Deficiency of WTAP in islet beta cells results in beta cell failure and diabetes in mice
Aims/hypothesis N 6 -methyladenosine (m 6 A) mRNA methylation and m 6 A-related proteins (methyltransferase-like 3 [METTL3], methyltransferase-like 14 [METTL14] and YTH domain containing 1 [YTHDC1]) have been shown to regulate islet beta cell function and the pathogenesis of diabetes. However, wheth...
Gespeichert in:
| Veröffentlicht in: | Diabetologia 2023-06, Vol.66 (6), p.1084-1096 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1096 |
|---|---|
| container_issue | 6 |
| container_start_page | 1084 |
| container_title | Diabetologia |
| container_volume | 66 |
| creator | Li, Xinzhi Yang, Ying Li, Zhenzhi Wang, Yuqin Qiao, Jingting Chen, Zheng |
| description | Aims/hypothesis
N
6
-methyladenosine (m
6
A) mRNA methylation and m
6
A-related proteins (methyltransferase-like 3 [METTL3], methyltransferase-like 14 [METTL14] and YTH domain containing 1 [YTHDC1]) have been shown to regulate islet beta cell function and the pathogenesis of diabetes. However, whether Wilms’ tumour 1-associating protein (WTAP), a key regulator of the m
6
A RNA methyltransferase complex, regulates islet beta cell failure during pathogenesis of diabetes is largely unknown. The present study aimed to investigate the role of WTAP in the regulation of islet beta cell failure and diabetes.
Methods
Islet beta cell-specific
Wtap
-knockout and beta cell-specific
Mettl3
-overexpressing mice were generated for this study. Blood glucose, glucose tolerance, serum insulin, glucose-stimulated insulin secretion (both in vivo and in vitro), insulin levels, glucagon levels and beta cell apoptosis were examined. RNA-seq and MeRIP-seq were performed, and the data were well analysed.
Results
WTAP was downregulated in islet beta cells in type 2 diabetes, due to lipotoxicity and chronic inflammation, and islet beta cell-specific deletion of
Wtap
(
Wtap
-betaKO) induced beta cell failure and diabetes.
Wtap
-betaKO mice showed severe hyperglycaemia (above 20 mmol/l [360 mg/dl]) from 8 weeks of age onwards. Mechanistically, WTAP deficiency decreased m
6
A mRNA modification and reduced the expression of islet beta cell-specific transcription factors and insulin secretion-related genes by reducing METTL3 protein levels. Islet beta cell-specific overexpression of
Mettl3
partially reversed the abnormalities observed in
Wtap
-betaKO mice.
Conclusions/interpretation
WTAP plays a key role in maintaining beta cell function by regulating m
6
A mRNA modification depending on METTL3, and the downregulation of WTAP leads to beta cell failure and diabetes.
Data availability
The RNA-seq and MeRIP-seq datasets generated during the current study are available in the Gene Expression Omnibus database repository (
https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE215156
;
https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE215360
).
Graphical abstract |
| doi_str_mv | 10.1007/s00125-023-05900-z |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2787212705</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2809961871</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-a740392fd76f31fe317a836fa4ec09929b4da55360af0167964e56f68ad804313</originalsourceid><addsrcrecordid>eNp9kMtKxDAUhoMoznh5ARcScOOmenJvl8N4BUEXirMLmfZEIp1Wk3ahT2_reAEXrgL5v_Ofw0fIAYMTBmBOEwDjKgMuMlAFQPa-QaZMCp6B5PkmmY55xnK9mJCdlJ4BQCipt8lE6IKD4nJKFmfoQxmwKd9o6-nj_eyOhoaGVGNHl9g5WmJdJxox9XWXxuznl3oX6j4idU1Fq-CGAD-JVShxj2x5Vyfc_3p3ycPF-f38Kru5vbyez26yUhjVZc5IEAX3ldFeMI-CGZcL7Z3EEoqCF0tZOaWEBueBaVNoiUp7nbsqBymY2CXH696X2L72mDq7Cmm8zjXY9slykxvOuAE1oEd_0Oe2j81wneX5sEyz3IyFfE2VsU0porcvMaxcfLMM7Ojdrr3bwbv99G7fh6HDr-p-ucLqZ-Rb9ACINZCGqHnC-Lv7n9oPDquLxA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2809961871</pqid></control><display><type>article</type><title>Deficiency of WTAP in islet beta cells results in beta cell failure and diabetes in mice</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Li, Xinzhi ; Yang, Ying ; Li, Zhenzhi ; Wang, Yuqin ; Qiao, Jingting ; Chen, Zheng</creator><creatorcontrib>Li, Xinzhi ; Yang, Ying ; Li, Zhenzhi ; Wang, Yuqin ; Qiao, Jingting ; Chen, Zheng</creatorcontrib><description>Aims/hypothesis
N
6
-methyladenosine (m
6
A) mRNA methylation and m
6
A-related proteins (methyltransferase-like 3 [METTL3], methyltransferase-like 14 [METTL14] and YTH domain containing 1 [YTHDC1]) have been shown to regulate islet beta cell function and the pathogenesis of diabetes. However, whether Wilms’ tumour 1-associating protein (WTAP), a key regulator of the m
6
A RNA methyltransferase complex, regulates islet beta cell failure during pathogenesis of diabetes is largely unknown. The present study aimed to investigate the role of WTAP in the regulation of islet beta cell failure and diabetes.
