Peroxiredoxin I deficiency increases pancreatic β‑cell apoptosis after streptozotocin stimulation via the AKT/GSK3β signaling pathway
Apoptosis of pancreatic β‑cells is involved in the pathogenesis of type I and II diabetes. Peroxiredoxin I (Prx I) serves an important role in regulating cellular apoptosis; however, the role of Prx I in pancreatic β‑cell apoptosis is not completely understood. In the present study, the role of pero...
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| Veröffentlicht in: | Molecular medicine reports 2020-09, Vol.22 (3), p.1831-1838 |
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| creator | Jin, Mei-Hua Shen, Gui-Nan Jin, Ying-Hua Sun, Hu-Nan Zhen, Xing Zhang, Yong-Qing Lee, Dong-Seok Cui, Yu-Dong Yu, Li-Yun Kim, Ji-Su Kwon, Taeho Han, Ying-Hao |
| description | Apoptosis of pancreatic β‑cells is involved in the pathogenesis of type I and II diabetes. Peroxiredoxin I (Prx I) serves an important role in regulating cellular apoptosis; however, the role of Prx I in pancreatic β‑cell apoptosis is not completely understood. In the present study, the role of peroxiredoxin 1 (Prx I) during streptozotocin (STZ)‑induced apoptosis of pancreatic β‑cells was investigated. The expression level of Prx I was decreased by STZ treatment in a time‑dependent manner, and apoptosis of Prx I knockdown MIN6 cells was increased by STZ stimulation, compared with untransduced MIN6 cells. Furthermore, an intraperitoneal injection of STZ increased pancreatic islet damage in Prx I knockout mice, compared with wild‑type and Prx II knockout mice. AKT and glycogen synthase kinase (GSK)‑3β phosphorylation significantly decreased following Prx I knockdown in MIN6 cells. However, phosphorylated β‑catenin and p65 levels significantly increased after STZ stimulation, compared with untransduced cells. The results of the present study indicate that deletion of Prx I mediated STZ‑induced pancreatic β‑cell death in vivo and in vitro by regulating the AKT/GSK‑3β/β‑catenin signaling pathway, as well as NF‑κB signaling. These findings provide a theoretical basis for treatment of pancreatic damage. |
| doi_str_mv | 10.3892/mmr.2020.11279 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7411341</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2431751636</sourcerecordid><originalsourceid>FETCH-LOGICAL-c418t-7f7cefb39afa5e3eeacc81eb2b78dd5ab668adf35d068fe6ee5176e13fd51b223</originalsourceid><addsrcrecordid>eNpVkUtuFDEQhi1EREJgyxJZYj0TP9rt7g1SFJGHEilIhLXldpdnHHXbje0JGVass-MGnCFH4AA5BCfBSYYINuUq119_2foQekPJnDct2xvHOGeEkTmlTLbP0A6VLZ1xQqrnm5y1rdxGL1O6JKQWTLQv0DZnkgjaVDvo5iPEcO0i9CX6Xz9PcA_WGQferLHzJoJOkPCkH9LsDL67_f39h4FhwHoKUw7JJaxthohTjlAuvoUcjPOldONqKDPB4yuncV4C3j-92Dv6dMrvbnFyC68H5xfFPC-_6vUrtGX1kOD15txFnw8_XBwcz87Oj04O9s9mpqJNnkkrDdiOt9pqARxAG9NQ6Fgnm74XuqvrRveWi57UjYUaQFBZA-W2F7RjjO-i94--06oboTfgc9SDmqIbdVyroJ36v-PdUi3ClZIVpbyixeDdxiCGLytIWV2GVSyfSYpVnEpBa14X1fxRZWJIKYJ92kCJumenCjt1z049sCsDb_9915P8Lyz-B95Xnl8</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2431751636</pqid></control><display><type>article</type><title>Peroxiredoxin I deficiency increases pancreatic β‑cell apoptosis after streptozotocin stimulation via the AKT/GSK3β signaling pathway</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Jin, Mei-Hua ; Shen, Gui-Nan ; Jin, Ying-Hua ; Sun, Hu-Nan ; Zhen, Xing ; Zhang, Yong-Qing ; Lee, Dong-Seok ; Cui, Yu-Dong ; Yu, Li-Yun ; Kim, Ji-Su ; Kwon, Taeho ; Han, Ying-Hao</creator><creatorcontrib>Jin, Mei-Hua ; Shen, Gui-Nan ; Jin, Ying-Hua ; Sun, Hu-Nan ; Zhen, Xing ; Zhang, Yong-Qing ; Lee, Dong-Seok ; Cui, Yu-Dong ; Yu, Li-Yun ; Kim, Ji-Su ; Kwon, Taeho ; Han, Ying-Hao</creatorcontrib><description>Apoptosis of pancreatic β‑cells is involved in the pathogenesis of type I and II diabetes. Peroxiredoxin I (Prx I) serves an important role in regulating cellular apoptosis; however, the role of Prx I in pancreatic β‑cell apoptosis is not completely understood. In the present study, the role of peroxiredoxin 