TMBIM protein family: ancestral regulators of cell death

The control of apoptosis in mammals has been historically associated with the activity of the BCL-2 family of proteins at the mitochondria. In the past years, a novel group of cell death regulators have emerged, known as the Transmembrane BAX Inhibitor-1 Motif-containing (TMBIM) protein family. This...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Oncogene 2015-01, Vol.34 (3), p.269-280
Hauptverfasser: Rojas-Rivera, D, Hetz, C
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 280
container_issue 3
container_start_page 269
container_title Oncogene
container_volume 34
creator Rojas-Rivera, D
Hetz, C
description The control of apoptosis in mammals has been historically associated with the activity of the BCL-2 family of proteins at the mitochondria. In the past years, a novel group of cell death regulators have emerged, known as the Transmembrane BAX Inhibitor-1 Motif-containing (TMBIM) protein family. This group of proteins is composed of at least six highly conserved members expressed in mammals, with homologs in insects, fish, plants, viruses and yeast. Different studies indicate that all TMBIM family members have inhibitory activities in different setting of apoptosis. Here, we overview and integrate possible mechanisms underlying the impact of the TMBIM protein family in the regulation of cell death, which include activities at diverse subcellular compartments, including death receptor regulation, modulation of endoplasmic reticulum (ER) calcium homeostasis, ER stress signaling, autophagy, reactive oxygen species production, among other effects. The possible intersection between the BCL-2 and TMBIM family in the control of cell death is also discussed, in addition to their implication in the progression of cancer.
doi_str_mv 10.1038/onc.2014.6
format Article
fullrecord <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1664209350</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A488535790</galeid><sourcerecordid>A488535790</sourcerecordid><originalsourceid>FETCH-LOGICAL-c651t-4fd94cdd5c3c53d41a7cc7d8892c7465a5eda2710720d9ac288965bccbb434733</originalsourceid><addsrcrecordid>eNqNkUtLAzEUhYMotlY3_gAZcCPK1Lwz406LL2hxU9chTTJ1ysykJjML_70prVIfiGQRyP3uybn3AHCM4BBBkl26Rg8xRHTId0AfUcFTxnK6C_owZzDNMcE9cBDCAkIocoj3QQ9TxhHDWR9k08nN4yRZetfaskkKVZfV21WiGm1D61WVeDvvKtU6HxJXJNpWVWKsal8OwV6hqmCPNvcAPN_dTkcP6fjp_nF0PU41Z6hNaWFyqo1hmmhGDEVKaC1MluVYC8qZYtYoLBAUGJpcaRwrnM20ns0ooYKQAThb60aLr100JesyrGyoxrouSMQ5xTAnDP4HhZRSQnBET7-hC9f5Jg4iMSGIExJl_6IQp4wJgfAWNVeVlWVTuLg4vfpaXtMsY4TFrUdq-AsVj7F1qV1jizK-f2k4Xzdo70LwtpBLX9bKv0kE5Sp3GXOXq9wlj_DJxmk3q635RD-CjsDFGgix1Myt3xrlp9w7hNmxkw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1645577124</pqid></control><display><type>article</type><title>TMBIM protein family: ancestral regulators of cell death</title><source>MEDLINE</source><source>SpringerLink Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Nature Journals Online</source><creator>Rojas-Rivera, D ; Hetz, C</creator><creatorcontrib>Rojas-Rivera, D ; Hetz, C</creatorcontrib><description>The control of apoptosis in mammals has been historically associated with the activity of the BCL-2 family of proteins at the mitochondria. In the past years, a novel group of cell death regulators have emerged, known as the Transmembrane BAX Inhibitor-1 Motif-containing (TMBIM) protein family. This group of proteins is composed of at least six highly conserved members expressed in mammals, with homologs in insects, fish, plants, viruses and yeast. Different studies indicate that all TMBIM family members have inhibitory activities in different setting of apoptosis. Here, we overview and integrate possible mechanisms underlying the impact of the TMBIM protein family in the regulation of cell death, which include activities at diverse subcellular compartments, including death receptor regulation, modulation of endoplasmic reticulum (ER) calcium homeostasis, ER stress signaling, autophagy, reactive oxygen species production, among other effects. The possible intersection between the BCL-2 and TMBIM family in the control of cell death is also discussed, in addition to their implication in the progression of cancer.