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Article: Induction of apoptosis and inhibition of cell growth by developmental regulator hTBX5

TitleInduction of apoptosis and inhibition of cell growth by developmental regulator hTBX5
Authors
KeywordsApoptosis
Growth inhibition
T box gene
Tbx5
Issue Date2002
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
Citation
Biochemical And Biophysical Research Communications, 2002, v. 297 n. 2, p. 185-192 How to Cite?
AbstractT box (Tbx) genes are a large family of transcription regulators that play critical roles in invertebrate and vertebrate development. Mutations in Tbx5 gene have been found to cause Holt-Oram syndrome (HOS) in humans. Partial dysfunction of TBX5 in mouse also causes HOS phenotype. Little is known about its molecular and cellular mechanism. Here, we report that ectopic expression of TBX5 inhibited colony formation, induced apoptosis, and decreased the growth rate of cells. The two point mutations in T domain and a truncated mutation in C-terminal found in human HOS patients produced TBX5 mutant proteins with a significantly reduction of colony suppression activity. Deletion of the DNA-binding domain, however, nearly completely abrogated its ability to suppress colony formation. These results reveal TBX5 as a new regulator of apoptosis and cell growth, suggesting a possible mechanism for Holt-Oram syndrome, and a potential reagent for controlling tumor growth. © 2002 Elsevier Science (USA). All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/87996
ISSN
2015 Impact Factor: 2.371
2015 SCImago Journal Rankings: 1.152
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHe, MLen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorPeng, Yen_HK
dc.contributor.authorJin, Den_HK
dc.contributor.authorDu, Den_HK
dc.contributor.authorWu, Jen_HK
dc.contributor.authorLu, Pen_HK
dc.contributor.authorLin, MCen_HK
dc.contributor.authorKung, HFen_HK
dc.date.accessioned2010-09-06T09:37:17Z-
dc.date.available2010-09-06T09:37:17Z-
dc.date.issued2002en_HK
dc.identifier.citationBiochemical And Biophysical Research Communications, 2002, v. 297 n. 2, p. 185-192en_HK
dc.identifier.issn0006-291Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/87996-
dc.description.abstractT box (Tbx) genes are a large family of transcription regulators that play critical roles in invertebrate and vertebrate development. Mutations in Tbx5 gene have been found to cause Holt-Oram syndrome (HOS) in humans. Partial dysfunction of TBX5 in mouse also causes HOS phenotype. Little is known about its molecular and cellular mechanism. Here, we report that ectopic expression of TBX5 inhibited colony formation, induced apoptosis, and decreased the growth rate of cells. The two point mutations in T domain and a truncated mutation in C-terminal found in human HOS patients produced TBX5 mutant proteins with a significantly reduction of colony suppression activity. Deletion of the DNA-binding domain, however, nearly completely abrogated its ability to suppress colony formation. These results reveal TBX5 as a new regulator of apoptosis and cell growth, suggesting a possible mechanism for Holt-Oram syndrome, and a potential reagent for controlling tumor growth. © 2002 Elsevier Science (USA). All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/descriptionen_HK
dc.relation.ispartofBiochemical and Biophysical Research Communicationsen_HK
dc.subjectApoptosisen_HK
dc.subjectGrowth inhibitionen_HK
dc.subjectT box geneen_HK
dc.subjectTbx5en_HK
dc.titleInduction of apoptosis and inhibition of cell growth by developmental regulator hTBX5en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-291X&volume=297&spage=185&epage=192&date=2002&atitle=Induction+of+apoptosis+and+inhibition+of+cell+growth+by+developmental+regulator+hTBX5en_HK
dc.identifier.emailLin, MC:mcllin@hkucc.hku.hken_HK
dc.identifier.authorityLin, MC=rp00746en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0006-291X(02)02142-3en_HK
dc.identifier.pmid12237100-
dc.identifier.scopuseid_2-s2.0-0036403185en_HK
dc.identifier.hkuros79018en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036403185&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume297en_HK
dc.identifier.issue2en_HK
dc.identifier.spage185en_HK
dc.identifier.epage192en_HK
dc.identifier.isiWOS:000178380400004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHe, ML=35080389700en_HK
dc.identifier.scopusauthoridChen, Y=7601425634en_HK
dc.identifier.scopusauthoridPeng, Y=7403419265en_HK
dc.identifier.scopusauthoridJin, D=15752969300en_HK
dc.identifier.scopusauthoridDu, D=55221634200en_HK
dc.identifier.scopusauthoridWu, J=7409250054en_HK
dc.identifier.scopusauthoridLu, P=55041426400en_HK
dc.identifier.scopusauthoridLin, MC=7404816359en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK

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