ER Stress via CHOP Pathway is Involved in FK506-Induced Apoptosis in Rat Fibroblasts
Abstract Background/Aims: Hypertrophic scars (HS) formation results from reduced apoptosis and increased proliferation of fibroblasts. Therefore, apoptosis of fibroblasts is a key target for the development of novel therapeutic strategies for HS. Previous reports demonstrated that FK506 could attenu...
Gespeichert in:
| Veröffentlicht in: | Cellular physiology and biochemistry 2016-01, Vol.39 (5), p.1965-1976 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1976 |
|---|---|
| container_issue | 5 |
| container_start_page | 1965 |
| container_title | Cellular physiology and biochemistry |
| container_volume | 39 |
| creator | Tang, Jian Ge, Yingbin Yang, Lei Xu, Xinyu Sui, Tao Ge, Dawei Que, Jun Cao, Xiaojian |
| description | Abstract
Background/Aims: Hypertrophic scars (HS) formation results from reduced apoptosis and increased proliferation of fibroblasts. Therefore, apoptosis of fibroblasts is a key target for the development of novel therapeutic strategies for HS. Previous reports demonstrated that FK506 could attenuate scar formation in vivo and FK506 could also induce endoplasmic reticulum stress (ER stress). However, the effects of FK506 on ER stress-mediated apoptosis in fibroblasts remain unclear. Methods: Rat skin fibroblasts were used in the study. Cell viability was examined using cell counting Kit-8. Apoptosis was detected by Annexin V/Propidium Iodide Double Staining. Gene silencing was performed using Small Interfering RNAs (siRNAs) or via lentiviral infection. The expression of apoptosis-related proteins was determined via Western blot. Interaction between proteins was explored by co-immunoprecipitation. Results: FK506 significantly reduced cell viability and induced apoptosis in fibroblasts. Interestingly, ER stress was also activated after FK506 treatment. We further demonstrated that FK506-induced apoptosis was mediated by ER stress via activating CHOP, evidenced by decreased apoptosis after inhibition of ER stress using TUDCA or silencing expression of CHOP. Furthermore, Co-immunoprecipitation results indicated that treatment of FK506 induced disassociation of FKBP12.6 from RyR2 and its translocation from ER membrane to cytosol, consequently promoting ER stress-mediated apoptosis. Conclusion: FK506-induced fibroblasts apoptosis was mediated by ER stress via CHOP signaling pathway. |
| doi_str_mv | 10.1159/000447894 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_karge</sourceid><recordid>TN_cdi_proquest_miscellaneous_1835521609</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_2cdc8f8ce2734d0da5c02c08441b073c</doaj_id><sourcerecordid>3040336602</sourcerecordid><originalsourceid>FETCH-LOGICAL-c463t-a756391f440abe121d7f5dcd46964ee99d9f34f12cd98ab03e09f189edc6be433</originalsourceid><addsrcrecordid>eNpt0U1v1DAQBmALgWgpHLgjFKkXegiMP-KPY1l16YpKXZVythzbKVmycWoni_rvMU3JAXGyPfP4la1B6C2GjxhX6hMAMCakYs_QMWYEl0oI-TzvAVelVFIcoVcp7SAfhSIv0RERQmCBq2N0e3FTfBujT6k4tKZYXV5vi60Zf_wyD0Wbik1_CN3Bu6Lti_XXCni56d1kc-F8CMMYUja5dWPGYt3WMdSdSWN6jV40pkv-zdN6gr6vL25Xl-XV9ZfN6vyqtIzTsTSi4lThhjEwtccEO9FUzjrGFWfeK-VUQ1mDiXVKmhqoB9VgqbyzvPaM0hO0mXNdMDs9xHZv4oMOptWPhRDvtIljazuvc4aVjbSeCMocOFNZIBYkY7gGQW3O-jBnDTHcTz6Net8m67vO9D5MSWNJq4pgDirT03_oLkyxzz_VFBhQyjmQrM5mZWNIKfpmeSAG_Wdsehlbtu-fEqd6790i_84pg3cz-GninY8LWO6f_re92n6ehR5cQ38D1CKjuA</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3040336602</pqid></control><display><type>article</type><title>ER Stress via CHOP Pathway is Involved in FK506-Induced Apoptosis in Rat Fibroblasts</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Karger Open Access</source><creator>Tang, Jian ; Ge, Yingbin ; Yang, Lei ; Xu, Xinyu ; Sui, Tao ; Ge, Dawei ; Que, Jun ; Cao, Xiaojian</creator><creatorcontrib>Tang, Jian ; Ge, Yingbin ; Yang, Lei ; Xu, Xinyu ; Sui, Tao ; Ge, Dawei ; Que, Jun ; Cao, Xiaojian</creatorcontrib><description>Abstract
