Regulation of TNFR1 and CD95 signalling by receptor compartmentalization
Tumour-necrosis factor receptor-1 (TNFR1) and CD95 can transduce pro-apoptotic and anti-apoptotic signals, but what determines the specificity of signalling events? It is possible that the endosomal compartment functions as a signalling organelle that selectively transmits death signals from TNFR1 a...
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| Veröffentlicht in: | Nature reviews. Molecular cell biology 2008-08, Vol.9 (8), p.655-662 |
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| creator | Schütze, Stefan Tchikov, Vladimir Schneider-Brachert, Wulf |
| description | Tumour-necrosis factor receptor-1 (TNFR1) and CD95 can transduce pro-apoptotic and anti-apoptotic signals, but what determines the specificity of signalling events? It is possible that the endosomal compartment functions as a signalling organelle that selectively transmits death signals from TNFR1 and CD95.
The death receptors tumour-necrosis factor receptor-1 (TNFR1) and CD95 (also known as FAS and APO-1) transduce signals that promote cell death by apoptosis. However, these receptors are also capable of inducing anti-apoptotic signals through the activation of the transcription factor nuclear factor-κB (NF-κB) or through activation of the proliferative mitogen-activated protein kinase (MAPK) cascade. Recent findings reveal a role for receptor internalization and endosomal trafficking in selectively transmitting the signals that lead either to apoptosis or to the survival of the cell. |
| doi_str_mv | 10.1038/nrm2430 |
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The death receptors tumour-necrosis factor receptor-1 (TNFR1) and CD95 (also known as FAS and APO-1) transduce signals that promote cell death by apoptosis. However, these receptors are also capable of inducing anti-apoptotic signals through the activation of the transcription factor nuclear factor-κB (NF-κB) or through activation of the proliferative mitogen-activated protein kinase (MAPK) cascade. Recent findings reveal a role for receptor internalization and endosomal trafficking in selectively transmitting the signals that lead either to apoptosis or to the survival of the cell.</description><identifier>ISSN: 1471-0072</identifier><identifier>EISSN: 1471-0080</identifier><identifier>DOI: 10.1038/nrm2430</identifier><identifier>PMID: 18545270</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Animals ; Apoptosis ; Apoptosis - physiology ; Biochemistry ; Biomedical and Life Sciences ; Cancer Research ; Cell Biology ; Cell Compartmentation - physiology ; Cell death ; Cell receptors ; Cellular signal transduction ; Developmental Biology ; Endocytosis ; fas Receptor - metabolism ; fas Receptor - physiology ; Growth factors ; Humans ; Kinases ; Life Sciences ; Ligands ; Models, Biological ; Mortality ; opinion-2 ; Physiological aspects ; Protein Transport - physiology ; Proteins ; Receptors, Tumor Necrosis Factor, Type I - metabolism ; Receptors, Tumor Necrosis Factor, Type I - physiology ; Signal transduction ; Signal Transduction - physiology ; Stem Cells ; Transcription factors</subject><ispartof>Nature reviews. Molecular cell biology, 2008-08, Vol.9 (8), p.655-662</ispartof><rights>Springer Nature Limited 2008</rights><rights>COPYRIGHT 2008 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Aug 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c440t-93dff82dce9839f54b3cc66a7e4147529084a3a380a2b4f93a6509839d1b6db73</citedby><cites>FETCH-LOGICAL-c440t-93dff82dce9839f54b3cc66a7e4147529084a3a380a2b4f93a6509839d1b6db73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nrm2430$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nrm2430$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18545270$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schütze, Stefan</creatorcontrib><creatorcontrib>Tchikov, Vladimir</creatorcontrib><creatorcontrib>Schneider-Brachert, Wulf</creatorcontrib><title>Regulation of TNFR1 and CD95 signalling by receptor compartmentalization</title><title>Nature reviews. Molecular cell biology</title><addtitle>Nat Rev Mol Cell Biol</addtitle><addtitle>Nat Rev Mol Cell Biol</addtitle><description>Tumour-necrosis factor receptor-1 (TNFR1) and CD95 can transduce pro-apoptotic and anti-apoptotic signals, but what determines the specificity of signalling events? It is possible that the endosomal compartment functions as a signalling organelle that selectively transmits death signals from TNFR1 and CD95.