Methods
Islet beta cell-specific
Wtap
-knockout and beta cell-specific
Mettl3
-overexpressing mice were generated for this study. Blood glucose, glucose tolerance, serum insulin, glucose-stimulated insulin secretion (both in vivo and in vitro), insulin levels, glucagon levels and beta cell apoptosis were examined. RNA-seq and MeRIP-seq were performed, and the data were well analysed.
Results
WTAP was downregulated in islet beta cells in type 2 diabetes, due to lipotoxicity and chronic inflammation, and islet beta cell-specific deletion of
Wtap
(
Wtap
-betaKO) induced beta cell failure and diabetes.
Wtap
-betaKO mice showed severe hyperglycaemia (above 20 mmol/l [360 mg/dl]) from 8 weeks of age onwards. Mechanistically, WTAP deficiency decreased m
6
A mRNA modification and reduced the expression of islet beta cell-specific transcription factors and insulin secretion-related genes by reducing METTL3 protein levels. Islet beta cell-specific overexpression of
Mettl3
partially reversed the abnormalities observed in
Wtap
-betaKO mice.
Conclusions/interpretation
WTAP plays a key role in maintaining beta cell function by regulating m
6
A mRNA modification depending on METTL3, and the downregulation of WTAP leads to beta cell failure and diabetes.
Data availability
The RNA-seq and MeRIP-seq datasets generated during the current study are available in the Gene Expression Omnibus database repository (
https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE215156
;
https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE215360
).
Graphical abstract</description><identifier>ISSN: 0012-186X</identifier><identifier>EISSN: 1432-0428</identifier><identifier>DOI: 10.1007/s00125-023-05900-z</identifier><identifier>PMID: 36920524</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Animals ; Apoptosis ; Beta cells ; Clonal deletion ; Diabetes ; Diabetes mellitus (non-insulin dependent) ; Diabetes Mellitus, Type 2 - metabolism ; Gene expression ; Glucagon ; Glucose ; Glucose tolerance ; Human Physiology ; Hyperglycemia ; Insulin ; Insulin secretion ; Insulins ; Internal Medicine ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Methyltransferases - genetics ; Methyltransferases - metabolism ; Mice ; N6-methyladenosine ; Pathogenesis ; RNA modification ; RNA, Messenger - metabolism ; Secretion ; Transcription factors</subject><ispartof>Diabetologia, 2023-06, Vol.66 (6), p.1084-1096</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-a740392fd76f31fe317a836fa4ec09929b4da55360af0167964e56f68ad804313</citedby><cites>FETCH-LOGICAL-c375t-a740392fd76f31fe317a836fa4ec09929b4da55360af0167964e56f68ad804313</cites><orcidid>0000-0001-7129-6644</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00125-023-05900-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00125-023-05900-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36920524$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Xinzhi</creatorcontrib><creatorcontrib>Yang, Ying</creatorcontrib><creatorcontrib>Li, Zhenzhi</creatorcontrib><creatorcontrib>Wang, Yuqin</creatorcontrib><creatorcontrib>Qiao, Jingting</creatorcontrib><creatorcontrib>Chen, Zheng</creatorcontrib><title>Deficiency of WTAP in islet beta cells results in beta cell failure and diabetes in mice</title><title>Diabetologia</title><addtitle>Diabetologia</addtitle><addtitle>Diabetologia</addtitle><description>Aims/hypothesis
N
6
-methyladenosine (m
6
A) mRNA methylation and m
6
A-related proteins (methyltransferase-like 3 [METTL3], methyltransferase-like 14 [METTL14] and YTH domain containing 1 [YTHDC1]) have been shown to regulate islet beta cell function and the pathogenesis of diabetes. However, whether Wilms’ tumour 1-associating protein (WTAP), a key regulator of the m
6
A RNA methyltransferase complex, regulates islet beta cell failure during pathogenesis of diabetes is largely unknown. The present study aimed to investigate the role of WTAP in the regulation of islet beta cell failure and diabetes.
