 (11), p.114853, Article 114853 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 11 |
| container_start_page | 114853 |
| container_title | Cell reports (Cambridge) |
| container_volume | 43 |
| creator | Merz, Sarah Senée, Valérie Philippi, Anne Oswald, Franz Shaigan, Mina Führer, Marita Drewes, Cosima Allgöwer, Chantal Öllinger, Rupert Heni, Martin Boland, Anne Deleuze, Jean-François Birkhofer, Franziska Gusmao, Eduardo G. Wagner, Martin Hohwieler, Meike Breunig, Markus Rad, Roland Siebert, Reiner Messerer, David Alexander Christian Costa, Ivan G. Alvarez, Fernando Julier, Cécile Kleger, Alexander Heller, Sandra |
| description | In a patient with permanent neonatal syndromic diabetes clinically similar to cases with ONECUT1 biallelic mutations, we identified a disease-causing deletion located upstream of ONECUT1. Through genetic, genomic, and functional studies, we identified a crucial regulatory region acting as an enhancer of ONECUT1 specifically during pancreatic development. This enhancer region contains a low-frequency variant showing a strong association with type 2 diabetes and other glycemic traits, thus extending the contribution of this region to common forms of diabetes. Clinical relevance is provided by experimentally tailored therapy options for patients carrying ONECUT1 coding or regulatory mutations.
[Display omitted]
•Compound heterozygous mutations in ONECUT1 and a non-coding region cause neonatal diabetes•Heterozygous deletion of the non-coding enhancer confirms cis-regulation of ONECUT1 expression•Changes in chromatin looping promote ONECUT1 enhancer activity during pancreatic development•ONECUT1 coding or enhancer mutations affect β cell performance, counteracted by T2D drugs
Merz et al. identify a disease-causing deletion upstream of ONECUT1. They uncover a cis-acting enhancer that regulates ONECUT1 expression during pancreatic development, harboring a low-frequency variant associated with type 2 diabetes. Additionally, they provide clinical relevance by experimentally testing in vitro therapeutic options for affected patients. |
| doi_str_mv | 10.1016/j.celrep.2024.114853 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_hal_p</sourceid><recordid>TN_cdi_proquest_miscellaneous_3118834522</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S221112472401204X</els_id><sourcerecordid>3118834522</sourcerecordid><originalsourceid>FETCH-LOGICAL-c275t-69a6619a7511437b8803dd049ebfb8b63e7a6bf430165e90f75012f05de439453</originalsourceid><addsrcrecordid>eNp9kE1rGzEQhkVoSILjfxDKHlvIuhpJ-3UpGOM0BZNc4rPQSrOJzFraSmtD_n1kNg05RReJ4Zl3Rg8hN0AXQKH8tVto7AMOC0aZWACIuuBn5IoxgByYqL59el-SeYw7mk5JARpxQS55I1jFob4iD8vs8WG92j5BFvD50KvRh9fbzHmXa2-sez6VrXeZddmgnA6oRqszg0fs_bBHN2bKmcxY1eKI8Zqcd6qPOH-_Z2R7t35a3eebxz9_V8tNrllVjHnZqLKERlVFWp1XbV1TbgwVDbZdW7clx0qVbSd4-muBDe2qggLraGFQpN0LPiM_p9wX1csh2L0Kr9IrK--XG3mqpSzaNCU9QmJ_TOwQ_L8DxlHubUz6euXQH6LkAHXNRcFYQsWE6uBjDNh9ZAOVJ_FyJyfx8iReTuJT2_f3CYd2j-aj6b_mBPyeAExOjhaDjNqi02hsQD1K4-3XE94AlPCSeg</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3118834522</pqid></control><display><type>article</type><title>A ONECUT1 regulatory, non-coding region in pancreatic development and diabetes</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Cell Press Free Archives</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Merz, Sarah ; Senée, Valérie ; Philippi, Anne ; Oswald, Franz ; Shaigan, Mina ; Führer, Marita ; Drewes, Cosima ; Allgöwer, Chantal ; Öllinger, Rupert ; Heni, Martin ; Boland, Anne ; Deleuze, Jean-François ; Birkhofer, Franziska ; Gusmao, Eduardo G. ; Wagner, Martin ; Hohwieler, Meike ; Breunig, Markus ; Rad, Roland ; Siebert, Reiner ; Messerer, David Alexander Christian ; Costa, Ivan G. ; Alvarez, Fernando ; Julier, Cécile ; Kleger, Alexander ; Heller, Sandra</creator><creatorcontrib>Merz, Sarah ; Senée, Valérie ; Philippi, Anne ; Oswald, Franz ; Shaigan, Mina ; Führer, Marita ; Drewes, Cosima ; Allgöwer, Chantal ; Öllinger, Rupert ; Heni, Martin ; Boland, Anne ; Deleuze, Jean-François ; Birkhofer, Franziska ; Gusmao, Eduardo G. ; Wagner, Martin ; Hohwieler, Meike ; Breunig, Markus ; Rad, Roland ; Siebert, Reiner ; Messerer, David Alexander Christian ; Costa, Ivan G. ; Alvarez, Fernando ; Julier, Cécile ; Kleger, Alexander ; Heller, Sandra</creatorcontrib><description>In a patient with permanent neonatal syndromic diabetes clinically similar to cases with ONECUT1 biallelic mutations, we identified a disease-causing deletion located upstream of ONECUT1. Through genetic, genomic, and functional studies, we identified a crucial regulatory region acting as an enhancer of ONECUT1 specifically during pancreatic development. This enhancer region contains a low-frequency variant showing a strong association with type 2 diabetes and other glycemic traits, thus extending the contribution of this region to common forms of diabetes. Clinical relevance is provided by experimentally tailored therapy options for patients carrying ONECUT1 coding or regulatory mutations.
[Display omitted]
•Compound heterozygous mutations in ONECUT1 and a non-coding region cause neonatal diabetes•Heterozygous deletion of the non-coding enhancer confirms cis-regulation of ONECUT1 expression•Changes in chromatin looping promote ONECUT1 enhancer activity during pancreatic development•ONECUT1 coding or enhancer mutations affect β cell performance, counteracted by T2D drugs
Merz et al. identify a disease-causing deletion upstream of ONECUT1. They uncover a cis-acting enhancer that regulates ONECUT1 expression during pancreatic development, harboring a low-frequency variant associated with type 2 diabetes. Additionally, they provide clinical relevance by experimentally testing in vitro therapeutic options for affected patients.</description><identifier>ISSN: 2211-1247</identifier><identifier>EISSN: 2211-1247</identifier><identifier>DOI: 10.1016/j.celrep.2024.114853</identifier><identifier>PMID: 39427318</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Cancer ; cis-regulatory enhancer ; Diabetes Mellitus - genetics ; Diabetes Mellitus - metabolism ; Diabetes Mellitus - pathology ; Diabetes Mellitus, Type 2 - genetics ; Diabetes Mellitus, Type 2 - metabolism ; Diabetes Mellitus, Type 2 - pathology ; Enhancer Elements, Genetic - genetics ; Female ; human embryonic stem cells ; Humans ; Life Sciences ; lncRNA ; Male ; Mice ; monogenic diabetes ; Mutation - genetics ; neonatal diabetes ; ONECUT1 ; Pancreas - metabolism ; Pancreas - pathology ; pancreas differentiation ; Regulatory Sequences, Nucleic Acid - genetics ; stem cell islets ; type 2 diabetes</subject><ispartof>Cell reports (Cambridge), 2024-11, Vol.43 (11), p.114853, Article 114853</ispartof><rights>2024 The Author(s)</rights><rights>Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c275t-69a6619a7511437b8803dd049ebfb8b63e7a6bf430165e90f75012f05de439453</cites><orcidid>0000-0003-0592-5232</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,860,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39427318$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-04909960$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Merz, Sarah</creatorcontrib><creatorcontrib>Senée, Valérie</creatorcontrib><creatorcontrib>Philippi, Anne</creatorcontrib><creatorcontrib>Oswald, Franz</creatorcontrib><creatorcontrib>Shaigan, Mina</creatorcontrib><creatorcontrib>Führer, Marita</creatorcontrib><creatorcontrib>Drewes, Cosima</creatorcontrib><creatorcontrib>Allgöwer, Chantal</creatorcontrib><creatorcontrib>Öllinger, Rupert</creatorcontrib><creatorcontrib>Heni, Martin</creatorcontrib><creatorcontrib>Boland, Anne</creatorcontrib><creatorcontrib>Deleuze, Jean-François</creatorcontrib><creatorcontrib>Birkhofer, Franziska</creatorcontrib><creatorcontrib>Gusmao, Eduardo G.</creatorcontrib><creatorcontrib>Wagner, Martin</creatorcontrib><creatorcontrib>Hohwieler, Meike</creatorcontrib><creatorcontrib>Breunig, Markus</creatorcontrib><creatorcontrib>Rad, Roland</creatorcontrib><creatorcontrib>Siebert, Reiner</creatorcontrib><creatorcontrib>Messerer, David Alexander Christian</creatorcontrib><creatorcontrib>Costa, Ivan G.