Serine protease hepsin regulates hepatocyte size and hemodynamic retention of tumor cells by hepatocyte growth factor signaling in mice
The liver architecture plays an important role in maintaining hemodynamic balance, but the mechanisms that underlie this role are not fully understood. Hepsin, a type II transmembrane serine protease, is predominantly expressed in the liver, but has no known physiological functions. Here, we report...
Gespeichert in:
| Veröffentlicht in: | Hepatology (Baltimore, Md.) Md.), 2012-11, Vol.56 (5), p.1913-1923 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1923 |
|---|---|
| container_issue | 5 |
| container_start_page | 1913 |
| container_title | Hepatology (Baltimore, Md.) |
| container_volume | 56 |
| creator | Hsu, Yu-Chen Huang, Hsiang-Po Yu, I-Shing Su, Kang-Yi Lin, Shu-Rung Lin, Wei-Chou Wu, Hua-Lin Shi, Guey-Yueh Tao, Mi-Hua Kao, Cheng-Heng Wu, Yao-Ming Martin, Patricia E. Lin, Shih-Yao Yang, Pan-Chyr Lin, Shu-Wha |
| description | The liver architecture plays an important role in maintaining hemodynamic balance, but the mechanisms that underlie this role are not fully understood. Hepsin, a type II transmembrane serine protease, is predominantly expressed in the liver, but has no known physiological functions. Here, we report that hemodynamic balance in the liver is regulated through hepsin. Deletion of hepsin (hepsin−/−) in mice resulted in enlarged hepatocytes and narrowed liver sinusoids. Using fluorescent microbeads and antihepsin treatment, we demonstrated that metastatic cancer cells preferentially colonized the hepsin−/− mouse liver as a result of the retention of tumor cells because of narrower sinusoids. The enlarged hepatocytes expressed increased levels of connexin, which resulted from defective prohepatocyte growth factor (pro‐HGF) processing and decreased c‐Met phosphorylation in the livers of hepsin−/− mice. Treatment of hepsin−/− mice with recombinant HGF rescued these phenotypes, and treatment of wild‐type mice with an HGF antagonist recapitulated the phenotypes observed in hepsin−/− mice. Conclusion: Our findings show that the maintenance of hepatic structural homeostasis occurs through HGF/c‐Met/connexin signaling by hepsin, and hepsin‐mediated changes in liver architecture significantly enhance tumor metastasis to the liver. (HEPATOLOGY 2012;56:1913–1923) |
| doi_str_mv | 10.1002/hep.25773 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1126580481</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2934244051</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4563-8849db9d1626558cf39e176eeb415ce267702c76ce11f9b945a1cc3f4eb4b5d13</originalsourceid><addsrcrecordid>eNp10d1qFDEUB_Agit1WL3wBCYigF9PmYzKZXEppu2JdBRUvQyZzZps6M1mTDO34Ar62WXdbRfAqcPid_0lyEHpGyTElhJ1cweaYCSn5A7SggsmCc0EeogVhkhSKcnWADmO8JoSoktWP0QFjgghG1AL9_ATBjYA3wScwEXDOim7EAdZTbxLEbcEkb-cEOLofgM3Y5trg23k0g7NZJhiT8yP2HU7T4AO20PcRN_Pfvevgb9IV7oxNWUS3Hk3vxjXOs3IKPEGPOtNHeLo_j9CX87PPp8vi8sPF29M3l4UtRcWLui5V26iWVqwSorYdV0BlBdCUVFhglZSEWVlZoLRTjSqFodbyrsygES3lR-jVLjc_-PsEMenBxe19zQh-iprSHFyTst7SF__Qaz-FfO2sOGOqlrJkWb3eKRt8jAE6vQluMGHWlOjtdnT-BP17O9k-3ydOzQDtvbxbRwYv98BEa_oumNG6-MdVlVRMyexOdu7G9TD_f6Jenn28G13sOlxMcHvfYcI3XUkuhf66utDl6v3q3ZKc6xX_BfpFtxE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1322987742</pqid></control><display><type>article</type><title>Serine protease hepsin regulates hepatocyte size and hemodynamic retention of tumor cells by hepatocyte growth factor signaling in mice</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Hsu, Yu-Chen ; Huang, Hsiang-Po ; Yu, I-Shing ; Su, Kang-Yi ; Lin, Shu-Rung ; Lin, Wei-Chou ; Wu, Hua-Lin ; Shi, Guey-Yueh ; Tao, Mi-Hua ; Kao, Cheng-Heng ; Wu, Yao-Ming ; Martin, Patricia E. ; Lin, Shih-Yao ; Yang, Pan-Chyr ; Lin, Shu-Wha</creator><creatorcontrib>Hsu, Yu-Chen ; Huang, Hsiang-Po ; Yu, I-Shing ; Su, Kang-Yi ; Lin, Shu-Rung ; Lin, Wei-Chou ; Wu, Hua-Lin ; Shi, Guey-Yueh ; Tao, Mi-Hua ; Kao, Cheng-Heng ; Wu, Yao-Ming ; Martin, Patricia E. ; Lin, Shih-Yao ; Yang, Pan-Chyr ; Lin, Shu-Wha</creatorcontrib><description>The liver architecture plays an important role in maintaining hemodynamic balance, but the mechanisms that underlie this role are not fully understood. Hepsin, a type II transmembrane serine protease, is predominantly expressed in the liver, but has no known physiological functions. Here, we report that hemodynamic balance in the liver is regulated through hepsin. Deletion of hepsin (hepsin−/−) in mice resulted in enlarged hepatocytes and narrowed liver sinusoids. Using fluorescent microbeads and antihepsin treatment, we demonstrated that metastatic cancer cells preferentially colonized the hepsin−/− mouse liver as a result of the retention of tumor cells because of narrower sinusoids. The enlarged hepatocytes expressed increased levels of connexin, which resulted from defective prohepatocyte growth factor (pro‐HGF) processing and decreased c‐Met phosphorylation in the livers of hepsin−/− mice. Treatment of hepsin−/− mice with recombinant HGF rescued these phenotypes, and treatment of wild‐type mice with an HGF antagonist recapitulated the phenotypes observed in hepsin−/− mice. Conclusion: Our findings show that the maintenance of hepatic structural homeostasis occurs through HGF/c‐Met/connexin signaling by hepsin, and hepsin‐mediated changes in liver architecture significantly enhance tumor metastasis to the liver. (HEPATOLOGY 2012;56:1913–1923)</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.25773</identifier><identifier>PMID: 22505209</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Biological and medical sciences ; Connexins - metabolism ; Gastroenterology. Liver. Pancreas. Abdomen ; Hemodynamics ; Hepatocyte Growth Factor - metabolism ; Hepatocyte Growth Factor - pharmacology ; Hepatocytes - drug effects ; Hepatocytes - metabolism ; Hepatocytes - pathology ; Hepatology ; Liver - drug effects ; Liver - metabolism ; Liver - pathology ; Liver Neoplasms - secondary ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Mice ; Mice, Knockout ; Microscopy, Electron, Transmission ; Neoplasm Metastasis - pathology ; Neoplasm Transplantation ; Phosphorylation ; Proteins ; Proto-Oncogene Proteins c-met - metabolism ; Retention ; Rodents ; Serine Endopeptidases - genetics ; Serine Endopeptidases - metabolism ; Signal Transduction</subject><ispartof>Hepatology (Baltimore, Md.), 2012-11, Vol.56 (5), p.1913-1923</ispartof><rights>Copyright © 2012 American Association for the Study of Liver Diseases</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2012 American Association for the Study of Liver Diseases.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4563-8849db9d1626558cf39e176eeb415ce267702c76ce11f9b945a1cc3f4eb4b5d13</citedby><cites>FETCH-LOGICAL-c4563-8849db9d1626558cf39e176eeb415ce267702c76ce11f9b945a1cc3f4eb4b5d13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fhep.25773$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fhep.25773$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26679297$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22505209$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hsu, Yu-Chen</creatorcontrib><creatorcontrib>Huang, Hsiang-Po</creatorcontrib><creatorcontrib>Yu, I-Shing</creatorcontrib><creatorcontrib>Su, Kang-Yi</creatorcontrib><creatorcontrib>Lin, Shu-Rung</creatorcontrib><creatorcontrib>Lin, Wei-Chou</creatorcontrib><creatorcontrib>Wu, Hua-Lin</creatorcontrib><creatorcontrib>Shi, Guey-Yueh</creatorcontrib><creatorcontrib>Tao, Mi-Hua</creatorcontrib><creatorcontrib>Kao, Cheng-Heng</creatorcontrib><creatorcontrib>Wu, Yao-Ming</creatorcontrib><creatorcontrib>Martin, Patricia E.