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dc.contributor.authorRamkumar, Charusheila
dc.contributor.authorKong, Yahui
dc.contributor.authorCui, Hang
dc.contributor.authorHao, Suyang
dc.contributor.authorJones, Stephen N.
dc.contributor.authorGerstein, Rachel M.
dc.contributor.authorZhang, Hong
dc.date2022-08-11T08:11:05.000
dc.date.accessioned2022-08-23T17:33:07Z
dc.date.available2022-08-23T17:33:07Z
dc.date.issued2012-06-01
dc.date.submitted2012-05-04
dc.identifier.citationRamkumar C, Kong Y, Cui H, Hao S, Jones SN, Gerstein RM, Zhang H. Smurf2 regulates the senescence response and suppresses tumorigenesis in mice. Cancer Res. 2012 Jun 1;72(11):2714-9. doi: 10.1158/0008-5472.CAN-11-3773. <a href="http://dx.doi.org/10.1158/0008-5472.CAN-11-3773">Link to article on publisher's website</a>
dc.identifier.issn1538-7445
dc.identifier.doi10.1158/0008-5472.CAN-11-3773
dc.identifier.pmid22552287
dc.identifier.urihttp://hdl.handle.net/20.500.14038/51100
dc.description<p>First author Charusheila Ramkumar is a student in the Cell Biology program in the Graduate School of Biomedical Sciences (GSBS) at UMass Medical School.</p>
dc.description.abstractThe E3 ubiquitin ligase Smurf2 mediates ubiquitination and degradation of several protein targets involved in tumorigenesis and induces senescence in human cells. However, the functional role of Smurf2 in tumorigenesis has not been fully evaluated. In this study, we generated a mouse model of Smurf2 deficiency to characterize the function of this E3 ligase in tumorigenesis. Smurf2 deficiency attenuated p16 expression and impaired the senescence response of primary mouse embryonic fibroblasts. In support of a functional role in controlling cancer, Smurf2 deficiency increased the susceptibility of mice to spontaneous tumorigenesis, most notably B cell lymphoma. At a premalignant stage of tumorigenesis, we documented a defective senescence response in the spleens of Smurf2-deficient mice, consistent with a mechanistic link between impaired senescence regulation and increased tumorigenesis. Taken together, our findings offer the genetic evidence of an important tumor suppressor function for Smurf2.
dc.language.isoen_US
dc.publisherAmerican Association for Cancer Research
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=22552287&dopt=Abstract">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1158/0008-5472.CAN-11-3773
dc.subjectUbiquitin-Protein Ligases
dc.subjectCell Aging
dc.subjectTumor Suppressor Proteins
dc.subjectCancer Biology
dc.subjectCell Biology
dc.titleSmurf2 regulates the senescence response and suppresses tumorigenesis in mice
dc.typeJournal Article
dc.source.journaltitleCancer research
dc.source.volume72
dc.source.issue11
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/zhang/12
dc.identifier.contextkey2821738
html.description.abstract<p>The E3 ubiquitin ligase Smurf2 mediates ubiquitination and degradation of several protein targets involved in tumorigenesis and induces senescence in human cells. However, the functional role of Smurf2 in tumorigenesis has not been fully evaluated. In this study, we generated a mouse model of Smurf2 deficiency to characterize the function of this E3 ligase in tumorigenesis. Smurf2 deficiency attenuated p16 expression and impaired the senescence response of primary mouse embryonic fibroblasts. In support of a functional role in controlling cancer, Smurf2 deficiency increased the susceptibility of mice to spontaneous tumorigenesis, most notably B cell lymphoma. At a premalignant stage of tumorigenesis, we documented a defective senescence response in the spleens of Smurf2-deficient mice, consistent with a mechanistic link between impaired senescence regulation and increased tumorigenesis. Taken together, our findings offer the genetic evidence of an important tumor suppressor function for Smurf2.</p>
dc.identifier.submissionpathzhang/12
dc.contributor.departmentDepartment of Microbiology and Physiological Systems
dc.contributor.departmentDepartment of Pathology
dc.contributor.departmentDepartment of Cell Biology
dc.source.pages2714-9


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