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Article: Antimorphic PV.1 causes secondary axis by inducing ectopic organizer

TitleAntimorphic PV.1 causes secondary axis by inducing ectopic organizer
Authors
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. 292 n. 4, p. 1081-1086 How to Cite?
AbstractXenopus homeobox gene, PV.1 ventralizes activin-induced dorsal mesoderm and inhibits neuralization of ectoderm in animal cap when overexpressed. Here we generated PV.1/engrailed fusion construct (N-PV1-EnR) to perform loss-of-function study for this transcription factor. N-PV1-EnR showed an extremely antimorphic effect, causing a partial secondary embryonic axis when expressed at ventral marginal zone of blastula. In ventral marginal zone cells, this chimeric protein induced organizer genes and suppressed ventral markers mimicking those effects reported for dominant negative BMP-4 receptor (DNBR). Moreover, N-PV1-EnR rescued the ventralized embryos caused by the ectopic dorsal expression of PV.1 but not by that of Xvent-2. These results suggested that PV.1 functions at downstream of BMP-4 as a ventralizing effector which acts separately from Xvent-2 and the dominant negative effect gained by this specific mutant is applicable for the further studies of BMP-4 downstream pathway.
Persistent Identifierhttp://hdl.handle.net/10722/222839
ISSN
2015 Impact Factor: 2.371
2015 SCImago Journal Rankings: 1.152

 

DC FieldValueLanguage
dc.contributor.authorHwang, YS-
dc.contributor.authorSeo, JJ-
dc.contributor.authorCha, SW-
dc.contributor.authorLee, HS-
dc.contributor.authorLee, SY-
dc.contributor.authorRoh, DH-
dc.contributor.authorKung, HF-
dc.contributor.authorKim, J-
dc.contributor.authorPark, MJ-
dc.date.accessioned2016-02-04T02:55:43Z-
dc.date.available2016-02-04T02:55:43Z-
dc.date.issued2002-
dc.identifier.citationBiochemical and Biophysical Research Communications, 2002, v. 292 n. 4, p. 1081-1086-
dc.identifier.issn0006-291X-
dc.identifier.urihttp://hdl.handle.net/10722/222839-
dc.description.abstractXenopus homeobox gene, PV.1 ventralizes activin-induced dorsal mesoderm and inhibits neuralization of ectoderm in animal cap when overexpressed. Here we generated PV.1/engrailed fusion construct (N-PV1-EnR) to perform loss-of-function study for this transcription factor. N-PV1-EnR showed an extremely antimorphic effect, causing a partial secondary embryonic axis when expressed at ventral marginal zone of blastula. In ventral marginal zone cells, this chimeric protein induced organizer genes and suppressed ventral markers mimicking those effects reported for dominant negative BMP-4 receptor (DNBR). Moreover, N-PV1-EnR rescued the ventralized embryos caused by the ectopic dorsal expression of PV.1 but not by that of Xvent-2. These results suggested that PV.1 functions at downstream of BMP-4 as a ventralizing effector which acts separately from Xvent-2 and the dominant negative effect gained by this specific mutant is applicable for the further studies of BMP-4 downstream pathway.-
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description-
dc.relation.ispartofBiochemical and Biophysical Research Communications-
dc.rights© <2002>. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/-
dc.subject.meshBody Patterning - drug effects - physiology-
dc.subject.meshHomeodomain Proteins - antagonists & inhibitors - genetics - pharmacology-
dc.subject.meshOrganizers, Embryonic - drug effects - metabolism-
dc.subject.meshProtein-Serine-Threonine Kinases-
dc.subject.meshReceptors, Growth Factor-
dc.titleAntimorphic PV.1 causes secondary axis by inducing ectopic organizer-
dc.typeArticle-
dc.identifier.emailKung, HF: hkung@hkucc.hku.hk-
dc.identifier.doi10.1006/bbrc.2002.6740-
dc.identifier.pmid11944926-
dc.identifier.hkuros79069-
dc.identifier.volume292-
dc.identifier.issue4-
dc.identifier.spage1081-
dc.identifier.epage1086-
dc.publisher.placeUnited States-

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