Background/Aims: Hypertrophic scars (HS) formation results from reduced apoptosis and increased proliferation of fibroblasts. Therefore, apoptosis of fibroblasts is a key target for the development of novel therapeutic strategies for HS. Previous reports demonstrated that FK506 could attenuate scar formation in vivo and FK506 could also induce endoplasmic reticulum stress (ER stress). However, the effects of FK506 on ER stress-mediated apoptosis in fibroblasts remain unclear. Methods: Rat skin fibroblasts were used in the study. Cell viability was examined using cell counting Kit-8. Apoptosis was detected by Annexin V/Propidium Iodide Double Staining. Gene silencing was performed using Small Interfering RNAs (siRNAs) or via lentiviral infection. The expression of apoptosis-related proteins was determined via Western blot. Interaction between proteins was explored by co-immunoprecipitation. Results: FK506 significantly reduced cell viability and induced apoptosis in fibroblasts. Interestingly, ER stress was also activated after FK506 treatment. We further demonstrated that FK506-induced apoptosis was mediated by ER stress via activating CHOP, evidenced by decreased apoptosis after inhibition of ER stress using TUDCA or silencing expression of CHOP. Furthermore, Co-immunoprecipitation results indicated that treatment of FK506 induced disassociation of FKBP12.6 from RyR2 and its translocation from ER membrane to cytosol, consequently promoting ER stress-mediated apoptosis. Conclusion: FK506-induced fibroblasts apoptosis was mediated by ER stress via CHOP signaling pathway.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000447894</identifier><identifier>PMID: 27771715</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animals ; Animals, Newborn ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Calcineurin Inhibitors - pharmacology ; Cell death ; CHOP ; Endoplasmic Reticulum - drug effects ; Endoplasmic Reticulum - metabolism ; Endoplasmic Reticulum Stress - drug effects ; Endoplasmic Reticulum Stress - genetics ; ER stress ; Experiments ; Fibroblast ; Fibroblasts ; Fibroblasts - cytology ; Fibroblasts - drug effects ; Fibroblasts - metabolism ; FK506 ; Fluorides ; Gene Expression Regulation ; Homeostasis ; Membranes ; Original Paper ; PERK ; Primary Cell Culture ; Proteins ; Rats ; Rats, Sprague-Dawley ; RNA, Small Interfering - genetics ; RNA, Small Interfering - metabolism ; Ryanodine Receptor Calcium Release Channel - genetics ; Ryanodine Receptor Calcium Release Channel - metabolism ; Signal Transduction ; Tacrolimus - pharmacology ; Tacrolimus Binding Proteins - genetics ; Tacrolimus Binding Proteins - metabolism ; Transcription Factor CHOP - antagonists & inhibitors ; Transcription Factor CHOP - genetics ; Transcription Factor CHOP - metabolism</subject><ispartof>Cellular physiology and biochemistry, 2016-01, Vol.39 (5), p.1965-1976</ispartof><rights>2016 The Author(s) Published by S. Karger AG, Basel</rights><rights>2016 The Author(s) Published by S. Karger AG, Basel.</rights><rights>2016 The Author(s) Published by S. Karger AG, Basel. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the associated terms available at: https://uk.sagepub.com/en-gb/eur/reusing-open-access-and-sage-choice-content</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-a756391f440abe121d7f5dcd46964ee99d9f34f12cd98ab03e09f189edc6be433</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,866,2106,27644,27933,27934</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27771715$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tang, Jian</creatorcontrib><creatorcontrib>Ge, Yingbin</creatorcontrib><creatorcontrib>Yang, Lei</creatorcontrib><creatorcontrib>Xu, Xinyu</creatorcontrib><creatorcontrib>Sui, Tao</creatorcontrib><creatorcontrib>Ge, Dawei</creatorcontrib><creatorcontrib>Que, Jun</creatorcontrib><creatorcontrib>Cao, Xiaojian</creatorcontrib><title>ER Stress via CHOP Pathway is Involved in FK506-Induced Apoptosis in Rat Fibroblasts</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Abstract