</creatorcontrib><creatorcontrib>Alvarez, Fernando</creatorcontrib><creatorcontrib>Julier, Cécile</creatorcontrib><creatorcontrib>Kleger, Alexander</creatorcontrib><creatorcontrib>Heller, Sandra</creatorcontrib><title>A ONECUT1 regulatory, non-coding region in pancreatic development and diabetes</title><title>Cell reports (Cambridge)</title><addtitle>Cell Rep</addtitle><description>In a patient with permanent neonatal syndromic diabetes clinically similar to cases with ONECUT1 biallelic mutations, we identified a disease-causing deletion located upstream of ONECUT1. Through genetic, genomic, and functional studies, we identified a crucial regulatory region acting as an enhancer of ONECUT1 specifically during pancreatic development. This enhancer region contains a low-frequency variant showing a strong association with type 2 diabetes and other glycemic traits, thus extending the contribution of this region to common forms of diabetes. Clinical relevance is provided by experimentally tailored therapy options for patients carrying ONECUT1 coding or regulatory mutations.
[Display omitted]
•Compound heterozygous mutations in ONECUT1 and a non-coding region cause neonatal diabetes•Heterozygous deletion of the non-coding enhancer confirms cis-regulation of ONECUT1 expression•Changes in chromatin looping promote ONECUT1 enhancer activity during pancreatic development•ONECUT1 coding or enhancer mutations affect β cell performance, counteracted by T2D drugs
Merz et al. identify a disease-causing deletion upstream of ONECUT1. They uncover a cis-acting enhancer that regulates ONECUT1 expression during pancreatic development, harboring a low-frequency variant associated with type 2 diabetes. Additionally, they provide clinical relevance by experimentally testing in vitro therapeutic options for affected patients.</description><subject>Animals</subject><subject>Cancer</subject><subject>cis-regulatory enhancer</subject><subject>Diabetes Mellitus - genetics</subject><subject>Diabetes Mellitus - metabolism</subject><subject>Diabetes Mellitus - pathology</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Diabetes Mellitus, Type 2 - pathology</subject><subject>Enhancer Elements, Genetic - genetics</subject><subject>Female</subject><subject>human embryonic stem cells</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>lncRNA</subject><subject>Male</subject><subject>Mice</subject><subject>monogenic diabetes</subject><subject>Mutation - genetics</subject><subject>neonatal diabetes</subject><subject>ONECUT1</subject><subject>Pancreas - metabolism</subject><subject>Pancreas - pathology</subject><subject>pancreas differentiation</subject><subject>Regulatory Sequences, Nucleic Acid - genetics</subject><subject>stem cell islets</subject><subject>type 2 diabetes</subject><issn>2211-1247</issn><issn>2211-1247</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1rGzEQhkVoSILjfxDKHlvIuhpJ-3UpGOM0BZNc4rPQSrOJzFraSmtD_n1kNg05RReJ4Zl3Rg8hN0AXQKH8tVto7AMOC0aZWACIuuBn5IoxgByYqL59el-SeYw7mk5JARpxQS55I1jFob4iD8vs8WG92j5BFvD50KvRh9fbzHmXa2-sez6VrXeZddmgnA6oRqszg0fs_bBHN2bKmcxY1eKI8Zqcd6qPOH-_Z2R7t35a3eebxz9_V8tNrllVjHnZqLKERlVFWp1XbV1TbgwVDbZdW7clx0qVbSd4-muBDe2qggLraGFQpN0LPiM_p9wX1csh2L0Kr9IrK--XG3mqpSzaNCU9QmJ_TOwQ_L8DxlHubUz6euXQH6LkAHXNRcFYQsWE6uBjDNh9ZAOVJ_FyJyfx8iReTuJT2_f3CYd2j-aj6b_mBPyeAExOjhaDjNqi02hsQD1K4-3XE94AlPCSeg</recordid><startdate>20241126</startdate><enddate>20241126</enddate><creator>Merz, Sarah</creator><creator>Senée, Valérie</creator><creator>Philippi, Anne</creator><creator>Oswald, Franz</creator><creator>Shaigan, Mina</creator><creator>Führer, Marita</creator><creator>Drewes, Cosima</creator><creator>Allgöwer, Chantal</creator><creator>Öllinger, Rupert</creator><creator>Heni, Martin</creator><creator>Boland, Anne</creator><creator>Deleuze, Jean-François</creator><creator>Birkhofer, Franziska</creator><creator>Gusmao, Eduardo G.