Tat‐antioxidant 1 protects against stress‐induced hippocampal HT‐22 cells death and attenuate ischaemic insult in animal model
Oxidative stress‐induced reactive oxygen species (ROS) are responsible for various neuronal diseases. Antioxidant 1 (Atox1) regulates copper homoeostasis and promotes cellular antioxidant defence against toxins generated by ROS. The roles of Atox1 protein in ischaemia, however, remain unclear. In th...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2015-06, Vol.19 (6), p.1333-1345 |
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| creator | Kim, So Mi Hwang, In Koo Yoo, Dae Young Eum, Won Sik Kim, Dae Won Shin, Min Jea Ahn, Eun Hee Jo, Hyo Sang Ryu, Eun Ji Yong, Ji In Cho, Sung‐Woo Kwon, Oh‐Shin Lee, Keun Wook Cho, Yoon Shin Han, Kyu Hyung Park, Jinseu Choi, Soo Young |
| description | Oxidative stress‐induced reactive oxygen species (ROS) are responsible for various neuronal diseases. Antioxidant 1 (Atox1) regulates copper homoeostasis and promotes cellular antioxidant defence against toxins generated by ROS. The roles of Atox1 protein in ischaemia, however, remain unclear. In this study, we generated a protein transduction domain fused Tat‐Atox1 and examined the roles of Tat‐Atox1 in oxidative stress‐induced hippocampal HT‐22 cell death and an ischaemic injury animal model. Tat‐Atox1 effectively transduced into HT‐22 cells and it protected cells against the effects of hydrogen peroxide (H2O2)‐induced toxicity including increasing of ROS levels and DNA fragmentation. At the same time, Tat‐Atox1 regulated cellular survival signalling such as p53, Bad/Bcl‐2, Akt and mitogen‐activate protein kinases (MAPKs). In the animal ischaemia model, transduced Tat‐Atox1 protected against neuronal cell death in the hippocampal CA1 region. In addition, Tat‐Atox1 significantly decreased the activation of astrocytes and microglia as well as lipid peroxidation in the CA1 region after ischaemic insult. Taken together, these results indicate that transduced Tat‐Atox1 protects against oxidative stress‐induced HT‐22 cell death and against neuronal damage in animal ischaemia model. Therefore, we suggest that Tat‐Atox1 has potential as a therapeutic agent for the treatment of oxidative stress‐induced ischaemic damage. |
| doi_str_mv | 10.1111/jcmm.12513 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4459847</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2290128023</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4483-d44d7606be589c57f69336c06f3b46c27d57381469173fc00cebe69c8c6c69703</originalsourceid><addsrcrecordid>eNp9kb1uFDEURi0EIiHQ8ADIEl2kTfw3HrtBQquEgBLRLLXlvfZkvZoZD7YnkC4FD8Az8iQ47CaCBjfX0j0-_qQPodeUnNB6TrcwDCeUNZQ_QYe0UWwhNBdP93equDpAL3LeEsIl5fo5OmBNqyhv-CH6sbLl191PO5YQvwdXJ6Z4SrF4KBnbaxvGXHAuyedcuTC6GbzDmzBNEeww2R5frOqCMQy-7zN23pYNtqPDthQ_zrZ4HDJsrB8C4Gqb-1JHJcJQHw_R-f4letbZPvtX-3mEvpyfrZYXi8vPHz4u318uQAjFF04I10oi175RGpq2k5pzCUR2fC0ksNY1LVdUSE1b3gEh4NdealAgQeqW8CP0bued5vXgHfixJNubKdUo6dZEG8y_mzFszHW8MUI0Wom2Ct7uBSl-nX0uZhvnNNbMhjFNKFOE8Uod7yhIMefku8cfKDH3jZn7xsyfxir85u9Mj-hDRRWgO-Bb6P3tf1Tm0_Lqaif9DThSpgY</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2290128023</pqid></control><display><type>article</type><title>Tat‐antioxidant 1 protects against stress‐induced hippocampal HT‐22 cells death and attenuate ischaemic insult in animal model</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Access via Wiley Online Library</source><source>Wiley Online Library Open Access</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Kim, So Mi ; Hwang, In Koo ; Yoo, Dae Young ; Eum, Won Sik ; Kim, Dae Won ; Shin, Min Jea ; Ahn, Eun Hee ; Jo, Hyo Sang ; Ryu, Eun Ji ; Yong, Ji In ; Cho, Sung‐Woo ; Kwon, Oh‐Shin ; Lee, Keun Wook ; Cho, Yoon Shin ; Han, Kyu Hyung ; Park, Jinseu ; Choi, Soo Young</creator><creatorcontrib>Kim, So Mi ; Hwang, In Koo ; Yoo, Dae Young ; Eum, Won Sik ; Kim, Dae Won ; Shin, Min Jea ; Ahn, Eun Hee ; Jo, Hyo Sang ; Ryu, Eun Ji ; Yong, Ji In ; Cho, Sung‐Woo ; Kwon, Oh‐Shin ; Lee, Keun Wook ; Cho, Yoon Shin ; Han, Kyu Hyung ; Park, Jinseu ; Choi, Soo