Background/Aims: Hypertrophic scars (HS) formation results from reduced apoptosis and increased proliferation of fibroblasts. Therefore, apoptosis of fibroblasts is a key target for the development of novel therapeutic strategies for HS. Previous reports demonstrated that FK506 could attenuate scar formation in vivo and FK506 could also induce endoplasmic reticulum stress (ER stress). However, the effects of FK506 on ER stress-mediated apoptosis in fibroblasts remain unclear. Methods: Rat skin fibroblasts were used in the study. Cell viability was examined using cell counting Kit-8. Apoptosis was detected by Annexin V/Propidium Iodide Double Staining. Gene silencing was performed using Small Interfering RNAs (siRNAs) or via lentiviral infection. The expression of apoptosis-related proteins was determined via Western blot. Interaction between proteins was explored by co-immunoprecipitation. Results: FK506 significantly reduced cell viability and induced apoptosis in fibroblasts. Interestingly, ER stress was also activated after FK506 treatment. We further demonstrated that FK506-induced apoptosis was mediated by ER stress via activating CHOP, evidenced by decreased apoptosis after inhibition of ER stress using TUDCA or silencing expression of CHOP. Furthermore, Co-immunoprecipitation results indicated that treatment of FK506 induced disassociation of FKBP12.6 from RyR2 and its translocation from ER membrane to cytosol, consequently promoting ER stress-mediated apoptosis. Conclusion: FK506-induced fibroblasts apoptosis was mediated by ER stress via CHOP signaling pathway.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Calcineurin Inhibitors - pharmacology</subject><subject>Cell death</subject><subject>CHOP</subject><subject>Endoplasmic Reticulum - drug effects</subject><subject>Endoplasmic Reticulum - metabolism</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>Endoplasmic Reticulum Stress - genetics</subject><subject>ER stress</subject><subject>Experiments</subject><subject>Fibroblast</subject><subject>Fibroblasts</subject><subject>Fibroblasts - cytology</subject><subject>Fibroblasts - drug effects</subject><subject>Fibroblasts - metabolism</subject><subject>FK506</subject><subject>Fluorides</subject><subject>Gene Expression Regulation</subject><subject>Homeostasis</subject><subject>Membranes</subject><subject>Original Paper</subject><subject>PERK</subject><subject>Primary Cell Culture</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>RNA, Small Interfering - genetics</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Ryanodine Receptor Calcium Release Channel - genetics</subject><subject>Ryanodine Receptor Calcium Release Channel - metabolism</subject><subject>Signal Transduction</subject><subject>Tacrolimus - pharmacology</subject><subject>Tacrolimus Binding Proteins - genetics</subject><subject>Tacrolimus Binding Proteins - metabolism</subject><subject>Transcription Factor CHOP - antagonists & inhibitors</subject><subject>Transcription Factor CHOP - genetics</subject><subject>Transcription Factor CHOP - metabolism</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNpt0U1v1DAQBmALgWgpHLgjFKkXegiMP-KPY1l16YpKXZVythzbKVmycWoni_rvMU3JAXGyPfP4la1B6C2GjxhX6hMAMCakYs_QMWYEl0oI-TzvAVelVFIcoVcp7SAfhSIv0RERQmCBq2N0e3FTfBujT6k4tKZYXV5vi60Zf_wyD0Wbik1_CN3Bu6Lti_XXCni56d1kc-F8CMMYUja5dWPGYt3WMdSdSWN6jV40pkv-zdN6gr6vL25Xl-XV9ZfN6vyqtIzTsTSi4lThhjEwtccEO9FUzjrGFWfeK-VUQ1mDiXVKmhqoB9VgqbyzvPaM0hO0mXNdMDs9xHZv4oMOptWPhRDvtIljazuvc4aVjbSeCMocOFNZIBYkY7gGQW3O-jBnDTHcTz6Net8m67vO9D5MSWNJq4pgDirT03_oLkyxzz_VFBhQyjmQrM5mZWNIKfpmeSAG_Wdsehlbtu-fEqd6790i_84pg3cz-GninY8LWO6f_re92n6ehR5cQ38D1CKjuA</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Tang, Jian</creator><creator>Ge, Yingbin</creator><creator>Yang, Lei</creator><creator>Xu, Xinyu</creator><creator>Sui, Tao</creator><creator>Ge, Dawei</creator><creator>Que, Jun</creator><creator>Cao, Xiaojian</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20160101</creationdate><title>ER Stress via CHOP Pathway is Involved in FK506-Induced Apoptosis in Rat Fibroblasts</title><author>Tang, Jian ; Ge, Yingbin ; Yang, Lei ; Xu, Xinyu ; Sui, Tao ; Ge, Dawei ; Que, Jun ; Cao, Xiaojian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-a756391f440abe121d7f5dcd46964ee99d9f34f12cd98ab03e09f189edc6be433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Calcineurin Inhibitors - pharmacology</topic><topic>Cell death</topic><topic>CHOP</topic><topic>Endoplasmic Reticulum - drug effects</topic><topic>Endoplasmic Reticulum - metabolism</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>Endoplasmic Reticulum Stress - genetics</topic><topic>ER stress</topic><topic>Experiments</topic><topic>Fibroblast</topic><topic>Fibroblasts</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - drug effects</topic><topic>Fibroblasts - metabolism</topic><topic>FK506</topic><topic>Fluorides</topic><topic>Gene Expression Regulation</topic><topic>Homeostasis</topic><topic>Membranes</topic><topic>Original Paper</topic><topic>PERK</topic><topic>Primary Cell Culture</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>RNA, Small Interfering - genetics</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Ryanodine Receptor Calcium Release Channel - genetics</topic><topic>Ryanodine Receptor Calcium Release Channel - metabolism</topic><topic>Signal Transduction</topic><topic>Tacrolimus - pharmacology</topic><topic>Tacrolimus Binding Proteins - genetics</topic><topic>Tacrolimus Binding Proteins - metabolism</topic><topic>Transcription Factor CHOP - antagonists & inhibitors</topic><topic>Transcription Factor CHOP - genetics</topic><topic>Transcription Factor CHOP - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tang, Jian</creatorcontrib><creatorcontrib>Ge, Yingbin</creatorcontrib><creatorcontrib>Yang, Lei</creatorcontrib><creatorcontrib>Xu, Xinyu</creatorcontrib><creatorcontrib>Sui, Tao</creatorcontrib><creatorcontrib>Ge, Dawei</creatorcontrib><creatorcontrib>Que, Jun</creatorcontrib><creatorcontrib>Cao, Xiaojian</creatorcontrib><collection>Karger 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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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>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><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tang, Jian</au><au>Ge, Yingbin</au><au>Yang, Lei</au><au>Xu, Xinyu</au><au>Sui, Tao</au><au>Ge, Dawei</au><au>Que, Jun</au><au>Cao, Xiaojian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ER Stress via CHOP Pathway is Involved in FK506-Induced Apoptosis in Rat Fibroblasts</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>39</volume><issue>5</issue><spage>1965</spage><epage>1976</epage><pages>1965-1976</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Abstract