</creatorcontrib><creatorcontrib>Lin, Shih-Yao</creatorcontrib><creatorcontrib>Yang, Pan-Chyr</creatorcontrib><creatorcontrib>Lin, Shu-Wha</creatorcontrib><title>Serine protease hepsin regulates hepatocyte size and hemodynamic retention of tumor cells by hepatocyte growth factor signaling in mice</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>The liver architecture plays an important role in maintaining hemodynamic balance, but the mechanisms that underlie this role are not fully understood. Hepsin, a type II transmembrane serine protease, is predominantly expressed in the liver, but has no known physiological functions. Here, we report that hemodynamic balance in the liver is regulated through hepsin. Deletion of hepsin (hepsin−/−) in mice resulted in enlarged hepatocytes and narrowed liver sinusoids. Using fluorescent microbeads and antihepsin treatment, we demonstrated that metastatic cancer cells preferentially colonized the hepsin−/− mouse liver as a result of the retention of tumor cells because of narrower sinusoids. The enlarged hepatocytes expressed increased levels of connexin, which resulted from defective prohepatocyte growth factor (pro‐HGF) processing and decreased c‐Met phosphorylation in the livers of hepsin−/− mice. Treatment of hepsin−/− mice with recombinant HGF rescued these phenotypes, and treatment of wild‐type mice with an HGF antagonist recapitulated the phenotypes observed in hepsin−/− mice. Conclusion: Our findings show that the maintenance of hepatic structural homeostasis occurs through HGF/c‐Met/connexin signaling by hepsin, and hepsin‐mediated changes in liver architecture significantly enhance tumor metastasis to the liver. (HEPATOLOGY 2012;56:1913–1923)</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Connexins - metabolism</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hemodynamics</subject><subject>Hepatocyte Growth Factor - metabolism</subject><subject>Hepatocyte Growth Factor - pharmacology</subject><subject>Hepatocytes - drug effects</subject><subject>Hepatocytes - metabolism</subject><subject>Hepatocytes - pathology</subject><subject>Hepatology</subject><subject>Liver - drug effects</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver Neoplasms - secondary</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Microscopy, Electron, Transmission</subject><subject>Neoplasm Metastasis - pathology</subject><subject>Neoplasm Transplantation</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-met - metabolism</subject><subject>Retention</subject><subject>Rodents</subject><subject>Serine Endopeptidases - genetics</subject><subject>Serine Endopeptidases - metabolism</subject><subject>Signal