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2014.6</identifier><identifier>PMID: 24561528</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/45/612/1237 ; 631/67/395 ; 631/80/82/23 ; 692/699/67 ; Animals ; Apoptosis ; Apoptosis - genetics ; Apoptosis Regulatory Proteins - genetics ; Apoptosis Regulatory Proteins - metabolism ; Autophagy ; BAX protein ; Bcl-2 protein ; Calcium (reticular) ; Calcium homeostasis ; Calcium signalling ; Cancer ; Carcinogenesis ; Cell Biology ; Cell death ; Cellular signal transduction ; Endoplasmic reticulum ; Endoplasmic Reticulum Stress - genetics ; Genetic aspects ; Health aspects ; Homeostasis ; Human Genetics ; Humans ; Internal Medicine ; Medicine ; Medicine &amp; Public Health ; Membrane proteins ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mitochondria ; Models, Genetic ; Multigene Family ; Neoplasms - genetics ; Oncology ; Pathology ; Phagocytosis ; Protein expression ; Proteins ; Reactive oxygen species ; Regulation ; review ; Signal Transduction - genetics</subject><ispartof>Oncogene, 2015-01, Vol.34 (3), p.269-280</ispartof><rights>Macmillan Publishers Limited 2015</rights><rights>COPYRIGHT 2015 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 15, 2015</rights><rights>Macmillan Publishers Limited 2015.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c651t-4fd94cdd5c3c53d41a7cc7d8892c7465a5eda2710720d9ac288965bccbb434733</citedby><cites>FETCH-LOGICAL-c651t-4fd94cdd5c3c53d41a7cc7d8892c7465a5eda2710720d9ac288965bccbb434733</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/onc.2014.6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2014.6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24561528$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rojas-Rivera, D</creatorcontrib><creatorcontrib>Hetz, C</creatorcontrib><title>TMBIM protein family: ancestral regulators of cell death</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>The control of apoptosis in mammals has been historically associated with the activity of the BCL-2 family of proteins at the mitochondria. In the past years, a novel group of cell death regulators have emerged, known as the Transmembrane BAX Inhibitor-1 Motif-containing (TMBIM) protein family. This group of proteins is composed of at least six highly conserved members expressed in mammals, with homologs in insects, fish, plants, viruses and yeast. Different studies indicate that all TMBIM family members have inhibitory activities in different setting of apoptosis. Here, we overview and integrate possible mechanisms underlying the impact of the TMBIM protein family in the regulation of cell death, which include activities at diverse subcellular compartments, including death receptor regulation, modulation of endoplasmic reticulum (ER) calcium homeostasis, ER stress signaling, autophagy, reactive oxygen species production, among other effects. The possible intersection between the BCL-2 and TMBIM family in the control of cell death is also discussed, in addition to their implication in the progression of cancer.</description><subject>631/45/612/1237</subject><subject>631/67/395</subject><subject>631/80/82/23</subject><subject>692/699/67</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Autophagy</subject><subject>BAX protein</subject><subject>Bcl-2 protein</subject><subject>Calcium (reticular)</subject><subject>Calcium homeostasis</subject><subject>Calcium signalling</subject><subject>Cancer</subject><subject>Carcinogenesis</subject><subject>Cell Biology</subject><subject>Cell death</subject><subject>Cellular signal transduction</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum Stress - genetics</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Homeostasis</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medicine</subject><subject>Medicine &amp; Public Health</subject><subject>Membrane proteins</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mitochondria</subject><subject>Models, Genetic</subject><subject>Multigene Family</subject><subject>Neoplasms - genetics</subject><subject>Oncology</subject><subject>Pathology</subject><subject>Phagocytosis</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Regulation</subject><subject>review</subject><subject>Signal Transduction - genetics</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkUtLAzEUhYMotlY3_gAZcCPK1Lwz406LL2hxU9chTTJ1ysykJjML_70prVIfiGQRyP3uybn3AHCM4BBBkl26Rg8xRHTId0AfUcFTxnK6C_owZzDNMcE9cBDCAkIocoj3QQ9TxhHDWR9k08nN4yRZetfaskkKVZfV21WiGm1D61WVeDvvKtU6HxJXJNpWVWKsal8OwV6hqmCPNvcAPN_dTkcP6fjp_nF0PU41Z6hNaWFyqo1hmmhGDEVKaC1MluVYC8qZYtYoLBAUGJpcaRwrnM20ns0ooYKQAThb60aLr100JesyrGyoxrouSMQ5xTAnDP4HhZRSQnBET7-hC9f5Jg4iMSGIExJl_6IQp4wJgfAWNVeVlWVTuLg4vfpaXtMsY4TFrUdq-AsVj7F1qV1jizK-f2k4Xzdo70LwtpBLX9bKv0kE5Sp3GXOXq9wlj_DJxmk3q635RD-CjsDFGgix1Myt3xrlp9w7hNmxkw</recordid><startdate>20150115</startdate><enddate>20150115</enddate><creator>Rojas-Rivera, D</creator><creator>Hetz, C</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>3V.