Tumour-suppression activity of the proapoptotic regulator Par4
The proapoptotic protein encoded by Par4 (prostate apoptosis response 4) has been implicated in tumour suppression, particularly in the prostate. We report here that Par4 ‐null mice are prone to develop tumours, both spontaneously and on carcinogenic treatment. The endometrium and prostate of Par4 ‐...
Gespeichert in:
| Veröffentlicht in: | EMBO reports 2005-06, Vol.6 (6), p.577-583 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 583 |
|---|---|
| container_issue | 6 |
| container_start_page | 577 |
| container_title | EMBO reports |
| container_volume | 6 |
| creator | García-Cao, Isabel Duran, Angeles Collado, Manuel Carrascosa, Maria J Martín-Caballero, Juan Flores, Juana M Diaz-Meco, Maria T Moscat, Jorge Serrano, Manuel |
| description | The proapoptotic protein encoded by
Par4
(prostate apoptosis response 4) has been implicated in tumour suppression, particularly in the prostate. We report here that
Par4
‐null mice are prone to develop tumours, both spontaneously and on carcinogenic treatment. The endometrium and prostate of
Par4
‐null mice were particularly sensitive to the development of proliferative lesions. Most (80%)
Par4
‐null females presented endometrial hyperplasia by 9 months of age, and a significant proportion (36%) developed endometrial adenocarcinomas after 1 year of age. Similarly,
Par4
‐null males showed a high incidence of prostate hyperplasia and prostatic intraepithelial neoplasias, and were extraordinarily sensitive to testosterone‐induced prostate hyperplasia. Finally, the uterus and prostate of young
Par4
‐null mice have increased levels of the apoptosis inhibitor XIAP (X‐chromosome‐linked inhibitor of apoptosis), supporting the previously proposed function of Par4 as an inhibitor of the ζPKC (atypical protein kinase)–NF‐κB (nuclear factor‐κB)–XIAP pathway. These data show that Par4 has an important role in tumour suppression, with a particular relevance in the endometrium and prostate. |
| doi_str_mv | 10.1038/sj.embor.7400421 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1369092</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>969884791</sourcerecordid><originalsourceid>FETCH-LOGICAL-c6041-2908f7f7a964e53901280864214d83531aa15c15a7d36b474e6f21bfb4c74c863</originalsourceid><addsrcrecordid>eNqFUctu1DAUtRCIlsKeDShiwS6Dr-34sakEVVuQyqsqKurGcjLO1EMSB9tpmb8nJdEMsIDVtXQe91wfhJ4CXgCm8lVcL2xb-rAQDGNG4B7aB8ZVTkHI-_ObEPi6hx7FuMYYF0rIh2gPCikEFmofHV4MrR9CHoe-DzZG57vMVMnduLTJfJ2la5v1wZve98knV2XBrobGJB-yTyawx-hBbZpon8zzAH05Ob44epuffTx9d_T6LK84ZpAThWUtamEUZ7agCgORWPIxMVtKWlAwBooKCiOWlJdMMMtrAmVdskqwSnJ6gA4n334oW7usbJeCaXQfXGvCRnvj9J9I5671yt9ooFxhRUaDl7NB8N8HG5NuXaxs05jO-iFqUJxIxulIfPEXcT3-TzcepwmWBRnD3ZHwRKqCjzHYepsEsL5rRse1_tWMnpsZJc9_v2AnmKsYCWoi3LrGbv5rqI_fvznfmcOkjaOsW9mwC_2PQM8mTWfSEOx24Q7PJ9zFZH9sYRO-aS6oKPTlh1N9xdjnKzgHfUl_Ak6RxsU</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>208524743</pqid></control><display><type>article</type><title>Tumour-suppression activity of the proapoptotic regulator Par4</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Wiley Free Content</source><source>PubMed Central</source><creator>García-Cao, Isabel ; Duran, Angeles ; Collado, Manuel ; Carrascosa, Maria J ; Martín-Caballero, Juan ; Flores, Juana M ; Diaz-Meco, Maria T ; Moscat, Jorge ; Serrano, Manuel</creator><creatorcontrib>García-Cao, Isabel ; Duran, Angeles ; Collado, Manuel ; Carrascosa, Maria J ; Martín-Caballero, Juan ; Flores, Juana M ; Diaz-Meco, Maria T ; Moscat, Jorge ; Serrano, Manuel</creatorcontrib><description>The proapoptotic protein encoded by
Par4
(prostate apoptosis response 4) has been implicated in tumour suppression, particularly in the prostate. We report here that
Par4
‐null mice are prone to develop tumours, both spontaneously and on carcinogenic treatment. The endometrium and prostate of
Par4
‐null mice were particularly sensitive to the development of proliferative lesions. Most (80%)
Par4
‐null females presented endometrial hyperplasia by 9 months of age, and a significant proportion (36%) developed endometrial adenocarcinomas after 1 year of age. Similarly,
Par4
‐null males showed a high incidence of prostate hyperplasia and prostatic intraepithelial neoplasias, and were extraordinarily sensitive to testosterone‐induced prostate hyperplasia. Finally, the uterus and prostate of young