1 (Prx I) during streptozotocin (STZ)‑induced apoptosis of pancreatic β‑cells was investigated. The expression level of Prx I was decreased by STZ treatment in a time‑dependent manner, and apoptosis of Prx I knockdown MIN6 cells was increased by STZ stimulation, compared with untransduced MIN6 cells. Furthermore, an intraperitoneal injection of STZ increased pancreatic islet damage in Prx I knockout mice, compared with wild‑type and Prx II knockout mice. AKT and glycogen synthase kinase (GSK)‑3β phosphorylation significantly decreased following Prx I knockdown in MIN6 cells. However, phosphorylated β‑catenin and p65 levels significantly increased after STZ stimulation, compared with untransduced cells. The results of the present study indicate that deletion of Prx I mediated STZ‑induced pancreatic β‑cell death in vivo and in vitro by regulating the AKT/GSK‑3β/β‑catenin signaling pathway, as well as NF‑κB signaling. These findings provide a theoretical basis for treatment of pancreatic damage.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2020.11279</identifier><identifier>PMID: 32705184</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>AKT protein ; Alcohol ; Animals ; Antibodies ; Apoptosis ; Beta cells ; Cell death ; Cell Line ; Cell Survival - drug effects ; Cellulose acetate ; Cytokines ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - chemically induced ; Diabetes Mellitus, Experimental - metabolism ; Down-Regulation ; Flow cytometry ; Gene Expression Regulation - drug effects ; Gene Knockout Techniques ; Glycogen ; Glycogen synthase kinase 3 ; Glycogen Synthase Kinase 3 beta - metabolism ; Hyperglycemia ; Insulin ; Insulin-Secreting Cells - cytology ; Insulin-Secreting Cells - drug effects ; Insulin-Secreting Cells - metabolism ; Kinases ; Male ; Mice ; NF-κB protein ; Pancreas ; Peroxiredoxin ; Peroxiredoxins - genetics ; Phosphorylation ; Proto-Oncogene Proteins c-akt - metabolism ; Signal transduction ; Signal Transduction - drug effects ; Streptozocin ; Streptozocin - adverse effects ; Viral infections ; β-Catenin</subject><ispartof>Molecular medicine reports, 2020-09, Vol.22 (3), p.1831-1838</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2020</rights><rights>Copyright: © Jin et al. 2020</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c418t-7f7cefb39afa5e3eeacc81eb2b78dd5ab668adf35d068fe6ee5176e13fd51b223</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32705184$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jin, Mei-Hua</creatorcontrib><creatorcontrib>Shen, Gui-Nan</creatorcontrib><creatorcontrib>Jin, Ying-Hua</creatorcontrib><creatorcontrib>Sun, Hu-Nan</creatorcontrib><creatorcontrib>Zhen, Xing</creatorcontrib><creatorcontrib>Zhang, Yong-Qing</creatorcontrib><creatorcontrib>Lee, Dong-Seok</creatorcontrib><creatorcontrib>Cui, Yu-Dong</creatorcontrib><creatorcontrib>Yu, Li-Yun</creatorcontrib><creatorcontrib>Kim, Ji-Su</creatorcontrib><creatorcontrib>Kwon, Taeho</creatorcontrib><creatorcontrib>Han, Ying-Hao</creatorcontrib><title>Peroxiredoxin I deficiency increases pancreatic β‑cell apoptosis after streptozotocin stimulation via the AKT/GSK3β signaling pathway</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Apoptosis of pancreatic β‑cells is involved in the pathogenesis of type I and II diabetes. Peroxiredoxin I (Prx I) serves an important role in regulating cellular apoptosis; however, the role of Prx I in pancreatic β‑cell apoptosis is not completely understood. In the present study, the role of peroxiredoxin 1 (Prx I) during streptozotocin (STZ)‑induced apoptosis of pancreatic β‑cells was investigated. The expression level of Prx I was decreased by STZ treatment in a time‑dependent manner, and apoptosis of Prx I knockdown MIN6 cells was increased by STZ stimulation, compared with untransduced MIN6 cells. Furthermore, an intraperitoneal injection of STZ increased pancreatic islet damage in Prx I knockout mice, compared with wild‑type and Prx II knockout mice. AKT and glycogen synthase kinase (GSK)‑3β phosphorylation significantly decreased following Prx I knockdown in MIN6 cells. However, phosphorylated β‑catenin and p65 levels significantly increased after STZ stimulation, compared with untransduced cells. The results of the present study indicate that deletion of Prx I mediated STZ‑induced pancreatic β‑cell death in vivo and in vitro by regulating the AKT/GSK‑3β/β‑catenin signaling pathway, as well as NF‑κB signaling. These findings provide a theoretical basis for treatment of pancreatic damage.