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Impact of Pdx1-associated chromatin modifiers on islet β-cells
Diabetes mellitus arises from insufficient insulin secretion from pancreatic islet β‐cells. In type 2 diabetes (T2D), β‐cell dysfunction is associated with inactivation and/or loss of transcription factor (TF) activity, including Pdx1. Notably, this particular TF is viewed as a master regulator of p...
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Published in: | Diabetes, obesity & metabolism obesity & metabolism, 2016-09, Vol.18 (S1), p.123-127 |
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container_title | Diabetes, obesity & metabolism |
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creator | Spaeth, J. M. Walker, E. M. Stein, R. |
description | Diabetes mellitus arises from insufficient insulin secretion from pancreatic islet β‐cells. In type 2 diabetes (T2D), β‐cell dysfunction is associated with inactivation and/or loss of transcription factor (TF) activity, including Pdx1. Notably, this particular TF is viewed as a master regulator of pancreas development and islet β‐cell formation, identity and function. TFs, like Pdx1, recruit coregulators to transduce activating and/or repressing signals to the general transcriptional machinery for controlling gene expression, including modifiers of DNA, histones and nucleosome architecture. These coregulators impart a secondary layer of control that can be exploited to modulate TF activity. In this review, we describe Pdx1‐recruited coregulators that impact chromatin structure, consequently influencing normal β‐cell function and likely Pdx1 activity in pathophysiological settings. |
doi_str_mv | 10.1111/dom.12730 |
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M. ; Walker, E. M. ; Stein, R.</creator><creatorcontrib>Spaeth, J. M. ; Walker, E. M. ; Stein, R.</creatorcontrib><description>Diabetes mellitus arises from insufficient insulin secretion from pancreatic islet β‐cells. In type 2 diabetes (T2D), β‐cell dysfunction is associated with inactivation and/or loss of transcription factor (TF) activity, including Pdx1. Notably, this particular TF is viewed as a master regulator of pancreas development and islet β‐cell formation, identity and function. TFs, like Pdx1, recruit coregulators to transduce activating and/or repressing signals to the general transcriptional machinery for controlling gene expression, including modifiers of DNA, histones and nucleosome architecture. These coregulators impart a secondary layer of control that can be exploited to modulate TF activity. 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M.</creatorcontrib><creatorcontrib>Walker, E. M.</creatorcontrib><creatorcontrib>Stein, R.</creatorcontrib><title>Impact of Pdx1-associated chromatin modifiers on islet β-cells</title><title>Diabetes, obesity & metabolism</title><addtitle>Diabetes Obes Metab</addtitle><description>Diabetes mellitus arises from insufficient insulin secretion from pancreatic islet β‐cells. In type 2 diabetes (T2D), β‐cell dysfunction is associated with inactivation and/or loss of transcription factor (TF) activity, including Pdx1. Notably, this particular TF is viewed as a master regulator of pancreas development and islet β‐cell formation, identity and function. TFs, like Pdx1, recruit coregulators to transduce activating and/or repressing signals to the general transcriptional machinery for controlling gene expression, including modifiers of DNA, histones and nucleosome architecture. These coregulators impart a secondary layer of control that can be exploited to modulate TF activity. In this review, we describe Pdx1‐recruited coregulators that impact chromatin structure, consequently influencing normal β‐cell function and likely Pdx1 activity in pathophysiological settings.</description><subject>Animals</subject><subject>Beta cells</subject><subject>Chromatin</subject><subject>Chromatin Assembly and Disassembly - genetics</subject><subject>coregulators</subject><subject>Diabetes</subject><subject>diabetes mellitus</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Diabetes Mellitus, Type 2 - genetics</subject><subject>Diabetes Mellitus, Type 2 - metabolism</subject><subject>DNA Methylation - genetics</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - genetics</subject><subject>Histone Code - genetics</subject><subject>Histones</subject><subject>Homeodomain Proteins - genetics</subject><subject>Humans</subject><subject>Insulin secretion</subject><subject>Insulin-Secreting Cells - metabolism</subject><subject>islet-enriched transcription factors</subject><subject>Mice</subject><subject>Nucleosomes</subject><subject>Pdx1</subject><subject>Trans-Activators - genetics</subject><subject>type 2 diabetes</subject><subject>β-cell dysfunction</subject><issn>1462-8902</issn><issn>1463-1326</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNp1kctKxDAUhoMo3he-gBTc6KKa07S5bBQZr3hdKIKbkElTjbbNmHS8vJYP4jMZHR1UMJsE8p2P__AjtAR4HeLZKF2zDhkjeALNQk5JCiSjk5_vLOUCZzNoLoQ7jHFOOJtGMxmjUEAOs2jrsBko3SWuSs7LZ0hVCE5b1Zky0bfeNaqzbdK40lbW-JC4NrGhNl3y9ppqU9dhAU1Vqg5m8eueR5d7uxe9g_T4bP-wt32c6pwDTgVRrE8FMYJzqHKe5wXTnBPKhWZ9DMAEFYJwbbDitBSiKGM-XPYJA8oxkHm0OfIOhv3GlNq0nVe1HHjbKP8inbLy909rb-WNe5SFAE5FEQWrXwLvHoYmdLKx4WMF1Ro3DBI4CMhijiyiK3_QOzf0bVxPElyIHFNaiEitjSjtXQjeVOMwgOVHLTLWIj9riezyz_Rj8ruHCGyMgCdbm5f_TXLn7ORbmY4mbOjM83hC-XtJGWGFvDrdlzvi9Irwo2vJyTv1QKQi</recordid><startdate>201609</startdate><enddate>201609</enddate><creator>Spaeth, J. M.