Transduction</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10d1qFDEUB_Agit1WL3wBCYigF9PmYzKZXEppu2JdBRUvQyZzZps6M1mTDO34Ar62WXdbRfAqcPid_0lyEHpGyTElhJ1cweaYCSn5A7SggsmCc0EeogVhkhSKcnWADmO8JoSoktWP0QFjgghG1AL9_ATBjYA3wScwEXDOim7EAdZTbxLEbcEkb-cEOLofgM3Y5trg23k0g7NZJhiT8yP2HU7T4AO20PcRN_Pfvevgb9IV7oxNWUS3Hk3vxjXOs3IKPEGPOtNHeLo_j9CX87PPp8vi8sPF29M3l4UtRcWLui5V26iWVqwSorYdV0BlBdCUVFhglZSEWVlZoLRTjSqFodbyrsygES3lR-jVLjc_-PsEMenBxe19zQh-iprSHFyTst7SF__Qaz-FfO2sOGOqlrJkWb3eKRt8jAE6vQluMGHWlOjtdnT-BP17O9k-3ydOzQDtvbxbRwYv98BEa_oumNG6-MdVlVRMyexOdu7G9TD_f6Jenn28G13sOlxMcHvfYcI3XUkuhf66utDl6v3q3ZKc6xX_BfpFtxE</recordid><startdate>201211</startdate><enddate>201211</enddate><creator>Hsu, Yu-Chen</creator><creator>Huang, Hsiang-Po</creator><creator>Yu, I-Shing</creator><creator>Su, Kang-Yi</creator><creator>Lin, Shu-Rung</creator><creator>Lin, Wei-Chou</creator><creator>Wu, Hua-Lin</creator><creator>Shi, Guey-Yueh</creator><creator>Tao, Mi-Hua</creator><creator>Kao, Cheng-Heng</creator><creator>Wu, Yao-Ming</creator><creator>Martin, Patricia E.</creator><creator>Lin, Shih-Yao</creator><creator>Yang, Pan-Chyr</creator><creator>Lin, Shu-Wha</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><general>Wolters Kluwer Health, Inc</general><scope>BSCLL</scope><scope>IQODW</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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201211</creationdate><title>Serine protease hepsin regulates hepatocyte size and hemodynamic retention of tumor cells by hepatocyte growth factor signaling in mice</title><author>Hsu, Yu-Chen ; Huang, Hsiang-Po ; Yu, I-Shing ; Su, Kang-Yi ; Lin, Shu-Rung ; Lin, Wei-Chou ; Wu, Hua-Lin ; Shi, Guey-Yueh ; Tao, Mi-Hua ; Kao, Cheng-Heng ; Wu, Yao-Ming ; Martin, Patricia E. ; Lin, Shih-Yao ; Yang, Pan-Chyr ; Lin, Shu-Wha</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4563-8849db9d1626558cf39e176eeb415ce267702c76ce11f9b945a1cc3f4eb4b5d13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Connexins - metabolism</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hemodynamics</topic><topic>Hepatocyte Growth Factor - metabolism</topic><topic>Hepatocyte Growth Factor - pharmacology</topic><topic>Hepatocytes - drug effects</topic><topic>Hepatocytes - metabolism</topic><topic>Hepatocytes - pathology</topic><topic>Hepatology</topic><topic>Liver - drug effects</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Liver Neoplasms - secondary</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Microscopy, Electron, Transmission</topic><topic>Neoplasm Metastasis - pathology</topic><topic>Neoplasm Transplantation</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-met - metabolism</topic><topic>Retention</topic><topic>Rodents</topic><topic>Serine Endopeptidases - genetics</topic><topic>Serine Endopeptidases - metabolism</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hsu, Yu-Chen</creatorcontrib><creatorcontrib>Huang, Hsiang-Po</creatorcontrib><creatorcontrib>Yu, I-Shing</creatorcontrib><creatorcontrib>Su, Kang-Yi</creatorcontrib><creatorcontrib>Lin, Shu-Rung</creatorcontrib><creatorcontrib>Lin, Wei-Chou</creatorcontrib><creatorcontrib>Wu, Hua-Lin</creatorcontrib><creatorcontrib>Shi, Guey-Yueh</creatorcontrib><creatorcontrib>Tao, Mi-Hua</creatorcontrib><creatorcontrib>Kao, Cheng-Heng</creatorcontrib><creatorcontrib>Wu, Yao-Ming</creatorcontrib><creatorcontrib>Martin, Patricia E.</creatorcontrib><creatorcontrib>Lin, Shih-Yao</creatorcontrib><creatorcontrib>Yang, Pan-Chyr</creatorcontrib><creatorcontrib>Lin, Shu-Wha</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hsu, Yu-Chen</au><au>Huang, Hsiang-Po</au><au>Yu, I-Shing</au><au>Su, Kang-Yi</au><au>Lin, Shu-Rung</au><au>Lin, Wei-Chou</au><au>Wu, Hua-Lin</au><au>Shi, Guey-Yueh</au><au>Tao, Mi-Hua</au><au>Kao, Cheng-Heng</au><au>Wu, Yao-Ming</au><au>Martin, Patricia E.