</description><subject>AKT protein</subject><subject>Alcohol</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Apoptosis</subject><subject>Beta cells</subject><subject>Cell death</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Cellulose acetate</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - chemically induced</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Down-Regulation</subject><subject>Flow cytometry</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Knockout Techniques</subject><subject>Glycogen</subject><subject>Glycogen synthase kinase 3</subject><subject>Glycogen Synthase Kinase 3 beta - metabolism</subject><subject>Hyperglycemia</subject><subject>Insulin</subject><subject>Insulin-Secreting Cells - cytology</subject><subject>Insulin-Secreting Cells - drug effects</subject><subject>Insulin-Secreting Cells - metabolism</subject><subject>Kinases</subject><subject>Male</subject><subject>Mice</subject><subject>NF-κB protein</subject><subject>Pancreas</subject><subject>Peroxiredoxin</subject><subject>Peroxiredoxins - genetics</subject><subject>Phosphorylation</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Streptozocin</subject><subject>Streptozocin - adverse effects</subject><subject>Viral infections</subject><subject>β-Catenin</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpVkUtuFDEQhi1EREJgyxJZYj0TP9rt7g1SFJGHEilIhLXldpdnHHXbje0JGVass-MGnCFH4AA5BCfBSYYINuUq119_2foQekPJnDct2xvHOGeEkTmlTLbP0A6VLZ1xQqrnm5y1rdxGL1O6JKQWTLQv0DZnkgjaVDvo5iPEcO0i9CX6Xz9PcA_WGQferLHzJoJOkPCkH9LsDL67_f39h4FhwHoKUw7JJaxthohTjlAuvoUcjPOldONqKDPB4yuncV4C3j-92Dv6dMrvbnFyC68H5xfFPC-_6vUrtGX1kOD15txFnw8_XBwcz87Oj04O9s9mpqJNnkkrDdiOt9pqARxAG9NQ6Fgnm74XuqvrRveWi57UjYUaQFBZA-W2F7RjjO-i94--06oboTfgc9SDmqIbdVyroJ36v-PdUi3ClZIVpbyixeDdxiCGLytIWV2GVSyfSYpVnEpBa14X1fxRZWJIKYJ92kCJumenCjt1z049sCsDb_9915P8Lyz-B95Xnl8</recordid><startdate>20200901</startdate><enddate>20200901</enddate><creator>Jin, Mei-Hua</creator><creator>Shen, Gui-Nan</creator><creator>Jin, Ying-Hua</creator><creator>Sun, Hu-Nan</creator><creator>Zhen, Xing</creator><creator>Zhang, Yong-Qing</creator><creator>Lee, Dong-Seok</creator><creator>Cui, Yu-Dong</creator><creator>Yu, Li-Yun</creator><creator>Kim, Ji-Su</creator><creator>Kwon, Taeho</creator><creator>Han, Ying-Hao</creator><general>Spandidos Publications UK Ltd</general><general>D.A. 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drug effects</topic><topic>Cellulose acetate</topic><topic>Cytokines</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - chemically induced</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Down-Regulation</topic><topic>Flow cytometry</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Knockout Techniques</topic><topic>Glycogen</topic><topic>Glycogen synthase kinase 3</topic><topic>Glycogen Synthase Kinase 3 beta - metabolism</topic><topic>Hyperglycemia</topic><topic>Insulin</topic><topic>Insulin-Secreting Cells - cytology</topic><topic>Insulin-Secreting Cells - drug effects</topic><topic>Insulin-Secreting Cells - metabolism</topic><topic>Kinases</topic><topic>Male</topic><topic>Mice</topic><topic>NF-κB protein</topic><topic>Pancreas</topic><topic>Peroxiredoxin</topic><topic>Peroxiredoxins - genetics</topic><topic>Phosphorylation</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Streptozocin</topic><topic>Streptozocin - adverse effects</topic><topic>Viral