Methods
Islet beta cell-specific
Wtap
-knockout and beta cell-specific
Mettl3
-overexpressing mice were generated for this study. Blood glucose, glucose tolerance, serum insulin, glucose-stimulated insulin secretion (both in vivo and in vitro), insulin levels, glucagon levels and beta cell apoptosis were examined. RNA-seq and MeRIP-seq were performed, and the data were well analysed.
Results
WTAP was downregulated in islet beta cells in type 2 diabetes, due to lipotoxicity and chronic inflammation, and islet beta cell-specific deletion of
Wtap
(
Wtap
-betaKO) induced beta cell failure and diabetes.
Wtap
-betaKO mice showed severe hyperglycaemia (above 20 mmol/l [360 mg/dl]) from 8 weeks of age onwards. Mechanistically, WTAP deficiency decreased m
6
A mRNA modification and reduced the expression of islet beta cell-specific transcription factors and insulin secretion-related genes by reducing METTL3 protein levels. Islet beta cell-specific overexpression of
Mettl3
partially reversed the abnormalities observed in
Wtap
-betaKO mice.
Conclusions/interpretation
WTAP plays a key role in maintaining beta cell function by regulating m
6
A mRNA modification depending on METTL3, and the downregulation of WTAP leads to beta cell failure and diabetes.
Data availability
The RNA-seq and MeRIP-seq datasets generated during the current study are available in the Gene Expression Omnibus database repository (
https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE215156
;
https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE215360
).
Graphical abstract</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Beta cells</subject><subject>Clonal deletion</subject><subject>Diabetes</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>Gene expression</subject><subject>Glucagon</subject><subject>Glucose</subject><subject>Glucose tolerance</subject><subject>Human Physiology</subject><subject>Hyperglycemia</subject><subject>Insulin</subject><subject>Insulin secretion</subject><subject>Insulins</subject><subject>Internal Medicine</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Methyltransferases - genetics</subject><subject>Methyltransferases - metabolism</subject><subject>Mice</subject><subject>N6-methyladenosine</subject><subject>Pathogenesis</subject><subject>RNA modification</subject><subject>RNA, Messenger - metabolism</subject><subject>Secretion</subject><subject>Transcription factors</subject><issn>0012-186X</issn><issn>1432-0428</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9kMtKxDAUhoMoznh5ARcScOOmenJvl8N4BUEXirMLmfZEIp1Wk3ahT2_reAEXrgL5v_Ofw0fIAYMTBmBOEwDjKgMuMlAFQPa-QaZMCp6B5PkmmY55xnK9mJCdlJ4BQCipt8lE6IKD4nJKFmfoQxmwKd9o6-nj_eyOhoaGVGNHl9g5WmJdJxox9XWXxuznl3oX6j4idU1Fq-CGAD-JVShxj2x5Vyfc_3p3ycPF-f38Kru5vbyez26yUhjVZc5IEAX3ldFeMI-CGZcL7Z3EEoqCF0tZOaWEBueBaVNoiUp7nbsqBymY2CXH696X2L72mDq7Cmm8zjXY9slykxvOuAE1oEd_0Oe2j81wneX5sEyz3IyFfE2VsU0porcvMaxcfLMM7Ojdrr3bwbv99G7fh6HDr-p-ucLqZ-Rb9ACINZCGqHnC-Lv7n9oPDquLxA</recordid><startdate>20230601</startdate><enddate>20230601</enddate><creator>Li, Xinzhi</creator><creator>Yang, Ying</creator><creator>Li, Zhenzhi</creator><creator>Wang, Yuqin</creator><creator>Qiao, Jingting</creator><creator>Chen, Zheng</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7129-6644</orcidid></search><sort><creationdate>20230601</creationdate><title>Deficiency of WTAP in islet beta cells results in beta cell failure and diabetes in mice</title><author>Li, Xinzhi ; Yang, Ying ; Li, Zhenzhi ; Wang, Yuqin ; Qiao, Jingting ; Chen, Zheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-a740392fd76f31fe317a836fa4ec09929b4da55360af0167964e56f68ad804313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Beta cells</topic><topic>Clonal deletion</topic><topic>Diabetes</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>Gene expression</topic><topic>Glucagon</topic><topic>Glucose</topic><topic>Glucose tolerance</topic><topic>Human Physiology</topic><topic>Hyperglycemia</topic><topic>Insulin</topic><topic>Insulin secretion</topic><topic>Insulins</topic><topic>Internal Medicine</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Methyltransferases - genetics</topic><topic>Methyltransferases - metabolism</topic><topic>Mice</topic><topic>N6-methyladenosine</topic><topic>Pathogenesis</topic><topic>RNA modification</topic><topic>RNA, Messenger - metabolism</topic><topic>Secretion</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Xinzhi</creatorcontrib><creatorcontrib>Yang, Ying</creatorcontrib><creatorcontrib>Li, Zhenzhi</creatorcontrib><creatorcontrib>Wang, Yuqin</creatorcontrib><creatorcontrib>Qiao, Jingting</creatorcontrib><creatorcontrib>Chen, Zheng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical 