The Ins and Outs of HOPS/TMUB1 in biology and pathology
HOPS/TMUB1 is an important player in controlling a number of important functions in the cell. Many investigations highlight the importance of HOPS/TMUB1 as protein modifier likewise SUMO or NEDD. HOPS/TMUB1 knockdown alters proper centrosome assembly, leading to genomic instability. HOPS/TMUB1 acts...
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| Veröffentlicht in: | The FEBS journal 2021-05, Vol.288 (9), p.2773-2783 |
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| creator | Della‐Fazia, Maria Agnese Castelli, Marilena Piobbico, Danilo Pieroni, Stefania Servillo, Giuseppe |
| description | HOPS/TMUB1 is an important player in controlling a number of important functions in the cell. Many investigations highlight the importance of HOPS/TMUB1 as protein modifier likewise SUMO or NEDD. HOPS/TMUB1 knockdown alters proper centrosome assembly, leading to genomic instability. HOPS/TMUB1 acts as a functional bridge between NPM and p19Arf, providing new mechanistic insight into proliferation control. HOPS/TMUB1 acts on p53 stability, directing p53 mitochondrial apoptosis and its cytoplasmic localization.
Liver regeneration represents an outstanding tool to study not only proliferation, but also other important processes such as inflammation, regenerative response or stem cell biology. Several novel genes have been identified as being involved in the proliferation of residual hepatocytes. One of them, HOPS/TMUB1, is proving to be a significant player in the control of proliferation, both contributing to genomic stability and as a partner of essential molecules. HOPS is an ubiquitin‐like protein, shuttling from nucleus to cytoplasm, and it is engaged in a number of biological and physiopathological functions. HOPS overexpression in tumour cell lines strongly reduces proliferation, arresting cell cycle in G0/G1. HOPS is involved in centrosome assembly and maintenance, and its knockdown causes genomic instability. Moreover, a direct interaction of HOPS with nucleophosmin (NPM) and p19Arf has been established, resulting in proper control of p19Arf stability and localization. These data indicate that HOPS acts as a functional bridge in the interaction between NPM and p19Arf, providing new mechanistic insight into how NPM and p19Arf will oppose cell proliferation. HOPS exerts a control in p53 stability, directing p53 mitochondrial apoptosis and cytoplasmic localization. HOPS plays a direct role as novel post‐translational modifier of p53, much like SUMO or NEDD. HOPS is overexpressed in a high number of human tumours in patients affected by large intestinal, CNS, liver and oesophageal tumours. This review highlights HOPS involvement in distinct cellular functions, establishing its role as a key player in cell biology and pathology in a broader context. |
| doi_str_mv | 10.1111/febs.15539 |
| format | Article |
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Liver regeneration represents an outstanding tool to study not only proliferation, but also other important processes such as inflammation, regenerative response or stem cell biology. Several novel genes have been identified as being involved in the proliferation of residual hepatocytes. One of them, HOPS/TMUB1, is proving to be a significant player in the control of proliferation, both contributing to genomic stability and as a partner of essential molecules. HOPS is an ubiquitin‐like protein, shuttling from nucleus to cytoplasm, and it is engaged in a number of biological