infections</topic><topic>β-Catenin</topic><toplevel>online_resources</toplevel><creatorcontrib>Jin, Mei-Hua</creatorcontrib><creatorcontrib>Shen, Gui-Nan</creatorcontrib><creatorcontrib>Jin, Ying-Hua</creatorcontrib><creatorcontrib>Sun, Hu-Nan</creatorcontrib><creatorcontrib>Zhen, Xing</creatorcontrib><creatorcontrib>Zhang, Yong-Qing</creatorcontrib><creatorcontrib>Lee, Dong-Seok</creatorcontrib><creatorcontrib>Cui, Yu-Dong</creatorcontrib><creatorcontrib>Yu, Li-Yun</creatorcontrib><creatorcontrib>Kim, Ji-Su</creatorcontrib><creatorcontrib>Kwon, Taeho</creatorcontrib><creatorcontrib>Han, Ying-Hao</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>British Nursing Database</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>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science 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>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jin, Mei-Hua</au><au>Shen, Gui-Nan</au><au>Jin, Ying-Hua</au><au>Sun, Hu-Nan</au><au>Zhen, Xing</au><au>Zhang, Yong-Qing</au><au>Lee, Dong-Seok</au><au>Cui, Yu-Dong</au><au>Yu, Li-Yun</au><au>Kim, Ji-Su</au><au>Kwon, Taeho</au><au>Han, Ying-Hao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peroxiredoxin I deficiency increases pancreatic β‑cell apoptosis after streptozotocin stimulation via the AKT/GSK3β signaling pathway</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2020-09-01</date><risdate>2020</risdate><volume>22</volume><issue>3</issue><spage>1831</spage><epage>1838</epage><pages>1831-1838</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Apoptosis of pancreatic β‑cells is involved in the pathogenesis of type I and II diabetes. Peroxiredoxin I (Prx I) serves an important role in regulating cellular apoptosis; however, the role of Prx I in pancreatic β‑cell apoptosis is not completely understood. In the present study, the role of peroxiredoxin 1 (Prx I) during streptozotocin (STZ)‑induced apoptosis of pancreatic β‑cells was investigated. The expression level of Prx I was decreased by STZ treatment in a time‑dependent manner, and apoptosis of Prx I knockdown MIN6 cells was increased by STZ stimulation, compared with untransduced MIN6 cells. Furthermore, an intraperitoneal injection of STZ increased pancreatic islet damage in Prx I knockout mice, compared with wild‑type and Prx II knockout mice. AKT and glycogen synthase kinase (GSK)‑3β phosphorylation significantly decreased following Prx I knockdown in MIN6 cells. However, phosphorylated β‑catenin and p65 levels significantly increased after STZ stimulation, compared with untransduced cells. The results of the present study indicate that deletion of Prx I mediated STZ‑induced pancreatic β‑cell death in vivo and in vitro by regulating the AKT/GSK‑3β/β‑catenin signaling pathway, as well as NF‑κB signaling. These findings provide a theoretical basis for treatment of pancreatic damage.</abstract><cop>Greece</cop><pub>Spandidos Publications UK Ltd</pub><pmid>32705184</pmid><doi>10.3892/mmr.2020.11279</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | AKT protein Alcohol Animals Antibodies Apoptosis Beta cells Cell death Cell Line Cell Survival - drug effects Cellulose acetate Cytokines Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - metabolism Down-Regulation Flow cytometry Gene Expression Regulation - drug effects Gene Knockout Techniques Glycogen Glycogen synthase kinase 3 Glycogen Synthase Kinase 3 beta - metabolism Hyperglycemia Insulin Insulin-Secreting Cells - cytology Insulin-Secreting Cells - drug effects Insulin-Secreting Cells - metabolism Kinases Male Mice NF-κB protein Pancreas Peroxiredoxin Peroxiredoxins - genetics Phosphorylation Proto-Oncogene Proteins c-akt - metabolism Signal transduction Signal Transduction - drug effects Streptozocin Streptozocin - adverse effects Viral infections β-Catenin |
| title | Peroxiredoxin I deficiency increases pancreatic β‑cell apoptosis after streptozotocin stimulation via the AKT/GSK3β signaling pathway |
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