</creator><creator>Wagner, Martin</creator><creator>Hohwieler, Meike</creator><creator>Breunig, Markus</creator><creator>Rad, Roland</creator><creator>Siebert, Reiner</creator><creator>Messerer, David Alexander Christian</creator><creator>Costa, Ivan G.</creator><creator>Alvarez, Fernando</creator><creator>Julier, Cécile</creator><creator>Kleger, Alexander</creator><creator>Heller, Sandra</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</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>1XC</scope><scope>VOOES</scope><orcidid>https://orcid.org/0000-0003-0592-5232</orcidid></search><sort><creationdate>20241126</creationdate><title>A ONECUT1 regulatory, non-coding region in pancreatic development and diabetes</title><author>Merz, Sarah ; Senée, Valérie ; Philippi, Anne ; Oswald, Franz ; Shaigan, Mina ; Führer, Marita ; Drewes, Cosima ; Allgöwer, Chantal ; Öllinger, Rupert ; Heni, Martin ; Boland, Anne ; Deleuze, Jean-François ; Birkhofer, Franziska ; Gusmao, Eduardo G. ; Wagner, Martin ; Hohwieler, Meike ; Breunig, Markus ; Rad, Roland ; Siebert, Reiner ; Messerer, David Alexander Christian ; Costa, Ivan G. ; Alvarez, Fernando ; Julier, Cécile ; Kleger, Alexander ; Heller, Sandra</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c275t-69a6619a7511437b8803dd049ebfb8b63e7a6bf430165e90f75012f05de439453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Cancer</topic><topic>cis-regulatory enhancer</topic><topic>Diabetes Mellitus - genetics</topic><topic>Diabetes Mellitus - metabolism</topic><topic>Diabetes Mellitus - pathology</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Diabetes Mellitus, Type 2 - pathology</topic><topic>Enhancer Elements, Genetic - genetics</topic><topic>Female</topic><topic>human embryonic stem cells</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>lncRNA</topic><topic>Male</topic><topic>Mice</topic><topic>monogenic diabetes</topic><topic>Mutation - genetics</topic><topic>neonatal diabetes</topic><topic>ONECUT1</topic><topic>Pancreas - metabolism</topic><topic>Pancreas - pathology</topic><topic>pancreas differentiation</topic><topic>Regulatory Sequences, Nucleic Acid - genetics</topic><topic>stem cell islets</topic><topic>type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Merz, Sarah</creatorcontrib><creatorcontrib>Senée, Valérie</creatorcontrib><creatorcontrib>Philippi, Anne</creatorcontrib><creatorcontrib>Oswald, Franz</creatorcontrib><creatorcontrib>Shaigan, Mina</creatorcontrib><creatorcontrib>Führer, Marita</creatorcontrib><creatorcontrib>Drewes, Cosima</creatorcontrib><creatorcontrib>Allgöwer, Chantal</creatorcontrib><creatorcontrib>Öllinger, Rupert</creatorcontrib><creatorcontrib>Heni, Martin</creatorcontrib><creatorcontrib>Boland, Anne</creatorcontrib><creatorcontrib>Deleuze, Jean-François</creatorcontrib><creatorcontrib>Birkhofer, Franziska</creatorcontrib><creatorcontrib>Gusmao, Eduardo G.</creatorcontrib><creatorcontrib>Wagner, Martin</creatorcontrib><creatorcontrib>Hohwieler, Meike</creatorcontrib><creatorcontrib>Breunig, Markus</creatorcontrib><creatorcontrib>Rad, Roland</creatorcontrib><creatorcontrib>Siebert, Reiner</creatorcontrib><creatorcontrib>Messerer, David Alexander Christian</creatorcontrib><creatorcontrib>Costa, Ivan G.</creatorcontrib><creatorcontrib>Alvarez, Fernando</creatorcontrib><creatorcontrib>Julier, Cécile</creatorcontrib><creatorcontrib>Kleger, Alexander</creatorcontrib><creatorcontrib>Heller, Sandra</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><jtitle>Cell reports (Cambridge)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Merz, Sarah</au><au>Senée, Valérie</au><au>Philippi, Anne</au><au>Oswald, Franz</au><au>Shaigan, Mina</au><au>Führer, Marita</au><au>Drewes, Cosima</au><au>Allgöwer, Chantal</au><au>Öllinger, Rupert</au><au>Heni, Martin</au><au>Boland, Anne</au><au>Deleuze, Jean-François</au><au>Birkhofer, Franziska</au><au>Gusmao, Eduardo G.