Young</creatorcontrib><description>Oxidative stress‐induced reactive oxygen species (ROS) are responsible for various neuronal diseases. Antioxidant 1 (Atox1) regulates copper homoeostasis and promotes cellular antioxidant defence against toxins generated by ROS. The roles of Atox1 protein in ischaemia, however, remain unclear. In this study, we generated a protein transduction domain fused Tat‐Atox1 and examined the roles of Tat‐Atox1 in oxidative stress‐induced hippocampal HT‐22 cell death and an ischaemic injury animal model. Tat‐Atox1 effectively transduced into HT‐22 cells and it protected cells against the effects of hydrogen peroxide (H2O2)‐induced toxicity including increasing of ROS levels and DNA fragmentation. At the same time, Tat‐Atox1 regulated cellular survival signalling such as p53, Bad/Bcl‐2, Akt and mitogen‐activate protein kinases (MAPKs). In the animal ischaemia model, transduced Tat‐Atox1 protected against neuronal cell death in the hippocampal CA1 region. In addition, Tat‐Atox1 significantly decreased the activation of astrocytes and microglia as well as lipid peroxidation in the CA1 region after ischaemic insult. Taken together, these results indicate that transduced Tat‐Atox1 protects against oxidative stress‐induced HT‐22 cell death and against neuronal damage in animal ischaemia model. Therefore, we suggest that Tat‐Atox1 has potential as a therapeutic agent for the treatment of oxidative stress‐induced ischaemic damage.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.12513</identifier><identifier>PMID: 25781353</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>AKT protein ; Animal models ; Animals ; Antioxidants ; Apoptosis ; Apoptosis - drug effects ; Astrocytes ; ATOX1 protein ; Biotechnology ; Blotting, Western ; Brain research ; Cell cycle ; Cell death ; Cell Line ; Cell Survival - drug effects ; Chemical compounds ; Copper ; Disease Models, Animal ; DNA fragmentation ; Dose-Response Relationship, Drug ; Gene Products, tat - genetics ; Gene Products, tat - metabolism ; Hippocampus ; Hippocampus - cytology ; Humans ; Hydrogen peroxide ; ischaemic injury ; Ischemia ; Ischemia - physiopathology ; Ischemia - prevention & control ; Lipid peroxidation ; Metabolism ; Metallochaperones - genetics ; Metallochaperones - metabolism ; Metallochaperones - pharmacology ; Mice ; Microglia ; Microscopy ; Microscopy, Confocal ; Microscopy, Fluorescence ; Motor Activity - drug effects ; Neurons - drug effects ; Neurons - metabolism ; Neuroprotective Agents - pharmacology ; Original ; Oxidative stress ; Oxidative Stress - drug effects ; p53 Protein ; Peptides ; Peroxidation ; Prosencephalon - blood supply ; Protein kinase ; protein therapy ; protein transduction domain ; Proteins ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Recombinant Fusion Proteins - genetics ; Recombinant Fusion Proteins - metabolism ; Recombinant Fusion Proteins - pharmacology ; Signal transduction ; Studies ; Tat‐Atox1 ; Toxicity</subject><ispartof>Journal of cellular and molecular medicine, 2015-06, Vol.19 (6), p.1333-1345</ispartof><rights>2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2015. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4483-d44d7606be589c57f69336c06f3b46c27d57381469173fc00cebe69c8c6c69703</citedby><cites>FETCH-LOGICAL-c4483-d44d7606be589c57f69336c06f3b46c27d57381469173fc00cebe69c8c6c69703</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459847/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459847/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25781353$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, So Mi</creatorcontrib><creatorcontrib>Hwang, In Koo</creatorcontrib><creatorcontrib>Yoo, Dae Young</creatorcontrib><creatorcontrib>Eum, Won Sik</creatorcontrib><creatorcontrib>Kim, Dae Won</creatorcontrib><creatorcontrib>Shin, Min Jea</creatorcontrib><creatorcontrib>Ahn, Eun Hee</creatorcontrib><creatorcontrib>Jo, Hyo Sang</creatorcontrib><creatorcontrib>Ryu, Eun Ji</creatorcontrib><creatorcontrib>Yong, Ji