and physiopathological functions. HOPS overexpression in tumour cell lines strongly reduces proliferation, arresting cell cycle in G0/G1. HOPS is involved in centrosome assembly and maintenance, and its knockdown causes genomic instability. Moreover, a direct interaction of HOPS with nucleophosmin (NPM) and p19Arf has been established, resulting in proper control of p19Arf stability and localization. These data indicate that HOPS acts as a functional bridge in the interaction between NPM and p19Arf, providing new mechanistic insight into how NPM and p19Arf will oppose cell proliferation. HOPS exerts a control in p53 stability, directing p53 mitochondrial apoptosis and cytoplasmic localization. HOPS plays a direct role as novel post‐translational modifier of p53, much like SUMO or NEDD. HOPS is overexpressed in a high number of human tumours in patients affected by large intestinal, CNS, liver and oesophageal tumours. This review highlights HOPS involvement in distinct cellular functions, establishing its role as a key player in cell biology and pathology in a broader context.</description><identifier>ISSN: 1742-464X</identifier><identifier>EISSN: 1742-4658</identifier><identifier>DOI: 10.1111/febs.15539</identifier><identifier>PMID: 32860479</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Apoptosis ; apoptosis protein modifier ; Biology ; Cell cycle ; Cell proliferation ; Control stability ; Cytoplasm ; Esophagus ; Genomic instability ; hepatocyte odd protein shuttling ; Hepatocytes ; Inflammation ; Intestine ; Liver ; liver regeneration ; Localization ; Mitochondria ; nucleophosmin ; p19 Arf ; p53 ; p53 Protein ; Pathology ; Regeneration ; Stem cells ; transmembrane and ubiquitin‐like domain‐containing 1 ; Tumor cell lines ; Tumors ; tumour suppressor gene ; Ubiquitin ; ubiquitin‐like protein</subject><ispartof>The FEBS journal, 2021-05, Vol.288 (9), p.2773-2783</ispartof><rights>2020 Federation of European Biochemical Societies</rights><rights>2020 Federation of European Biochemical Societies.</rights><rights>Copyright © 2021 Federation of European Biochemical Societies</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3939-4e604bb128f2b03b04fea3564c1874328c948868acfe9c516d51643477efa1863</citedby><cites>FETCH-LOGICAL-c3939-4e604bb128f2b03b04fea3564c1874328c948868acfe9c516d51643477efa1863</cites><orcidid>0000-0002-5373-8477 ; 0000-0001-7960-7689</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Ffebs.15539$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Ffebs.15539$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32860479$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Della‐Fazia, Maria Agnese</creatorcontrib><creatorcontrib>Castelli, Marilena</creatorcontrib><creatorcontrib>Piobbico, Danilo</creatorcontrib><creatorcontrib>Pieroni, Stefania</creatorcontrib><creatorcontrib>Servillo, Giuseppe</creatorcontrib><title>The Ins and Outs of HOPS/TMUB1 in biology and pathology</title><title>The FEBS journal</title><addtitle>FEBS J</addtitle><description>HOPS/TMUB1 is an important player in controlling a number of important functions in the cell. Many investigations highlight the importance of HOPS/TMUB1 as protein modifier likewise SUMO or NEDD. HOPS/TMUB1 knockdown alters proper centrosome assembly, leading to genomic instability. HOPS/TMUB1 acts as a functional bridge between NPM and p19Arf, providing new mechanistic insight into proliferation control. HOPS/TMUB1 acts on p53 stability, directing p53 mitochondrial apoptosis and its cytoplasmic localization.