The death receptors tumour-necrosis factor receptor-1 (TNFR1) and CD95 (also known as FAS and APO-1) transduce signals that promote cell death by apoptosis. However, these receptors are also capable of inducing anti-apoptotic signals through the activation of the transcription factor nuclear factor-κB (NF-κB) or through activation of the proliferative mitogen-activated protein kinase (MAPK) cascade. Recent findings reveal a role for receptor internalization and endosomal trafficking in selectively transmitting the signals that lead either to apoptosis or to the survival of the cell.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer Research</subject><subject>Cell Biology</subject><subject>Cell Compartmentation - physiology</subject><subject>Cell death</subject><subject>Cell receptors</subject><subject>Cellular signal transduction</subject><subject>Developmental Biology</subject><subject>Endocytosis</subject><subject>fas Receptor - metabolism</subject><subject>fas Receptor - physiology</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Ligands</subject><subject>Models, Biological</subject><subject>Mortality</subject><subject>opinion-2</subject><subject>Physiological aspects</subject><subject>Protein Transport - physiology</subject><subject>Proteins</subject><subject>Receptors, Tumor Necrosis Factor, Type I - metabolism</subject><subject>Receptors, Tumor Necrosis Factor, Type I - physiology</subject><subject>Signal transduction</subject><subject>Signal Transduction - physiology</subject><subject>Stem Cells</subject><subject>Transcription factors</subject><issn>1471-0072</issn><issn>1471-0080</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpt0V1LHDEUBuAgFrUq_QdlsFDrxdp8z-RStloFUdjqdchkkiEyk2yTDNT--mbdpbIiuUhInveQwwHgE4LnCJLmu48jpgTugANEazSDsIG7_8813gcfU3qCEHFUsz2wjxpGGa7hAbhemH4aVHbBV8FWD3dXC1Qp31XzH4JVyfVeDYPzfdU-V9Fos8whVjqMSxXzaHxWg_v7kj4CH6wakjne7Ifg8eryYX49u73_eTO_uJ1pSmGeCdJZ2-BOG9EQYRltidacq9rQ8luGBWyoIoo0UOGWWkEUZ3BFO9Tyrq3JIfi6rruM4fdkUpajS9oMg_ImTElyQUpYoAJP3sCnMMXSTpIYU84xw6ygL2vUq8FI523IUelVRXmBBKai4YgXdf6OKqszo9PBG-vK_VbgbCtQTDZ_cq-mlOTNr8W2PV1bHUNK0Vi5jG5U8VkiKFfDlZvhFvl509HUjqZ7dZtpFvBtDVJ58r2Jry2_rfUP20-oNw</recordid><startdate>20080801</startdate><enddate>20080801</enddate><creator>Schütze, Stefan</creator><creator>Tchikov, Vladimir</creator><creator>Schneider-Brachert, Wulf</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>ISR</scope><scope>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7RV</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PCBAR</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20080801</creationdate><title>Regulation of TNFR1 and CD95 signalling by receptor compartmentalization</title><author>Schütze, Stefan ; Tchikov, Vladimir ; Schneider-Brachert, Wulf</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c440t-93dff82dce9839f54b3cc66a7e4147529084a3a380a2b4f93a6509839d1b6db73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - physiology</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cancer Research</topic><topic>Cell Biology</topic><topic>Cell Compartmentation - physiology</topic><topic>Cell death</topic><topic>Cell receptors</topic><topic>Cellular signal transduction</topic><topic>Developmental Biology</topic><topic>Endocytosis</topic><topic>fas Receptor - metabolism</topic><topic>fas Receptor - physiology</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>Ligands</topic><topic>Models, Biological</topic><topic>Mortality</topic><topic>opinion-2</topic><topic>Physiological aspects</topic><topic>Protein Transport - physiology</topic><topic>Proteins</topic><topic>Receptors, Tumor Necrosis Factor, Type I - metabolism</topic><topic>Receptors, Tumor Necrosis Factor, Type I - physiology</topic><topic>Signal transduction</topic><topic>Signal Transduction - physiology</topic><topic>Stem Cells</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schütze, Stefan</creatorcontrib><creatorcontrib>Tchikov, Vladimir</creatorcontrib><creatorcontrib>Schneider-Brachert, Wulf</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research 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 One Sustainability</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>Earth, Atmospheric & Aquatic Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Earth, Atmospheric & Aquatic 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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Nature reviews. Molecular cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schütze, Stefan</au><au>Tchikov, Vladimir</au><au>Schneider-Brachert, Wulf</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of TNFR1 and CD95 signalling by receptor compartmentalization</atitle><jtitle>Nature reviews. Molecular cell biology</jtitle><stitle>Nat Rev Mol Cell Biol</stitle><addtitle>Nat Rev Mol Cell Biol</addtitle><date>2008-08-01</date><risdate>2008</risdate><volume>9</volume><issue>8</issue><spage>655</spage><epage>662</epage><pages>655-662</pages><issn>1471-0072</issn><eissn>1471-0080</eissn><abstract>Tumour-necrosis factor receptor-1 (TNFR1) and CD95 can transduce pro-apoptotic and anti-apoptotic signals, but what determines the specificity of signalling events? It is possible that the endosomal compartment functions as a signalling organelle that selectively transmits death signals from TNFR1 and CD95.
The death receptors tumour-necrosis factor receptor-1 (TNFR1) and CD95 (also known as FAS and APO-1) transduce signals that promote cell death by apoptosis. However, these receptors are also capable of inducing anti-apoptotic signals through the activation of the transcription factor nuclear factor-κB (NF-κB) or through activation of the proliferative mitogen-activated protein kinase (MAPK) cascade. Recent findings reveal a role for receptor internalization and endosomal trafficking in selectively transmitting the signals that lead either to apoptosis or to the survival of the cell.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>18545270</pmid><doi>10.1038/nrm2430</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Apoptosis Apoptosis - physiology Biochemistry Biomedical and Life Sciences Cancer Research Cell Biology Cell Compartmentation - physiology Cell death Cell receptors Cellular signal transduction Developmental Biology Endocytosis fas Receptor - metabolism fas Receptor - physiology Growth factors Humans Kinases Life Sciences Ligands Models, Biological Mortality opinion-2 Physiological aspects Protein Transport - physiology Proteins Receptors, Tumor Necrosis Factor, Type I - metabolism Receptors, Tumor Necrosis Factor, Type I - physiology Signal transduction Signal Transduction - physiology Stem Cells Transcription factors |
| title | Regulation of TNFR1 and CD95 signalling by receptor compartmentalization |
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