In</creatorcontrib><creatorcontrib>Cho, Sung‐Woo</creatorcontrib><creatorcontrib>Kwon, Oh‐Shin</creatorcontrib><creatorcontrib>Lee, Keun Wook</creatorcontrib><creatorcontrib>Cho, Yoon Shin</creatorcontrib><creatorcontrib>Han, Kyu Hyung</creatorcontrib><creatorcontrib>Park, Jinseu</creatorcontrib><creatorcontrib>Choi, Soo Young</creatorcontrib><title>Tat‐antioxidant 1 protects against stress‐induced hippocampal HT‐22 cells death and attenuate ischaemic insult in animal model</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Oxidative stress‐induced reactive oxygen species (ROS) are responsible for various neuronal diseases. Antioxidant 1 (Atox1) regulates copper homoeostasis and promotes cellular antioxidant defence against toxins generated by ROS. The roles of Atox1 protein in ischaemia, however, remain unclear. In this study, we generated a protein transduction domain fused Tat‐Atox1 and examined the roles of Tat‐Atox1 in oxidative stress‐induced hippocampal HT‐22 cell death and an ischaemic injury animal model. Tat‐Atox1 effectively transduced into HT‐22 cells and it protected cells against the effects of hydrogen peroxide (H2O2)‐induced toxicity including increasing of ROS levels and DNA fragmentation. At the same time, Tat‐Atox1 regulated cellular survival signalling such as p53, Bad/Bcl‐2, Akt and mitogen‐activate protein kinases (MAPKs). In the animal ischaemia model, transduced Tat‐Atox1 protected against neuronal cell death in the hippocampal CA1 region. In addition, Tat‐Atox1 significantly decreased the activation of astrocytes and microglia as well as lipid peroxidation in the CA1 region after ischaemic insult. Taken together, these results indicate that transduced Tat‐Atox1 protects against oxidative stress‐induced HT‐22 cell death and against neuronal damage in animal ischaemia model. Therefore, we suggest that Tat‐Atox1 has potential as a therapeutic agent for the treatment of oxidative stress‐induced ischaemic damage.</description><subject>AKT protein</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Astrocytes</subject><subject>ATOX1 protein</subject><subject>Biotechnology</subject><subject>Blotting, Western</subject><subject>Brain research</subject><subject>Cell cycle</subject><subject>Cell death</subject><subject>Cell Line</subject><subject>Cell Survival - drug effects</subject><subject>Chemical compounds</subject><subject>Copper</subject><subject>Disease Models, Animal</subject><subject>DNA fragmentation</subject><subject>Dose-Response Relationship, Drug</subject><subject>Gene Products, tat - genetics</subject><subject>Gene Products, tat - metabolism</subject><subject>Hippocampus</subject><subject>Hippocampus - cytology</subject><subject>Humans</subject><subject>Hydrogen peroxide</subject><subject>ischaemic injury</subject><subject>Ischemia</subject><subject>Ischemia - physiopathology</subject><subject>Ischemia - prevention & control</subject><subject>Lipid peroxidation</subject><subject>Metabolism</subject><subject>Metallochaperones - genetics</subject><subject>Metallochaperones - metabolism</subject><subject>Metallochaperones - pharmacology</subject><subject>Mice</subject><subject>Microglia</subject><subject>Microscopy</subject><subject>Microscopy, Confocal</subject><subject>Microscopy, Fluorescence</subject><subject>Motor Activity - drug effects</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Original</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>p53 Protein</subject><subject>Peptides</subject><subject>Peroxidation</subject><subject>Prosencephalon - blood supply</subject><subject>Protein kinase</subject><subject>protein therapy</subject><subject>protein transduction domain</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Recombinant Fusion Proteins - genetics</subject><subject>Recombinant Fusion Proteins - metabolism</subject><subject>Recombinant Fusion Proteins - pharmacology</subject><subject>Signal