Par4
‐null mice have increased levels of the apoptosis inhibitor XIAP (X‐chromosome‐linked inhibitor of apoptosis), supporting the previously proposed function of Par4 as an inhibitor of the ζPKC (atypical protein kinase)–NF‐κB (nuclear factor‐κB)–XIAP pathway. These data show that Par4 has an important role in tumour suppression, with a particular relevance in the endometrium and prostate.</description><identifier>ISSN: 1469-221X</identifier><identifier>EISSN: 1469-3178</identifier><identifier>EISSN: 1469-221X</identifier><identifier>DOI: 10.1038/sj.embor.7400421</identifier><identifier>PMID: 15877079</identifier><identifier>CODEN: ERMEAX</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Age Factors ; Animals ; apoptosis ; Apoptosis - physiology ; Butylhydroxybutylnitrosamine - toxicity ; Endometrial Neoplasms - chemically induced ; Endometrial Neoplasms - metabolism ; endometrium ; Estradiol - toxicity ; Female ; Histological Techniques ; Immunoblotting ; Lesions ; Male ; Mice ; Mice, Mutant Strains ; Par4 ; Phenotype ; prostate ; Prostatic Neoplasms - chemically induced ; Prostatic Neoplasms - metabolism ; protein kinase C ; Proteins - metabolism ; Receptors, Thrombin - metabolism ; Scientific Report ; Testosterone - toxicity ; Tumors ; tumour suppression ; Urinary Bladder Neoplasms - chemically induced ; Urinary Bladder Neoplasms - metabolism ; X-Linked Inhibitor of Apoptosis Protein</subject><ispartof>EMBO reports, 2005-06, Vol.6 (6), p.577-583</ispartof><rights>European Molecular Biology Organization 2005</rights><rights>Copyright © 2005 European Molecular Biology Organization</rights><rights>Copyright Nature Publishing Group Jun 2005</rights><rights>Copyright © 2005, European Molecular Biology Organization 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6041-2908f7f7a964e53901280864214d83531aa15c15a7d36b474e6f21bfb4c74c863</citedby><cites>FETCH-LOGICAL-c6041-2908f7f7a964e53901280864214d83531aa15c15a7d36b474e6f21bfb4c74c863</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/PMC1369092/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1369092/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,725,778,782,883,1414,1430,27911,27912,45561,45562,46396,46820,53778,53780</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15877079$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>García-Cao, Isabel</creatorcontrib><creatorcontrib>Duran, Angeles</creatorcontrib><creatorcontrib>Collado, Manuel</creatorcontrib><creatorcontrib>Carrascosa, Maria J</creatorcontrib><creatorcontrib>Martín-Caballero, Juan</creatorcontrib><creatorcontrib>Flores, Juana M</creatorcontrib><creatorcontrib>Diaz-Meco, Maria T</creatorcontrib><creatorcontrib>Moscat, Jorge</creatorcontrib><creatorcontrib>Serrano, Manuel</creatorcontrib><title>Tumour-suppression activity of the proapoptotic regulator Par4</title><title>EMBO reports</title><addtitle>EMBO Rep</addtitle><addtitle>EMBO Rep</addtitle><description>The proapoptotic protein encoded by
Par4
(prostate apoptosis response 4) has been implicated in tumour suppression, particularly in the prostate. We report here that
Par4
‐null mice are prone to develop tumours, both spontaneously and on carcinogenic treatment. The endometrium and prostate of
Par4
‐null mice were particularly sensitive to the development of proliferative lesions. Most (80%)
Par4
‐null females presented endometrial hyperplasia by 9 months of age, and a significant proportion (36%) developed endometrial adenocarcinomas after 1 year of age. Similarly,
Par4
‐null males showed a high incidence of prostate hyperplasia and prostatic intraepithelial neoplasias, and were extraordinarily sensitive to testosterone‐induced prostate hyperplasia. Finally, the uterus and prostate of young
Par4
