Engagement of CD99 Induces Apoptosis Through a Calcineurin-Independent Pathway in Ewing's Sarcoma Cells
Programmed cell death (PCD) is a prominent feature of the development of the immune and nervous systems. In both systems, widespread PCD occurs in primitive progenitor cells during development. In this study, we demonstrated that Ewing's sarcoma (ES) cells, undifferentiated neural precursors, u...
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| Veröffentlicht in: | The American journal of pathology 1998-12, Vol.153 (6), p.1937-1945 |
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| creator | Sohn, Hae Won Choi, Eun Young Kim, Soon Ha Lee, Im-soon Chung, Doo Hyun Sung, Uhn A Hwang, Duck Ho Cho, Sa Sun Jun, Byung Hoon Jang, Ja June Chi, Je Geun Park, Seong Hoe |
| description | Programmed cell death (PCD) is a prominent feature of the development of the immune and nervous systems. In both systems, widespread PCD occurs in primitive progenitor cells during development. In this study, we demonstrated that Ewing's sarcoma (ES) cells, undifferentiated neural precursors, underwent apoptosis upon engagement of CD99 with anti-CD99 monoclonal antibody. Apoptosis via CD99 occurred only in the undifferentiated state of ES cells, but not in differentiated ES cells. CD99-induced apoptosis in ES cells appeared to require
de novo synthesis of RNA and protein as well as caspase activation. Cyclosporin A, known to be a potent inhibitor of both calcineurin activation and mitochondrial permeability transition pore opening, inhibited CD99-mediated apoptosis, whereas FK-506, a specific calcineurin inhibitor, did not, indicating the induction of CD99-mediated apoptosis through a calcineurin-independent pathway. Furthermore, the dying cells displayed the reduction of mitochondrial transmembrane potential (ΔΨm). These results suggest that CD99 engagement induce CsA-inhibitable mitochondrial permeability transition pore opening, followed by a reduction of ΔΨm and caspase activation, thereby leading to apoptosis. Based on these results, we suggest the possible involvement of CD99 in the apoptotic processes that occur during nervous system development and also its application in immunotherapeutic trials for ES cases. |
| doi_str_mv | 10.1016/S0002-9440(10)65707-0 |
| format | Article |
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de novo synthesis of RNA and protein as well as caspase activation. Cyclosporin A, known to be a potent inhibitor of both calcineurin activation and mitochondrial permeability transition pore opening, inhibited CD99-mediated apoptosis, whereas FK-506, a specific calcineurin inhibitor, did not, indicating the induction of CD99-mediated apoptosis through a calcineurin-independent pathway. Furthermore, the dying cells displayed the reduction of mitochondrial transmembrane potential (ΔΨm). These results suggest that CD99 engagement induce CsA-inhibitable mitochondrial permeability transition pore opening, followed by a reduction of ΔΨm and caspase activation, thereby leading to apoptosis. Based on these results, we suggest the possible involvement of CD99 in the apoptotic processes that occur during nervous system development and also its application in immunotherapeutic trials for ES cases.