transduction</subject><subject>Studies</subject><subject>Tat‐Atox1</subject><subject>Toxicity</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><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>eNp9kb1uFDEURi0EIiHQ8ADIEl2kTfw3HrtBQquEgBLRLLXlvfZkvZoZD7YnkC4FD8Az8iQ47CaCBjfX0j0-_qQPodeUnNB6TrcwDCeUNZQ_QYe0UWwhNBdP93equDpAL3LeEsIl5fo5OmBNqyhv-CH6sbLl191PO5YQvwdXJ6Z4SrF4KBnbaxvGXHAuyedcuTC6GbzDmzBNEeww2R5frOqCMQy-7zN23pYNtqPDthQ_zrZ4HDJsrB8C4Gqb-1JHJcJQHw_R-f4letbZPvtX-3mEvpyfrZYXi8vPHz4u318uQAjFF04I10oi175RGpq2k5pzCUR2fC0ksNY1LVdUSE1b3gEh4NdealAgQeqW8CP0bued5vXgHfixJNubKdUo6dZEG8y_mzFszHW8MUI0Wom2Ct7uBSl-nX0uZhvnNNbMhjFNKFOE8Uod7yhIMefku8cfKDH3jZn7xsyfxir85u9Mj-hDRRWgO-Bb6P3tf1Tm0_Lqaif9DThSpgY</recordid><startdate>201506</startdate><enddate>201506</enddate><creator>Kim, So Mi</creator><creator>Hwang, In Koo</creator><creator>Yoo, Dae Young</creator><creator>Eum, Won Sik</creator><creator>Kim, Dae Won</creator><creator>Shin, Min Jea</creator><creator>Ahn, Eun Hee</creator><creator>Jo, Hyo Sang</creator><creator>Ryu, Eun Ji</creator><creator>Yong, Ji In</creator><creator>Cho, Sung‐Woo</creator><creator>Kwon, Oh‐Shin</creator><creator>Lee, Keun Wook</creator><creator>Cho, Yoon Shin</creator><creator>Han, Kyu Hyung</creator><creator>Park, Jinseu</creator><creator>Choi, Soo Young</creator><general>John Wiley & Sons, Inc</general><general>BlackWell Publishing 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1 protects against stress‐induced hippocampal HT‐22 cells death and attenuate ischaemic insult in animal model</title><author>Kim, So Mi ; Hwang, In Koo ; Yoo, Dae Young ; Eum, Won Sik ; Kim, Dae Won ; Shin, Min Jea ; Ahn, Eun Hee ; Jo, Hyo Sang ; Ryu, Eun Ji ; Yong, Ji In ; Cho, Sung‐Woo ; Kwon, Oh‐Shin ; Lee, Keun Wook ; Cho, Yoon Shin ; Han, Kyu Hyung ; Park, Jinseu ; Choi, Soo Young</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4483-d44d7606be589c57f69336c06f3b46c27d57381469173fc00cebe69c8c6c69703</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>AKT protein</topic><topic>Animal models</topic><topic>Animals</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Astrocytes</topic><topic>ATOX1 protein</topic><topic>Biotechnology</topic><topic>Blotting, Western</topic><topic>Brain research</topic><topic>Cell cycle</topic><topic>Cell death</topic><topic>Cell Line</topic><topic>Cell Survival - drug effects</topic><topic>Chemical compounds</topic><topic>Copper</topic><topic>Disease Models, Animal</topic><topic>DNA fragmentation</topic><topic>Dose-Response Relationship, Drug</topic><topic>Gene Products, tat - genetics</topic><topic>Gene Products, tat - metabolism</topic><topic>Hippocampus</topic><topic>Hippocampus - cytology</topic><topic>Humans</topic><topic>Hydrogen peroxide</topic><topic>ischaemic injury</topic><topic>Ischemia</topic><topic>Ischemia - physiopathology</topic><topic>Ischemia - prevention & control</topic><topic>Lipid peroxidation</topic><topic>Metabolism</topic><topic>Metallochaperones - genetics</topic><topic>Metallochaperones - metabolism</topic><topic>Metallochaperones - pharmacology</topic><topic>Mice</topic><topic>Microglia</topic><topic>Microscopy</topic><topic>Microscopy, Confocal</topic><topic>Microscopy, Fluorescence</topic><topic>Motor Activity - drug effects</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Original</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>p53 Protein</topic><topic>Peptides</topic><topic>Peroxidation</topic><topic>Prosencephalon - blood supply</topic><topic>Protein kinase</topic><topic>protein therapy</topic><topic>protein transduction domain</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Recombinant Fusion Proteins - genetics</topic><topic>Recombinant Fusion Proteins - metabolism</topic><topic>Recombinant Fusion Proteins - pharmacology</topic><topic>Signal transduction</topic><topic>Studies</topic><topic>Tat‐Atox1</topic><topic>Toxicity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, So Mi</creatorcontrib><creatorcontrib>Hwang, In 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Shin</au><au>Han, Kyu Hyung</au><au>Park, Jinseu</au><au>Choi, Soo Young</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tat‐antioxidant 1 protects against stress‐induced hippocampal HT‐22 cells death and attenuate ischaemic insult in animal