</creator><creator>Walker, E. M.</creator><creator>Stein, R.</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7T5</scope><scope>7TK</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201609</creationdate><title>Impact of Pdx1-associated chromatin modifiers on islet β-cells</title><author>Spaeth, J. M. ; Walker, E. M. ; Stein, R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4810-93a7b693e9881f484457c883689c7b0117969938ce0a86d995d5140db37168013</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Beta cells</topic><topic>Chromatin</topic><topic>Chromatin Assembly and Disassembly - genetics</topic><topic>coregulators</topic><topic>Diabetes</topic><topic>diabetes mellitus</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Diabetes Mellitus, Type 2 - genetics</topic><topic>Diabetes Mellitus, Type 2 - metabolism</topic><topic>DNA Methylation - genetics</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - genetics</topic><topic>Histone Code - genetics</topic><topic>Histones</topic><topic>Homeodomain Proteins - genetics</topic><topic>Humans</topic><topic>Insulin secretion</topic><topic>Insulin-Secreting Cells - metabolism</topic><topic>islet-enriched transcription factors</topic><topic>Mice</topic><topic>Nucleosomes</topic><topic>Pdx1</topic><topic>Trans-Activators - genetics</topic><topic>type 2 diabetes</topic><topic>β-cell dysfunction</topic><toplevel>online_resources</toplevel><creatorcontrib>Spaeth, J. M.</creatorcontrib><creatorcontrib>Walker, E. M.</creatorcontrib><creatorcontrib>Stein, R.</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Diabetes, obesity & metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Spaeth, J. M.</au><au>Walker, E. M.</au><au>Stein, R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of Pdx1-associated chromatin modifiers on islet β-cells</atitle><jtitle>Diabetes, obesity & metabolism</jtitle><addtitle>Diabetes Obes Metab</addtitle><date>2016-09</date><risdate>2016</risdate><volume>18</volume><issue>S1</issue><spage>123</spage><epage>127</epage><pages>123-127</pages><issn>1462-8902</issn><eissn>1463-1326</eissn><notes>National Institute of Diabetes and Digestive Kidney Disease - No. R01DK050203; No. R01DK090570</notes><notes>istex:CBF349A099C75F3F791F2CE8F4418053869C951E</notes><notes>American Diabetes Association - No. 1-16-PDF-109</notes><notes>ark:/67375/WNG-D9NW38KZ-8</notes><notes>ArticleID:DOM12730</notes><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-3</notes><notes>content type line 23</notes><notes>ObjectType-Review-1</notes><abstract>Diabetes mellitus arises from insufficient insulin secretion from pancreatic islet β‐cells. In type 2 diabetes (T2D), β‐cell dysfunction is associated with inactivation and/or loss of transcription factor (TF) activity, including Pdx1. Notably, this particular TF is viewed as a master regulator of pancreas development and islet β‐cell formation, identity and function. TFs, like Pdx1, recruit coregulators to transduce activating and/or repressing signals to the general transcriptional machinery for controlling gene expression, including modifiers of DNA, histones and nucleosome architecture. These coregulators impart a secondary layer of control that can be exploited to modulate TF activity. In this review, we describe Pdx1‐recruited coregulators that impact chromatin structure, consequently influencing normal β‐cell function and likely Pdx1 activity in pathophysiological settings.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>27615141</pmid><doi>10.1111/dom.12730</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Beta cells Chromatin Chromatin Assembly and Disassembly - genetics coregulators Diabetes diabetes mellitus Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - genetics Diabetes Mellitus, Type 2 - metabolism DNA Methylation - genetics Gene expression Gene Expression Regulation - genetics Histone Code - genetics Histones Homeodomain Proteins - genetics Humans Insulin secretion Insulin-Secreting Cells - metabolism islet-enriched transcription factors Mice Nucleosomes Pdx1 Trans-Activators - genetics type 2 diabetes β-cell dysfunction |
title | Impact of Pdx1-associated chromatin modifiers on islet β-cells |
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