‐null mice have increased levels of the apoptosis inhibitor XIAP (X‐chromosome‐linked inhibitor of apoptosis), supporting the previously proposed function of Par4 as an inhibitor of the ζPKC (atypical protein kinase)–NF‐κB (nuclear factor‐κB)–XIAP pathway. These data show that Par4 has an important role in tumour suppression, with a particular relevance in the endometrium and prostate.</description><subject>Age Factors</subject><subject>Animals</subject><subject>apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Butylhydroxybutylnitrosamine - toxicity</subject><subject>Endometrial Neoplasms - chemically induced</subject><subject>Endometrial Neoplasms - metabolism</subject><subject>endometrium</subject><subject>Estradiol - toxicity</subject><subject>Female</subject><subject>Histological Techniques</subject><subject>Immunoblotting</subject><subject>Lesions</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Par4</subject><subject>Phenotype</subject><subject>prostate</subject><subject>Prostatic Neoplasms - chemically induced</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>protein kinase C</subject><subject>Proteins - metabolism</subject><subject>Receptors, Thrombin - metabolism</subject><subject>Scientific Report</subject><subject>Testosterone - toxicity</subject><subject>Tumors</subject><subject>tumour suppression</subject><subject>Urinary Bladder Neoplasms - chemically induced</subject><subject>Urinary Bladder Neoplasms - metabolism</subject><subject>X-Linked Inhibitor of Apoptosis Protein</subject><issn>1469-221X</issn><issn>1469-3178</issn><issn>1469-221X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</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>eNqFUctu1DAUtRCIlsKeDShiwS6Dr-34sakEVVuQyqsqKurGcjLO1EMSB9tpmb8nJdEMsIDVtXQe91wfhJ4CXgCm8lVcL2xb-rAQDGNG4B7aB8ZVTkHI-_ObEPi6hx7FuMYYF0rIh2gPCikEFmofHV4MrR9CHoe-DzZG57vMVMnduLTJfJ2la5v1wZve98knV2XBrobGJB-yTyawx-hBbZpon8zzAH05Ob44epuffTx9d_T6LK84ZpAThWUtamEUZ7agCgORWPIxMVtKWlAwBooKCiOWlJdMMMtrAmVdskqwSnJ6gA4n334oW7usbJeCaXQfXGvCRnvj9J9I5671yt9ooFxhRUaDl7NB8N8HG5NuXaxs05jO-iFqUJxIxulIfPEXcT3-TzcepwmWBRnD3ZHwRKqCjzHYepsEsL5rRse1_tWMnpsZJc9_v2AnmKsYCWoi3LrGbv5rqI_fvznfmcOkjaOsW9mwC_2PQM8mTWfSEOx24Q7PJ9zFZH9sYRO-aS6oKPTlh1N9xdjnKzgHfUl_Ak6RxsU</recordid><startdate>200506</startdate><enddate>200506</enddate><creator>García-Cao, Isabel</creator><creator>Duran, Angeles</creator><creator>Collado, Manuel</creator><creator>Carrascosa, Maria J</creator><creator>Martín-Caballero, Juan</creator><creator>Flores, Juana M</creator><creator>Diaz-Meco, Maria T</creator><creator>Moscat, Jorge</creator><creator>Serrano, Manuel</creator><general>John Wiley & Sons, Ltd</general><general>Nature Publishing Group UK</general><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>7QL</scope><scope>7T5</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>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</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>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>200506</creationdate><title>Tumour-suppression activity of the proapoptotic regulator Par4</title><author>García-Cao, Isabel ; Duran, Angeles ; Collado, Manuel ; Carrascosa, Maria J ; Martín-Caballero, Juan ; Flores, Juana M ; Diaz-Meco, Maria T ; Moscat, Jorge ; Serrano, Manuel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6041-2908f7f7a964e53901280864214d83531aa15c15a7d36b474e6f21bfb4c74c863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Age Factors</topic><topic>Animals</topic><topic>apoptosis</topic><topic>Apoptosis - physiology</topic><topic>Butylhydroxybutylnitrosamine - toxicity</topic><topic>Endometrial Neoplasms - chemically induced</topic><topic>Endometrial Neoplasms - metabolism</topic><topic>endometrium</topic><topic>Estradiol - toxicity</topic><topic>Female</topic><topic>Histological Techniques</topic><topic>Immunoblotting</topic><topic>Lesions</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Par4</topic><topic>Phenotype</topic><topic>prostate</topic><topic>Prostatic Neoplasms - chemically induced</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>protein kinase C</topic><topic>Proteins - metabolism</topic><topic>Receptors, Thrombin - metabolism</topic><topic>Scientific Report</topic><topic>Testosterone - toxicity</topic><topic>Tumors</topic><topic>tumour suppression</topic><topic>Urinary Bladder Neoplasms - chemically induced</topic><topic>Urinary Bladder Neoplasms - metabolism</topic><topic>X-Linked Inhibitor of Apoptosis Protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>García-Cao, Isabel</creatorcontrib><creatorcontrib>Duran, Angeles</creatorcontrib><creatorcontrib>Collado, Manuel</creatorcontrib><creatorcontrib>Carrascosa, Maria J</creatorcontrib><creatorcontrib>Martín-Caballero, Juan</creatorcontrib><creatorcontrib>Flores, Juana M</creatorcontrib><creatorcontrib>Diaz-Meco, Maria