</description><identifier>ISSN: 0002-9440</identifier><identifier>EISSN: 1525-2191</identifier><identifier>DOI: 10.1016/S0002-9440(10)65707-0</identifier><identifier>PMID: 9846983</identifier><identifier>CODEN: AJPAA4</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>12E7 Antigen ; Antibodies, Monoclonal - pharmacology ; Antigens, CD - immunology ; Antigens, CD - physiology ; Apoptosis ; Calcineurin ; Calcium - physiology ; Caspase Inhibitors ; Caspases - physiology ; Cell Adhesion Molecules - immunology ; Cell Adhesion Molecules - physiology ; Cell Differentiation ; Cyclosporine - pharmacology ; Dactinomycin - pharmacology ; Fluorescent Antibody Technique, Indirect ; Humans ; Membrane Potentials ; Microscopy, Confocal ; Microscopy, Electron ; Neuroblastoma - pathology ; Neuroectodermal Tumors, Primitive - pathology ; Regular ; Sarcoma, Ewing - pathology ; Tacrolimus - pharmacology ; Tumor Cells, Cultured</subject><ispartof>The American journal of pathology, 1998-12, Vol.153 (6), p.1937-1945</ispartof><rights>1998 American Society for Investigative Pathology</rights><rights>Copyright American Society for Investigative Pathology Dec 1998</rights><rights>Copyright © 1998, American Society for Investigative Pathology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c587t-f91d6c608c68b9af1693662c29086d010004e469d81df207b45b42ae8d9303043</citedby><cites>FETCH-LOGICAL-c587t-f91d6c608c68b9af1693662c29086d010004e469d81df207b45b42ae8d9303043</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/PMC1866321/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0002-9440(10)65707-0$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,3548,27922,27923,45993,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9846983$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sohn, Hae Won</creatorcontrib><creatorcontrib>Choi, Eun Young</creatorcontrib><creatorcontrib>Kim, Soon Ha</creatorcontrib><creatorcontrib>Lee, Im-soon</creatorcontrib><creatorcontrib>Chung, Doo Hyun</creatorcontrib><creatorcontrib>Sung, Uhn A</creatorcontrib><creatorcontrib>Hwang, Duck Ho</creatorcontrib><creatorcontrib>Cho, Sa Sun</creatorcontrib><creatorcontrib>Jun, Byung Hoon</creatorcontrib><creatorcontrib>Jang, Ja June</creatorcontrib><creatorcontrib>Chi, Je Geun</creatorcontrib><creatorcontrib>Park, Seong Hoe</creatorcontrib><title>Engagement of CD99 Induces Apoptosis Through a Calcineurin-Independent Pathway in Ewing's Sarcoma Cells</title><title>The American journal of pathology</title><addtitle>Am J Pathol</addtitle><description>Programmed cell death (PCD) is a prominent feature of the development of the immune and nervous systems. In both systems, widespread PCD occurs in primitive progenitor cells during development. In this study, we demonstrated that Ewing's sarcoma (ES) cells, undifferentiated neural precursors, underwent apoptosis upon engagement of CD99 with anti-CD99 monoclonal antibody. Apoptosis via CD99 occurred only in the undifferentiated state of ES cells, but not in differentiated ES cells. CD99-induced apoptosis in ES cells appeared to require
de novo synthesis of RNA and protein as well as caspase activation. Cyclosporin A, known to be a potent inhibitor of both calcineurin activation and mitochondrial permeability transition pore opening, inhibited CD99-mediated apoptosis, whereas FK-506, a specific calcineurin inhibitor, did not, indicating the induction of CD99-mediated apoptosis through a calcineurin-independent pathway. Furthermore, the dying cells displayed the reduction of mitochondrial transmembrane potential (ΔΨm). These results suggest that CD99 engagement induce CsA-inhibitable mitochondrial permeability transition pore opening, followed by a reduction of ΔΨm and caspase activation, thereby leading to apoptosis. Based on these results, we suggest the possible involvement of CD99 in the apoptotic processes that occur during nervous system development and also its application in immunotherapeutic trials for ES cases.