</au><au>Wagner, Martin</au><au>Hohwieler, Meike</au><au>Breunig, Markus</au><au>Rad, Roland</au><au>Siebert, Reiner</au><au>Messerer, David Alexander Christian</au><au>Costa, Ivan G.</au><au>Alvarez, Fernando</au><au>Julier, Cécile</au><au>Kleger, Alexander</au><au>Heller, Sandra</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A ONECUT1 regulatory, non-coding region in pancreatic development and diabetes</atitle><jtitle>Cell reports (Cambridge)</jtitle><addtitle>Cell Rep</addtitle><date>2024-11-26</date><risdate>2024</risdate><volume>43</volume><issue>11</issue><spage>114853</spage><pages>114853-</pages><artnum>114853</artnum><issn>2211-1247</issn><eissn>2211-1247</eissn><abstract>In a patient with permanent neonatal syndromic diabetes clinically similar to cases with ONECUT1 biallelic mutations, we identified a disease-causing deletion located upstream of ONECUT1. Through genetic, genomic, and functional studies, we identified a crucial regulatory region acting as an enhancer of ONECUT1 specifically during pancreatic development. This enhancer region contains a low-frequency variant showing a strong association with type 2 diabetes and other glycemic traits, thus extending the contribution of this region to common forms of diabetes. Clinical relevance is provided by experimentally tailored therapy options for patients carrying ONECUT1 coding or regulatory mutations.
[Display omitted]
•Compound heterozygous mutations in ONECUT1 and a non-coding region cause neonatal diabetes•Heterozygous deletion of the non-coding enhancer confirms cis-regulation of ONECUT1 expression•Changes in chromatin looping promote ONECUT1 enhancer activity during pancreatic development•ONECUT1 coding or enhancer mutations affect β cell performance, counteracted by T2D drugs
Merz et al. identify a disease-causing deletion upstream of ONECUT1. They uncover a cis-acting enhancer that regulates ONECUT1 expression during pancreatic development, harboring a low-frequency variant associated with type 2 diabetes. Additionally, they provide clinical relevance by experimentally testing in vitro therapeutic options for affected patients.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>39427318</pmid><doi>10.1016/j.celrep.2024.114853</doi><orcidid>https://orcid.org/0000-0003-0592-5232</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2211-1247 |
| ispartof | Cell reports (Cambridge), 2024-11, Vol.43 (11), p.114853, Article 114853 |
| issn | 2211-1247 2211-1247 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_3118834522 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Cell Press Free Archives; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Cancer cis-regulatory enhancer Diabetes Mellitus - genetics Diabetes Mellitus - metabolism Diabetes Mellitus - pathology Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism Diabetes Mellitus, Type 2 - pathology Enhancer Elements, Genetic - genetics Female human embryonic stem cells Humans Life Sciences lncRNA Male Mice monogenic diabetes Mutation - genetics neonatal diabetes ONECUT1 Pancreas - metabolism Pancreas - pathology pancreas differentiation Regulatory Sequences, Nucleic Acid - genetics stem cell islets type 2 diabetes |
| title | A ONECUT1 regulatory, non-coding region in pancreatic development and diabetes |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-05T14%3A25%3A44IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_hal_p&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=A%20ONECUT1%20regulatory,%20non-coding%20region%20in%20pancreatic%20development%20and%20diabetes&rft.jtitle=Cell%20reports%20(Cambridge)&rft.au=Merz,%20Sarah&rft.date=2024-11-26&rft.volume=43&rft.issue=11&rft.spage=114853&rft.pages=114853-&rft.artnum=114853&rft.issn=2211-1247&rft.eissn=2211-1247&rft_id=info:doi/10.1016/j.celrep.2024.114853&rft_dat=%3Cproquest_hal_p%3E3118834522%3C/proquest_hal_p%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=3118834522&rft_id=info:pmid/39427318&rft_els_id=S221112472401204X&rfr_iscdi=true |