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Article: MADR2 maps to 18q21 and encodes a TGFβ-regulated MAD-related protein that is functionally mutated in colorectal carcinoma

TitleMADR2 maps to 18q21 and encodes a TGFβ-regulated MAD-related protein that is functionally mutated in colorectal carcinoma
Authors
Issue Date1996
PublisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/cell
Citation
Cell, 1996, v. 86 n. 4, p. 543-552 How to Cite?
AbstractThe MAD-related (MADR) family of proteins are essential components in the signaling pathways of serine/threonine kinase receptors for the transforming growth factor β (TGFβ) superfamily. We demonstrate that MADR2 is specifically regulated by TGFβ and not bone morphogenetic proteins. The gene for MADR2 was found to reside on chromosome 18q21, near DPC4, another MADR protein implicated in pancreatic cancer. Mutational analysis of MADR2 in sporadic tumors identified four missense mutations in colorectal carcinomas, two of which display a loss of heterozygosity. Biochemical and functional analysis of three of these demonstrates that the mutations are inactivating. These findings suggest that MADR2 is a tumor suppressor and that mutations acquired in colorectal carcinomas may function to disrupt TGFβ signaling.
Persistent Identifierhttp://hdl.handle.net/10722/44305
ISSN
2015 Impact Factor: 28.71
2015 SCImago Journal Rankings: 28.188
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorEppert, Ken_HK
dc.contributor.authorScherer, SWen_HK
dc.contributor.authorOzcelik, Hen_HK
dc.contributor.authorPirone, Ren_HK
dc.contributor.authorHoodless, Pen_HK
dc.contributor.authorKim, Hen_HK
dc.contributor.authorTsui, LCen_HK
dc.contributor.authorBapat, Ben_HK
dc.contributor.authorGallinger, Sen_HK
dc.contributor.authorAndrulis, ILen_HK
dc.contributor.authorThomsen, GHen_HK
dc.contributor.authorWrana, JLen_HK
dc.contributor.authorAttisano, Len_HK
dc.date.accessioned2007-09-12T03:51:02Z-
dc.date.available2007-09-12T03:51:02Z-
dc.date.issued1996en_HK
dc.identifier.citationCell, 1996, v. 86 n. 4, p. 543-552en_HK
dc.identifier.issn0092-8674en_HK
dc.identifier.urihttp://hdl.handle.net/10722/44305-
dc.description.abstractThe MAD-related (MADR) family of proteins are essential components in the signaling pathways of serine/threonine kinase receptors for the transforming growth factor β (TGFβ) superfamily. We demonstrate that MADR2 is specifically regulated by TGFβ and not bone morphogenetic proteins. The gene for MADR2 was found to reside on chromosome 18q21, near DPC4, another MADR protein implicated in pancreatic cancer. Mutational analysis of MADR2 in sporadic tumors identified four missense mutations in colorectal carcinomas, two of which display a loss of heterozygosity. Biochemical and functional analysis of three of these demonstrates that the mutations are inactivating. These findings suggest that MADR2 is a tumor suppressor and that mutations acquired in colorectal carcinomas may function to disrupt TGFβ signaling.en_HK
dc.languageengen_HK
dc.publisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/cellen_HK
dc.relation.ispartofCellen_HK
dc.rightsThis paper has been submitted to Cancer Cell for considerationen_HK
dc.subject.meshChromosomes, human, pair 18en_HK
dc.subject.meshColorectal neoplasms - geneticsen_HK
dc.subject.meshDna-binding proteins - geneticsen_HK
dc.subject.meshGenes, tumor suppressoren_HK
dc.subject.meshTrans-activatorsen_HK
dc.titleMADR2 maps to 18q21 and encodes a TGFβ-regulated MAD-related protein that is functionally mutated in colorectal carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0092-8674&volume=86&issue=4&spage=543&epage=552&date=1996&atitle=MADR2+maps+to+18q21+and+encodes+a+TGFbeta-regulated+MAD-related+protein+that+is+functionally+mutated+in+colorectal+carcinomaen_HK
dc.identifier.emailTsui, LC: tsuilc@hkucc.hku.hken_HK
dc.identifier.authorityTsui, LC=rp00058en_HK
dc.description.naturelink_to_subscribed_fulltexten_HK
dc.identifier.doi10.1016/S0092-8674(00)80128-2en_HK
dc.identifier.pmid8752209-
dc.identifier.scopuseid_2-s2.0-16044369574en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-16044369574&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume86en_HK
dc.identifier.issue4en_HK
dc.identifier.spage543en_HK
dc.identifier.epage552en_HK
dc.identifier.isiWOS:A1996VE23500005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridEppert, K=8307015700en_HK
dc.identifier.scopusauthoridScherer, SW=35374654500en_HK
dc.identifier.scopusauthoridOzcelik, H=7003751595en_HK
dc.identifier.scopusauthoridPirone, R=7004041562en_HK
dc.identifier.scopusauthoridHoodless, P=6602719972en_HK
dc.identifier.scopusauthoridKim, H=7410127763en_HK
dc.identifier.scopusauthoridTsui, LC=7102754167en_HK
dc.identifier.scopusauthoridBapat, B=7006372475en_HK
dc.identifier.scopusauthoridGallinger, S=34975072000en_HK
dc.identifier.scopusauthoridAndrulis, IL=7005655442en_HK
dc.identifier.scopusauthoridThomsen, GH=7006498441en_HK
dc.identifier.scopusauthoridWrana, JL=35413866700en_HK
dc.identifier.scopusauthoridAttisano, L=7005900387en_HK

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