</au><au>Lin, Shih-Yao</au><au>Yang, Pan-Chyr</au><au>Lin, Shu-Wha</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Serine protease hepsin regulates hepatocyte size and hemodynamic retention of tumor cells by hepatocyte growth factor signaling in mice</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>2012-11</date><risdate>2012</risdate><volume>56</volume><issue>5</issue><spage>1913</spage><epage>1923</epage><pages>1913-1923</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract>The liver architecture plays an important role in maintaining hemodynamic balance, but the mechanisms that underlie this role are not fully understood. Hepsin, a type II transmembrane serine protease, is predominantly expressed in the liver, but has no known physiological functions. Here, we report that hemodynamic balance in the liver is regulated through hepsin. Deletion of hepsin (hepsin−/−) in mice resulted in enlarged hepatocytes and narrowed liver sinusoids. Using fluorescent microbeads and antihepsin treatment, we demonstrated that metastatic cancer cells preferentially colonized the hepsin−/− mouse liver as a result of the retention of tumor cells because of narrower sinusoids. The enlarged hepatocytes expressed increased levels of connexin, which resulted from defective prohepatocyte growth factor (pro‐HGF) processing and decreased c‐Met phosphorylation in the livers of hepsin−/− mice. Treatment of hepsin−/− mice with recombinant HGF rescued these phenotypes, and treatment of wild‐type mice with an HGF antagonist recapitulated the phenotypes observed in hepsin−/− mice. Conclusion: Our findings show that the maintenance of hepatic structural homeostasis occurs through HGF/c‐Met/connexin signaling by hepsin, and hepsin‐mediated changes in liver architecture significantly enhance tumor metastasis to the liver. (HEPATOLOGY 2012;56:1913–1923)</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>22505209</pmid><doi>10.1002/hep.25773</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0270-9139 |
| ispartof | Hepatology (Baltimore, Md.), 2012-11, Vol.56 (5), p.1913-1923 |
| issn | 0270-9139 1527-3350 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1126580481 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Biological and medical sciences Connexins - metabolism Gastroenterology. Liver. Pancreas. Abdomen Hemodynamics Hepatocyte Growth Factor - metabolism Hepatocyte Growth Factor - pharmacology Hepatocytes - drug effects Hepatocytes - metabolism Hepatocytes - pathology Hepatology Liver - drug effects Liver - metabolism Liver - pathology Liver Neoplasms - secondary Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Mice Mice, Knockout Microscopy, Electron, Transmission Neoplasm Metastasis - pathology Neoplasm Transplantation Phosphorylation Proteins Proto-Oncogene Proteins c-met - metabolism Retention Rodents Serine Endopeptidases - genetics Serine Endopeptidases - metabolism Signal Transduction |
| title | Serine protease hepsin regulates hepatocyte size and hemodynamic retention of tumor cells by hepatocyte growth factor signaling in mice |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-09T05%3A38%3A35IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Serine%20protease%20hepsin%20regulates%20hepatocyte%20size%20and%20hemodynamic%20retention%20of%20tumor%20cells%20by%20hepatocyte%20growth%20factor%20signaling%20in%20mice&rft.jtitle=Hepatology%20(Baltimore,%20Md.)&rft.au=Hsu,%20Yu-Chen&rft.date=2012-11&rft.volume=56&rft.issue=5&rft.spage=1913&rft.epage=1923&rft.pages=1913-1923&rft.issn=0270-9139&rft.eissn=1527-3350&rft.coden=HPTLD9&rft_id=info:doi/10.1002/hep.25773&rft_dat=%3Cproquest_cross%3E2934244051%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1322987742&rft_id=info:pmid/22505209&rfr_iscdi=true |