Background/Aims: Hypertrophic scars (HS) formation results from reduced apoptosis and increased proliferation of fibroblasts. Therefore, apoptosis of fibroblasts is a key target for the development of novel therapeutic strategies for HS. Previous reports demonstrated that FK506 could attenuate scar formation in vivo and FK506 could also induce endoplasmic reticulum stress (ER stress). However, the effects of FK506 on ER stress-mediated apoptosis in fibroblasts remain unclear. Methods: Rat skin fibroblasts were used in the study. Cell viability was examined using cell counting Kit-8. Apoptosis was detected by Annexin V/Propidium Iodide Double Staining. Gene silencing was performed using Small Interfering RNAs (siRNAs) or via lentiviral infection. The expression of apoptosis-related proteins was determined via Western blot. Interaction between proteins was explored by co-immunoprecipitation. Results: FK506 significantly reduced cell viability and induced apoptosis in fibroblasts. Interestingly, ER stress was also activated after FK506 treatment. We further demonstrated that FK506-induced apoptosis was mediated by ER stress via activating CHOP, evidenced by decreased apoptosis after inhibition of ER stress using TUDCA or silencing expression of CHOP. Furthermore, Co-immunoprecipitation results indicated that treatment of FK506 induced disassociation of FKBP12.6 from RyR2 and its translocation from ER membrane to cytosol, consequently promoting ER stress-mediated apoptosis. Conclusion: FK506-induced fibroblasts apoptosis was mediated by ER stress via CHOP signaling pathway.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>27771715</pmid><doi>10.1159/000447894</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1015-8987 |
| ispartof | Cellular physiology and biochemistry, 2016-01, Vol.39 (5), p.1965-1976 |
| issn | 1015-8987 1421-9778 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1835521609 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Karger Open Access |
| subjects | Animals Animals, Newborn Apoptosis Apoptosis - drug effects Apoptosis - genetics Calcineurin Inhibitors - pharmacology Cell death CHOP Endoplasmic Reticulum - drug effects Endoplasmic Reticulum - metabolism Endoplasmic Reticulum Stress - drug effects Endoplasmic Reticulum Stress - genetics ER stress Experiments Fibroblast Fibroblasts Fibroblasts - cytology Fibroblasts - drug effects Fibroblasts - metabolism FK506 Fluorides Gene Expression Regulation Homeostasis Membranes Original Paper PERK Primary Cell Culture Proteins Rats Rats, Sprague-Dawley RNA, Small Interfering - genetics RNA, Small Interfering - metabolism Ryanodine Receptor Calcium Release Channel - genetics Ryanodine Receptor Calcium Release Channel - metabolism Signal Transduction Tacrolimus - pharmacology Tacrolimus Binding Proteins - genetics Tacrolimus Binding Proteins - metabolism Transcription Factor CHOP - antagonists & inhibitors Transcription Factor CHOP - genetics Transcription Factor CHOP - metabolism |
| title | ER Stress via CHOP Pathway is Involved in FK506-Induced Apoptosis in Rat Fibroblasts |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-02T22%3A09%3A31IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_karge&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=ER%20Stress%20via%20CHOP%20Pathway%20is%20Involved%20in%20FK506-Induced%20Apoptosis%20in%20Rat%20Fibroblasts&rft.jtitle=Cellular%20physiology%20and%20biochemistry&rft.au=Tang,%20Jian&rft.date=2016-01-01&rft.volume=39&rft.issue=5&rft.spage=1965&rft.epage=1976&rft.pages=1965-1976&rft.issn=1015-8987&rft.eissn=1421-9778&rft_id=info:doi/10.1159/000447894&rft_dat=%3Cproquest_karge%3E3040336602%3C/proquest_karge%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=3040336602&rft_id=info:pmid/27771715&rft_doaj_id=oai_doaj_org_article_2cdc8f8ce2734d0da5c02c08441b073c&rfr_iscdi=true |