</description><subject>12E7 Antigen</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Antigens, CD - immunology</subject><subject>Antigens, CD - physiology</subject><subject>Apoptosis</subject><subject>Calcineurin</subject><subject>Calcium - physiology</subject><subject>Caspase Inhibitors</subject><subject>Caspases - physiology</subject><subject>Cell Adhesion Molecules - immunology</subject><subject>Cell Adhesion Molecules - physiology</subject><subject>Cell Differentiation</subject><subject>Cyclosporine - pharmacology</subject><subject>Dactinomycin - pharmacology</subject><subject>Fluorescent Antibody Technique, Indirect</subject><subject>Humans</subject><subject>Membrane Potentials</subject><subject>Microscopy, Confocal</subject><subject>Microscopy, Electron</subject><subject>Neuroblastoma - pathology</subject><subject>Neuroectodermal Tumors, Primitive - pathology</subject><subject>Regular</subject><subject>Sarcoma, Ewing - pathology</subject><subject>Tacrolimus - pharmacology</subject><subject>Tumor Cells, Cultured</subject><issn>0002-9440</issn><issn>1525-2191</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</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>eNqFkUFv1DAQhS0EKkvhJ1SyOFA4BGwncewLqFq2tFIlkFrOltdxEq8SO9hJV_33zHZXq8KlF1v2fG_0Zh5CZ5R8poTyL7eEEJbJoiAfKfnEy4pUGXmBFrRkZcaopC_R4oi8Rm9S2sCT54KcoBMpCi5FvkDtyre6tYP1Ew4NXn6XEl_7ejY24YsxjFNILuG7Loa57bDGS90b5-0cnc-As6OFA7S_9NRt9QN2Hq-2zrfnCd_qaMIAEtv36S161eg-2XeH-xT9vlzdLa-ym58_rpcXN5kpRTVljaQ1N5wIw8Va6oZymXPODJNE8JpQmKCwYL0WtG4YqdZFuS6YtqKWOclJkZ-ir_u-47webG3AW9S9GqMbdHxQQTv1b8W7TrXhXlHBec4oNPhwaBDDn9mmSQ0uGRhBexvmpCowUYBBAN__B27CHD0MpxgVsFzJJEDlHjIxpBRtc3RCidrFqB5jVLuMdl-PMSoCurOnYxxVh9ygfr6vd67tti5alQbd90BTpTcjLXPFFZV5BeS3PWlh6_fORpWMs97YGlRmUnVwz3j5C3NxuQ4</recordid><startdate>19981201</startdate><enddate>19981201</enddate><creator>Sohn, Hae Won</creator><creator>Choi, Eun Young</creator><creator>Kim, Soon Ha</creator><creator>Lee, Im-soon</creator><creator>Chung, Doo Hyun</creator><creator>Sung, Uhn A</creator><creator>Hwang, Duck Ho</creator><creator>Cho, Sa Sun</creator><creator>Jun, Byung Hoon</creator><creator>Jang, Ja June</creator><creator>Chi, Je Geun</creator><creator>Park, Seong Hoe</creator><general>Elsevier Inc</general><general>ASIP</general><general>American Society for Investigative Pathology</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19981201</creationdate><title>Engagement of CD99 Induces Apoptosis Through a Calcineurin-Independent Pathway in Ewing's Sarcoma Cells</title><author>Sohn, Hae Won ; Choi, Eun Young ; Kim, Soon Ha ; Lee, Im-soon ; Chung, Doo Hyun ; Sung, Uhn A ; Hwang, Duck Ho ; Cho, Sa Sun ; Jun, Byung Hoon ; Jang, Ja June ; Chi, Je Geun ; Park, Seong Hoe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c587t-f91d6c608c68b9af1693662c29086d010004e469d81df207b45b42ae8d9303043</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>12E7 Antigen</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Antigens, CD - immunology</topic><topic>Antigens, CD - physiology</topic><topic>Apoptosis</topic><topic>Calcineurin</topic><topic>Calcium - physiology</topic><topic>Caspase Inhibitors</topic><topic>Caspases - physiology</topic><topic>Cell Adhesion Molecules - immunology</topic><topic>Cell Adhesion Molecules - physiology</topic><topic>Cell Differentiation</topic><topic>Cyclosporine - pharmacology</topic><topic>Dactinomycin - pharmacology</topic><topic>Fluorescent Antibody Technique, Indirect</topic><topic>Humans</topic><topic>Membrane Potentials</topic><topic>Microscopy, Confocal</topic><topic>Microscopy, Electron</topic><topic>Neuroblastoma - pathology</topic><topic>Neuroectodermal Tumors, Primitive - pathology</topic><topic>Regular</topic><topic>Sarcoma, Ewing - pathology</topic><topic>Tacrolimus - pharmacology</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sohn, Hae Won</creatorcontrib><creatorcontrib>Choi, Eun Young</creatorcontrib><creatorcontrib>Kim, Soon Ha</creatorcontrib><creatorcontrib>Lee, Im-soon</creatorcontrib><creatorcontrib>Chung, Doo Hyun</creatorcontrib><creatorcontrib>Sung, Uhn