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><jtitle>Diabetologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Xinzhi</au><au>Yang, Ying</au><au>Li, Zhenzhi</au><au>Wang, Yuqin</au><au>Qiao, Jingting</au><au>Chen, Zheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deficiency of WTAP in islet beta cells results in beta cell failure and diabetes in mice</atitle><jtitle>Diabetologia</jtitle><stitle>Diabetologia</stitle><addtitle>Diabetologia</addtitle><date>2023-06-01</date><risdate>2023</risdate><volume>66</volume><issue>6</issue><spage>1084</spage><epage>1096</epage><pages>1084-1096</pages><issn>0012-186X</issn><eissn>1432-0428</eissn><abstract>Aims/hypothesis
N
6
-methyladenosine (m
6
A) mRNA methylation and m
6
A-related proteins (methyltransferase-like 3 [METTL3], methyltransferase-like 14 [METTL14] and YTH domain containing 1 [YTHDC1]) have been shown to regulate islet beta cell function and the pathogenesis of diabetes. However, whether Wilms’ tumour 1-associating protein (WTAP), a key regulator of the m
6
A RNA methyltransferase complex, regulates islet beta cell failure during pathogenesis of diabetes is largely unknown. The present study aimed to investigate the role of WTAP in the regulation of islet beta cell failure and diabetes.
Methods
Islet beta cell-specific
Wtap
-knockout and beta cell-specific
Mettl3
-overexpressing mice were generated for this study. Blood glucose, glucose tolerance, serum insulin, glucose-stimulated insulin secretion (both in vivo and in vitro), insulin levels, glucagon levels and beta cell apoptosis were examined. RNA-seq and MeRIP-seq were performed, and the data were well analysed.
Results
WTAP was downregulated in islet beta cells in type 2 diabetes, due to lipotoxicity and chronic inflammation, and islet beta cell-specific deletion of
Wtap
(
Wtap
-betaKO) induced beta cell failure and diabetes.
Wtap
-betaKO mice showed severe hyperglycaemia (above 20 mmol/l [360 mg/dl]) from 8 weeks of age onwards. Mechanistically, WTAP deficiency decreased m
6
A mRNA modification and reduced the expression of islet beta cell-specific transcription factors and insulin secretion-related genes by reducing METTL3 protein levels. Islet beta cell-specific overexpression of
Mettl3
partially reversed the abnormalities observed in
Wtap
-betaKO mice.
Conclusions/interpretation
WTAP plays a key role in maintaining beta cell function by regulating m
6
A mRNA modification depending on METTL3, and the downregulation of WTAP leads to beta cell failure and diabetes.
Data availability
The RNA-seq and MeRIP-seq datasets generated during the current study are available in the Gene Expression Omnibus database repository (
https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE215156
;
https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE215360
).
Graphical abstract</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>36920524</pmid><doi>10.1007/s00125-023-05900-z</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-7129-6644</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0012-186X |
| ispartof | Diabetologia, 2023-06, Vol.66 (6), p.1084-1096 |
| issn | 0012-186X 1432-0428 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2787212705 |
| source | MEDLINE; SpringerNature Journals |
| subjects | Animals Apoptosis Beta cells Clonal deletion Diabetes Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - metabolism Gene expression Glucagon Glucose Glucose tolerance Human Physiology Hyperglycemia Insulin Insulin secretion Insulins Internal Medicine Medicine Medicine & Public Health Metabolic Diseases Methyltransferases - genetics Methyltransferases - metabolism Mice N6-methyladenosine Pathogenesis RNA modification RNA, Messenger - metabolism Secretion Transcription factors |
| title | Deficiency of WTAP in islet beta cells results in beta cell failure and diabetes in mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-28T20%3A42%3A15IST&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=Deficiency%20of%20WTAP%20in%20islet%20beta%20cells%20results%20in%20beta%20cell%20failure%20and%20diabetes%20in%20mice&rft.jtitle=Diabetologia&rft.au=Li,%20Xinzhi&rft.date=2023-06-01&rft.volume=66&rft.issue=6&rft.spage=1084&rft.epage=1096&rft.pages=1084-1096&rft.issn=0012-186X&rft.eissn=1432-0428&rft_id=info:doi/10.1007/s00125-023-05900-z&rft_dat=%3Cproquest_cross%3E2809961871%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2809961871&rft_id=info:pmid/36920524&rfr_iscdi=true |