Liver regeneration represents an outstanding tool to study not only proliferation, but also other important processes such as inflammation, regenerative response or stem cell biology. Several novel genes have been identified as being involved in the proliferation of residual hepatocytes. One of them, HOPS/TMUB1, is proving to be a significant player in the control of proliferation, both contributing to genomic stability and as a partner of essential molecules. HOPS is an ubiquitin‐like protein, shuttling from nucleus to cytoplasm, and it is engaged in a number of biological and physiopathological functions. HOPS overexpression in tumour cell lines strongly reduces proliferation, arresting cell cycle in G0/G1. HOPS is involved in centrosome assembly and maintenance, and its knockdown causes genomic instability. Moreover, a direct interaction of HOPS with nucleophosmin (NPM) and p19Arf has been established, resulting in proper control of p19Arf stability and localization. These data indicate that HOPS acts as a functional bridge in the interaction between NPM and p19Arf, providing new mechanistic insight into how NPM and p19Arf will oppose cell proliferation. HOPS exerts a control in p53 stability, directing p53 mitochondrial apoptosis and cytoplasmic localization. HOPS plays a direct role as novel post‐translational modifier of p53, much like SUMO or NEDD. HOPS is overexpressed in a high number of human tumours in patients affected by large intestinal, CNS, liver and oesophageal tumours. This review highlights HOPS involvement in distinct cellular functions, establishing its role as a key player in cell biology and pathology in a broader context.</description><subject>Apoptosis</subject><subject>apoptosis protein modifier</subject><subject>Biology</subject><subject>Cell cycle</subject><subject>Cell proliferation</subject><subject>Control stability</subject><subject>Cytoplasm</subject><subject>Esophagus</subject><subject>Genomic instability</subject><subject>hepatocyte odd protein shuttling</subject><subject>Hepatocytes</subject><subject>Inflammation</subject><subject>Intestine</subject><subject>Liver</subject><subject>liver regeneration</subject><subject>Localization</subject><subject>Mitochondria</subject><subject>nucleophosmin</subject><subject>p19 Arf</subject><subject>p53</subject><subject>p53 Protein</subject><subject>Pathology</subject><subject>Regeneration</subject><subject>Stem cells</subject><subject>transmembrane and ubiquitin‐like domain‐containing 1</subject><subject>Tumor cell lines</subject><subject>Tumors</subject><subject>tumour suppressor gene</subject><subject>Ubiquitin</subject><subject>ubiquitin‐like protein</subject><issn>1742-464X</issn><issn>1742-4658</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9kF1rwjAUhsPYmM7tZj9gFHYzBtWkSfNxOUWn4HCgwu5CWpNZqY1rLMN_v9g6L3axA4eTwMNzDi8A9wh2ka-e0YnrojjG4gK0ESNRSGjML89v8tECN85tIMQxEeIatHDEKSRMtAFbrHUwKVygilUwq_YusCYYz97nvcXbso-CrAiSzOb281ATO7Vf179bcGVU7vTdaXbAcjRcDMbhdPY6GbxMwxQLLEKi_Z4kQRE3UQJxAonRCseUpIgz4s9IBeGccpUaLdIY0ZVvgglj2ijEKe6Ap8a7K-1Xpd1ebjOX6jxXhbaVkxHBnDJGMfbo4x90Y6uy8NfJKI4g802OwueGSkvrXKmN3JXZVpUHiaA8ximPcco6Tg8_nJRVstWrM_qbnwdQA3xnuT78o5KjYX_eSH8AlWh7Sg</recordid><startdate>202105</startdate><enddate>202105</enddate><creator>Della‐Fazia, Maria Agnese</creator><creator>Castelli, Marilena</creator><creator>Piobbico, Danilo</creator><creator>Pieroni, Stefania</creator><creator>Servillo, Giuseppe</creator><general>Blackwell Publishing Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-5373-8477</orcidid><orcidid>https://orcid.org/0000-0001-7960-7689</orcidid></search><sort><creationdate>202105</creationdate><title>The Ins and Outs of HOPS/TMUB1 in biology and pathology</title><author>Della‐Fazia, Maria Agnese ; Castelli, Marilena ; Piobbico, Danilo ; Pieroni, Stefania ; Servillo, Giuseppe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3939-4e604bb128f2b03b04fea3564c1874328c948868acfe9c516d51643477efa1863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Apoptosis</topic><topic>apoptosis protein modifier</topic><topic>Biology</topic><topic>Cell cycle</topic><topic>Cell proliferation</topic><topic>Control stability</topic><topic>Cytoplasm</topic><topic>Esophagus</topic><topic>Genomic instability</topic><topic>hepatocyte odd protein shuttling</topic><topic>Hepatocytes</topic><topic>Inflammation</topic><topic>Intestine</topic><topic>Liver</topic><topic>liver