T</creatorcontrib><creatorcontrib>Moscat, Jorge</creatorcontrib><creatorcontrib>Serrano, Manuel</creatorcontrib><collection>Istex</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors 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>Research Library (Alumni Edition)</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>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>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</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>Research Library</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</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 Basic</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>EMBO reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>García-Cao, Isabel</au><au>Duran, Angeles</au><au>Collado, Manuel</au><au>Carrascosa, Maria J</au><au>Martín-Caballero, Juan</au><au>Flores, Juana M</au><au>Diaz-Meco, Maria T</au><au>Moscat, Jorge</au><au>Serrano, Manuel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumour-suppression activity of the proapoptotic regulator Par4</atitle><jtitle>EMBO reports</jtitle><stitle>EMBO Rep</stitle><addtitle>EMBO Rep</addtitle><date>2005-06</date><risdate>2005</risdate><volume>6</volume><issue>6</issue><spage>577</spage><epage>583</epage><pages>577-583</pages><issn>1469-221X</issn><eissn>1469-3178</eissn><eissn>1469-221X</eissn><coden>ERMEAX</coden><abstract>The proapoptotic protein encoded by
Par4
(prostate apoptosis response 4) has been implicated in tumour suppression, particularly in the prostate. We report here that
Par4
‐null mice are prone to develop tumours, both spontaneously and on carcinogenic treatment. The endometrium and prostate of
Par4
‐null mice were particularly sensitive to the development of proliferative lesions. Most (80%)
Par4
‐null females presented endometrial hyperplasia by 9 months of age, and a significant proportion (36%) developed endometrial adenocarcinomas after 1 year of age. Similarly,
Par4
‐null males showed a high incidence of prostate hyperplasia and prostatic intraepithelial neoplasias, and were extraordinarily sensitive to testosterone‐induced prostate hyperplasia. Finally, the uterus and prostate of young
Par4
‐null mice have increased levels of the apoptosis inhibitor XIAP (X‐chromosome‐linked inhibitor of apoptosis), supporting the previously proposed function of Par4 as an inhibitor of the ζPKC (atypical protein kinase)–NF‐κB (nuclear factor‐κB)–XIAP pathway. These data show that Par4 has an important role in tumour suppression, with a particular relevance in the endometrium and prostate.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>15877079</pmid><doi>10.1038/sj.embor.7400421</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1469-221X |
| ispartof | EMBO reports, 2005-06, Vol.6 (6), p.577-583 |
| issn | 1469-221X 1469-3178 1469-221X |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1369092 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley Free Content; PubMed Central |
| subjects | Age Factors Animals apoptosis Apoptosis - physiology Butylhydroxybutylnitrosamine - toxicity Endometrial Neoplasms - chemically induced Endometrial Neoplasms - metabolism endometrium Estradiol - toxicity Female Histological Techniques Immunoblotting Lesions Male Mice Mice, Mutant Strains Par4 Phenotype prostate Prostatic Neoplasms - chemically induced Prostatic Neoplasms - metabolism protein kinase C Proteins - metabolism Receptors, Thrombin - metabolism Scientific Report Testosterone - toxicity Tumors tumour suppression Urinary Bladder Neoplasms - chemically induced Urinary Bladder Neoplasms - metabolism X-Linked Inhibitor of Apoptosis Protein |
| title | Tumour-suppression activity of the proapoptotic regulator Par4 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-16T00%3A10%3A49IST&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=Tumour-suppression%20activity%20of%20the%20proapoptotic%20regulator%20Par4&rft.jtitle=EMBO%20reports&rft.au=Garc%C3%ADa-Cao,%20Isabel&rft.date=2005-06&rft.volume=6&rft.issue=6&rft.spage=577&rft.epage=583&rft.pages=577-583&rft.issn=1469-221X&rft.eissn=1469-3178&rft.coden=ERMEAX&rft_id=info:doi/10.1038/sj.embor.7400421&rft_dat=%3Cproquest_pubme%3E969884791%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=208524743&rft_id=info:pmid/15877079&rfr_iscdi=true |