A</creatorcontrib><creatorcontrib>Hwang, Duck Ho</creatorcontrib><creatorcontrib>Cho, Sa Sun</creatorcontrib><creatorcontrib>Jun, Byung Hoon</creatorcontrib><creatorcontrib>Jang, Ja June</creatorcontrib><creatorcontrib>Chi, Je Geun</creatorcontrib><creatorcontrib>Park, Seong Hoe</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>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Public Health Database</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>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>Science 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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The American journal of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sohn, Hae Won</au><au>Choi, Eun Young</au><au>Kim, Soon Ha</au><au>Lee, Im-soon</au><au>Chung, Doo Hyun</au><au>Sung, Uhn A</au><au>Hwang, Duck Ho</au><au>Cho, Sa Sun</au><au>Jun, Byung Hoon</au><au>Jang, Ja June</au><au>Chi, Je Geun</au><au>Park, Seong Hoe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Engagement of CD99 Induces Apoptosis Through a Calcineurin-Independent Pathway in Ewing's Sarcoma Cells</atitle><jtitle>The American journal of pathology</jtitle><addtitle>Am J Pathol</addtitle><date>1998-12-01</date><risdate>1998</risdate><volume>153</volume><issue>6</issue><spage>1937</spage><epage>1945</epage><pages>1937-1945</pages><issn>0002-9440</issn><eissn>1525-2191</eissn><coden>AJPAA4</coden><abstract>Programmed cell death (PCD) is a prominent feature of the development of the immune and nervous systems. In both systems, widespread PCD occurs in primitive progenitor cells during development. In this study, we demonstrated that Ewing's sarcoma (ES) cells, undifferentiated neural precursors, underwent apoptosis upon engagement of CD99 with anti-CD99 monoclonal antibody. Apoptosis via CD99 occurred only in the undifferentiated state of ES cells, but not in differentiated ES cells. CD99-induced apoptosis in ES cells appeared to require
de novo synthesis of RNA and protein as well as caspase activation. Cyclosporin A, known to be a potent inhibitor of both calcineurin activation and mitochondrial permeability transition pore opening, inhibited CD99-mediated apoptosis, whereas FK-506, a specific calcineurin inhibitor, did not, indicating the induction of CD99-mediated apoptosis through a calcineurin-independent pathway. Furthermore, the dying cells displayed the reduction of mitochondrial transmembrane potential (ΔΨm). These results suggest that CD99 engagement induce CsA-inhibitable mitochondrial permeability transition pore opening, followed by a reduction of ΔΨm and caspase activation, thereby leading to apoptosis. Based on these results, we suggest the possible involvement of CD99 in the apoptotic processes that occur during nervous system development and also its application in immunotherapeutic trials for ES cases.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>9846983</pmid><doi>10.1016/S0002-9440(10)65707-0</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 12E7 Antigen Antibodies, Monoclonal - pharmacology Antigens, CD - immunology Antigens, CD - physiology Apoptosis Calcineurin Calcium - physiology Caspase Inhibitors Caspases - physiology Cell Adhesion Molecules - immunology Cell Adhesion Molecules - physiology Cell Differentiation Cyclosporine - pharmacology Dactinomycin - pharmacology Fluorescent Antibody Technique, Indirect Humans Membrane Potentials Microscopy, Confocal Microscopy, Electron Neuroblastoma - pathology Neuroectodermal Tumors, Primitive - pathology Regular Sarcoma, Ewing - pathology Tacrolimus - pharmacology Tumor Cells, Cultured |
| title | Engagement of CD99 Induces Apoptosis Through a Calcineurin-Independent Pathway in Ewing's Sarcoma Cells |
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