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Conference Paper: Homodimerization of the deleted in liver cancer 2 (DLC2) is not mediated by the SAM domain

TitleHomodimerization of the deleted in liver cancer 2 (DLC2) is not mediated by the SAM domain
Authors
Issue Date2005
PublisherBlackwell
Citation
The 30th Federation of Biochemical Societies (FEBS) Congress & 9th International Union of Biochemistry and Molecular Biology (IUBMB) Conference, Budapest, Hungary, 2-7 July 2005. In The FEBS Journal, 2005, v. 272 n. S1, p. 328 Abstract no. E4-015P How to Cite?
AbstractDeleted in liver cancer 2 (DLC2) is a novel tumor suppressorgene which is found to be frequently deleted in hepatocellularcarcinoma. Although DLC2 is consisted of a RhoGAP homologydomain, a START domain and a sterile-a-motif (SAM) domain,the role of DLC2 in cellular function remains elusive. To gaininsight on the function of DLC2, we expressed and purified arecombinant13C and15N doubled DLC2 SAM domain. Circulardichromism analysis showed that DLC2 SAM contains high heli-ces. We further determined the structure of the DLC2 SAMdomain by 2D and 3D NMR experiments together with simula-ted annealing calculations. Our data revealed that the structureof DLC2 SAM is slightly different from other known SAMdomains and adapts a monomeric structure with four alpha heli-ces in solution. Consistent with the structural data, cross-linkingexperiment also suggested that DLC SAM exists in predomin-antly monomeric form in vitro. On the other hand, co-immuno-precipitation experiments suggested that the DLC2 protein ishomodimerized. Analysis of the deletion mutants revealed thatthe homodimerization is not mediated by the SAM domain, butthrough a distinct region on the DLC2 protein.
Persistent Identifierhttp://hdl.handle.net/10722/97019
ISSN

 

DC FieldValueLanguage
dc.contributor.authorFung, KLen_HK
dc.contributor.authorLi, HYYan, Hen_HK
dc.contributor.authorNg, IOLen_HK
dc.contributor.authorChing, YPen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorSun, Hen_HK
dc.contributor.authorKo, BCBen_HK
dc.date.accessioned2010-09-25T16:53:29Z-
dc.date.available2010-09-25T16:53:29Z-
dc.date.issued2005en_HK
dc.identifier.citationThe 30th Federation of Biochemical Societies (FEBS) Congress & 9th International Union of Biochemistry and Molecular Biology (IUBMB) Conference, Budapest, Hungary, 2-7 July 2005. In The FEBS Journal, 2005, v. 272 n. S1, p. 328 Abstract no. E4-015P-
dc.identifier.issn1742-4658-
dc.identifier.urihttp://hdl.handle.net/10722/97019-
dc.description.abstractDeleted in liver cancer 2 (DLC2) is a novel tumor suppressorgene which is found to be frequently deleted in hepatocellularcarcinoma. Although DLC2 is consisted of a RhoGAP homologydomain, a START domain and a sterile-a-motif (SAM) domain,the role of DLC2 in cellular function remains elusive. To gaininsight on the function of DLC2, we expressed and purified arecombinant13C and15N doubled DLC2 SAM domain. Circulardichromism analysis showed that DLC2 SAM contains high heli-ces. We further determined the structure of the DLC2 SAMdomain by 2D and 3D NMR experiments together with simula-ted annealing calculations. Our data revealed that the structureof DLC2 SAM is slightly different from other known SAMdomains and adapts a monomeric structure with four alpha heli-ces in solution. Consistent with the structural data, cross-linkingexperiment also suggested that DLC SAM exists in predomin-antly monomeric form in vitro. On the other hand, co-immuno-precipitation experiments suggested that the DLC2 protein ishomodimerized. Analysis of the deletion mutants revealed thatthe homodimerization is not mediated by the SAM domain, butthrough a distinct region on the DLC2 protein.-
dc.languageengen_HK
dc.publisherBlackwell-
dc.relation.ispartofThe FEBS Journalen_HK
dc.titleHomodimerization of the deleted in liver cancer 2 (DLC2) is not mediated by the SAM domainen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailFung, KL: klfung@hkucc.hku.hken_HK
dc.identifier.emailChing, YP: ypching@hkucc.hku.hken_HK
dc.identifier.emailNg, IOL: iolng@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.emailSun, H: hsun@hku.hken_HK
dc.identifier.authorityChing, YP=rp00469en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authoritySun, H=rp00777en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1742-4658.2005.4739_7.x-
dc.identifier.hkuros105821en_HK

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