</scope><scope>7TM</scope><scope>7TO</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>8G5</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20150115</creationdate><title>TMBIM protein family: ancestral regulators of cell death</title><author>Rojas-Rivera, D ; Hetz, C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c651t-4fd94cdd5c3c53d41a7cc7d8892c7465a5eda2710720d9ac288965bccbb434733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>631/45/612/1237</topic><topic>631/67/395</topic><topic>631/80/82/23</topic><topic>692/699/67</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Autophagy</topic><topic>BAX protein</topic><topic>Bcl-2 protein</topic><topic>Calcium (reticular)</topic><topic>Calcium homeostasis</topic><topic>Calcium signalling</topic><topic>Cancer</topic><topic>Carcinogenesis</topic><topic>Cell Biology</topic><topic>Cell death</topic><topic>Cellular signal transduction</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum Stress - genetics</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Homeostasis</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Medicine</topic><topic>Medicine &amp; Public Health</topic><topic>Membrane proteins</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mitochondria</topic><topic>Models, Genetic</topic><topic>Multigene Family</topic><topic>Neoplasms - genetics</topic><topic>Oncology</topic><topic>Pathology</topic><topic>Phagocytosis</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>Regulation</topic><topic>review</topic><topic>Signal Transduction - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rojas-Rivera, D</creatorcontrib><creatorcontrib>Hetz, C</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>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health &amp; 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>Research Library (Alumni Edition)</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>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rojas-Rivera, D</au><au>Hetz, C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TMBIM protein family: ancestral regulators of cell death</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2015-01-15</date><risdate>2015</risdate><volume>34</volume><issue>3</issue><spage>269</spage><epage>280</epage><pages>269-280</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>The control of apoptosis in mammals has been historically associated with the activity of the BCL-2 family of proteins at the mitochondria. In the past years, a novel group of cell death regulators have emerged, known as the Transmembrane BAX Inhibitor-1 Motif-containing (TMBIM) protein family. This group of proteins is composed of at least six highly conserved members expressed in mammals, with homologs in insects, fish, plants, viruses and yeast. Different studies indicate that all TMBIM family members have inhibitory activities in different setting of apoptosis. Here, we overview and integrate possible mechanisms underlying the impact of the TMBIM protein family in the regulation of cell death, which include activities at diverse subcellular compartments, including death receptor regulation, modulation of endoplasmic reticulum (ER) calcium homeostasis, ER stress signaling, autophagy, reactive oxygen species production, among other effects. The possible intersection between the BCL-2 and TMBIM family in the control of cell death is also discussed, in addition to their implication in the progression of cancer.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24561528</pmid><doi>10.1038/onc.2014.6</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0950-9232
ispartof Oncogene, 2015-01, Vol.34 (3), p.269-280
issn 0950-9232
1476-5594
language eng
recordid cdi_proquest_miscellaneous_1664209350
source MEDLINE; SpringerLink Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Nature Journals Online
subjects 631/45/612/1237
631/67/395
631/80/82/23
692/699/67
Animals
Apoptosis
Apoptosis - genetics
Apoptosis Regulatory Proteins - genetics
Apoptosis Regulatory Proteins - metabolism
Autophagy
BAX protein
Bcl-2 protein
Calcium (reticular)
Calcium homeostasis
Calcium signalling
Cancer
Carcinogenesis
Cell Biology
Cell death
Cellular signal transduction
Endoplasmic reticulum
Endoplasmic Reticulum Stress - genetics
Genetic aspects
Health aspects
Homeostasis
Human Genetics
Humans
Internal Medicine
Medicine
Medicine & Public Health
Membrane proteins
Membrane Proteins - genetics
Membrane Proteins - metabolism
Mitochondria
Models, Genetic
Multigene Family
Neoplasms - genetics
Oncology
Pathology
Phagocytosis
Protein expression
Proteins
Reactive oxygen species
Regulation
review
Signal Transduction - genetics
title TMBIM protein family: ancestral regulators of cell death
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-19T16%3A24%3A08IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=TMBIM%20protein%20family:%20ancestral%20regulators%20of%20cell%20death&rft.jtitle=Oncogene&rft.au=Rojas-Rivera,%20D&rft.date=2015-01-15&rft.volume=34&rft.issue=3&rft.spage=269&rft.epage=280&rft.pages=269-280&rft.issn=0950-9232&rft.eissn=1476-5594&rft.coden=ONCNES&rft_id=info:doi/10.1038/onc.2014.6&rft_dat=%3Cgale_proqu%3EA488535790%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1645577124&rft_id=info:pmid/24561528&rft_galeid=A488535790&rfr_iscdi=true