regeneration</topic><topic>Localization</topic><topic>Mitochondria</topic><topic>nucleophosmin</topic><topic>p19 Arf</topic><topic>p53</topic><topic>p53 Protein</topic><topic>Pathology</topic><topic>Regeneration</topic><topic>Stem cells</topic><topic>transmembrane and ubiquitin‐like domain‐containing 1</topic><topic>Tumor cell lines</topic><topic>Tumors</topic><topic>tumour suppressor gene</topic><topic>Ubiquitin</topic><topic>ubiquitin‐like protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Della‐Fazia, Maria Agnese</creatorcontrib><creatorcontrib>Castelli, Marilena</creatorcontrib><creatorcontrib>Piobbico, Danilo</creatorcontrib><creatorcontrib>Pieroni, Stefania</creatorcontrib><creatorcontrib>Servillo, Giuseppe</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The FEBS journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Della‐Fazia, Maria Agnese</au><au>Castelli, Marilena</au><au>Piobbico, Danilo</au><au>Pieroni, Stefania</au><au>Servillo, Giuseppe</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Ins and Outs of HOPS/TMUB1 in biology and pathology</atitle><jtitle>The FEBS journal</jtitle><addtitle>FEBS J</addtitle><date>2021-05</date><risdate>2021</risdate><volume>288</volume><issue>9</issue><spage>2773</spage><epage>2783</epage><pages>2773-2783</pages><issn>1742-464X</issn><eissn>1742-4658</eissn><abstract>HOPS/TMUB1 is an important player in controlling a number of important functions in the cell. Many investigations highlight the importance of HOPS/TMUB1 as protein modifier likewise SUMO or NEDD. HOPS/TMUB1 knockdown alters proper centrosome assembly, leading to genomic instability. HOPS/TMUB1 acts as a functional bridge between NPM and p19Arf, providing new mechanistic insight into proliferation control. HOPS/TMUB1 acts on p53 stability, directing p53 mitochondrial apoptosis and its cytoplasmic localization.
Liver regeneration represents an outstanding tool to study not only proliferation, but also other important processes such as inflammation, regenerative response or stem cell biology. Several novel genes have been identified as being involved in the proliferation of residual hepatocytes. One of them, HOPS/TMUB1, is proving to be a significant player in the control of proliferation, both contributing to genomic stability and as a partner of essential molecules. HOPS is an ubiquitin‐like protein, shuttling from nucleus to cytoplasm, and it is engaged in a number of biological and physiopathological functions. HOPS overexpression in tumour cell lines strongly reduces proliferation, arresting cell cycle in G0/G1. HOPS is involved in centrosome assembly and maintenance, and its knockdown causes genomic instability. Moreover, a direct interaction of HOPS with nucleophosmin (NPM) and p19Arf has been established, resulting in proper control of p19Arf stability and localization. These data indicate that HOPS acts as a functional bridge in the interaction between NPM and p19Arf, providing new mechanistic insight into how NPM and p19Arf will oppose cell proliferation. HOPS exerts a control in p53 stability, directing p53 mitochondrial apoptosis and cytoplasmic localization. HOPS plays a direct role as novel post‐translational modifier of p53, much like SUMO or NEDD. HOPS is overexpressed in a high number of human tumours in patients affected by large intestinal, CNS, liver and oesophageal tumours. This review highlights HOPS involvement in distinct cellular functions, establishing its role as a key player in cell biology and pathology in a broader context.</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>32860479</pmid><doi>10.1111/febs.15539</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-5373-8477</orcidid><orcidid>https://orcid.org/0000-0001-7960-7689</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis apoptosis protein modifier Biology Cell cycle Cell proliferation Control stability Cytoplasm Esophagus Genomic instability hepatocyte odd protein shuttling Hepatocytes Inflammation Intestine Liver liver regeneration Localization Mitochondria nucleophosmin p19 Arf p53 p53 Protein Pathology Regeneration Stem cells transmembrane and ubiquitin‐like domain‐containing 1 Tumor cell lines Tumors tumour suppressor gene Ubiquitin ubiquitin‐like protein |
| title | The Ins and Outs of HOPS/TMUB1 in biology and pathology |
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