model</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2015-06</date><risdate>2015</risdate><volume>19</volume><issue>6</issue><spage>1333</spage><epage>1345</epage><pages>1333-1345</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Oxidative stress‐induced reactive oxygen species (ROS) are responsible for various neuronal diseases. Antioxidant 1 (Atox1) regulates copper homoeostasis and promotes cellular antioxidant defence against toxins generated by ROS. The roles of Atox1 protein in ischaemia, however, remain unclear. In this study, we generated a protein transduction domain fused Tat‐Atox1 and examined the roles of Tat‐Atox1 in oxidative stress‐induced hippocampal HT‐22 cell death and an ischaemic injury animal model. Tat‐Atox1 effectively transduced into HT‐22 cells and it protected cells against the effects of hydrogen peroxide (H2O2)‐induced toxicity including increasing of ROS levels and DNA fragmentation. At the same time, Tat‐Atox1 regulated cellular survival signalling such as p53, Bad/Bcl‐2, Akt and mitogen‐activate protein kinases (MAPKs). In the animal ischaemia model, transduced Tat‐Atox1 protected against neuronal cell death in the hippocampal CA1 region. In addition, Tat‐Atox1 significantly decreased the activation of astrocytes and microglia as well as lipid peroxidation in the CA1 region after ischaemic insult. Taken together, these results indicate that transduced Tat‐Atox1 protects against oxidative stress‐induced HT‐22 cell death and against neuronal damage in animal ischaemia model. Therefore, we suggest that Tat‐Atox1 has potential as a therapeutic agent for the treatment of oxidative stress‐induced ischaemic damage.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>25781353</pmid><doi>10.1111/jcmm.12513</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4459847 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Access via Wiley Online Library; Wiley Online Library Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | AKT protein Animal models Animals Antioxidants Apoptosis Apoptosis - drug effects Astrocytes ATOX1 protein Biotechnology Blotting, Western Brain research Cell cycle Cell death Cell Line Cell Survival - drug effects Chemical compounds Copper Disease Models, Animal DNA fragmentation Dose-Response Relationship, Drug Gene Products, tat - genetics Gene Products, tat - metabolism Hippocampus Hippocampus - cytology Humans Hydrogen peroxide ischaemic injury Ischemia Ischemia - physiopathology Ischemia - prevention & control Lipid peroxidation Metabolism Metallochaperones - genetics Metallochaperones - metabolism Metallochaperones - pharmacology Mice Microglia Microscopy Microscopy, Confocal Microscopy, Fluorescence Motor Activity - drug effects Neurons - drug effects Neurons - metabolism Neuroprotective Agents - pharmacology Original Oxidative stress Oxidative Stress - drug effects p53 Protein Peptides Peroxidation Prosencephalon - blood supply Protein kinase protein therapy protein transduction domain Proteins Reactive oxygen species Reactive Oxygen Species - metabolism Recombinant Fusion Proteins - genetics Recombinant Fusion Proteins - metabolism Recombinant Fusion Proteins - pharmacology Signal transduction Studies Tat‐Atox1 Toxicity |
| title | Tat‐antioxidant 1 protects against stress‐induced hippocampal HT‐22 cells death and attenuate ischaemic insult in animal model |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-28T21%3A41%3A16IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Tat%E2%80%90antioxidant%201%20protects%20against%20stress%E2%80%90induced%20hippocampal%20HT%E2%80%9022%20cells%20death%20and%20attenuate%20ischaemic%20insult%20in%20animal%20model&rft.jtitle=Journal%20of%20cellular%20and%20molecular%20medicine&rft.au=Kim,%20So%20Mi&rft.date=2015-06&rft.volume=19&rft.issue=6&rft.spage=1333&rft.epage=1345&rft.pages=1333-1345&rft.issn=1582-1838&rft.eissn=1582-4934&rft_id=info:doi/10.1111/jcmm.12513&rft_dat=%3Cproquest_pubme%3E2290128023%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2290128023&rft_id=info:pmid/25781353&rfr_iscdi=true |