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Conference Paper: Identification of 3' splicing variants of receptor tyrosine kinase encoding gene RET in mouse and expression study of RET splicing variants in developing mouse embryo

TitleIdentification of 3' splicing variants of receptor tyrosine kinase encoding gene RET in mouse and expression study of RET splicing variants in developing mouse embryo
Authors
Issue Date2000
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/cellbi
Academic Press.
Citation
The 7th International Congress of Cell Biology, Gold Coast, QLD., Australia, 24–28 September 2000. In Cell Biology International, 2000, v. 24 n. 12, p. 968 How to Cite?
AbstractHuman RET proto-oncogene is composed of 21 exons and encodes trans-membrane receptor tyrosine kinase. RET plays a crucial role in the development of peripheral nervous systems (PNS) and excretory system. Activating mutations of RET gene are responsible for familial multiple endocrine neoplasia and medullary thyroid carcinoma. On the other hand, inactivating mutations of RET gene cause PNS defects. Alternative splicing of sequence 3 of exon 19 of RET gene generates splicing variants. Translation of the 3 splicing variants generates several isoforms including RET9, RET43 and RET51. RET isoforms differ in their C-terminus and present distinct transforming activity in cell transfection. Differential expression of various RET isoforms were described in developing human kidney and in tumor cell lines. The mouse Ret gene was shown to contain only 20 exons and expression study of various 3 splicing variants of Ret gene in mouse is lacking. In order to study function of various Ret isoforms in mouse development, we identify the alternative spliced exon 21 in the mouse Ret gene and analyse the expression pattern of various splicing variants during mouse embryonic development. DNA sequencing of 3 end of the mouse Ret gene identified the presence of exon 21. The mouse exon 21 shares 71.7% similarity at the nucleotide level with the respective exon in human RET gene. Expression of various 3 splicing variants of Ret gene in developing mouse embryos was analysed using RT-PCR with primers specific for exons 19, 20 and 21. We showed that the Ret 3 splicing variant equivalent of human RET51 encoding variant was the only predominant Ret transcript in the developing mouse embryos from 9.5 to 14.5 d.p.c. Differential expression of different Ret isoforms during mouse embryonic development suggesting that splicing of Ret gene is developmentally regulated and different Ret isoforms may have specific function in embryonic development. EMBR
Descriptionpp. 913-1021 entitled: Meeting Abstracts
Persistent Identifierhttp://hdl.handle.net/10722/96201
ISSN
2015 Impact Factor: 1.663
2015 SCImago Journal Rankings: 0.705

 

DC FieldValueLanguage
dc.contributor.authorSamy, ETen_HK
dc.contributor.authorSham, MHen_HK
dc.contributor.authorTam, PKHen_HK
dc.contributor.authorLui, VCHen_HK
dc.date.accessioned2010-09-25T16:26:30Z-
dc.date.available2010-09-25T16:26:30Z-
dc.date.issued2000en_HK
dc.identifier.citationThe 7th International Congress of Cell Biology, Gold Coast, QLD., Australia, 24–28 September 2000. In Cell Biology International, 2000, v. 24 n. 12, p. 968en_HK
dc.identifier.issn1065-6995en_HK
dc.identifier.urihttp://hdl.handle.net/10722/96201-
dc.descriptionpp. 913-1021 entitled: Meeting Abstracts-
dc.description.abstractHuman RET proto-oncogene is composed of 21 exons and encodes trans-membrane receptor tyrosine kinase. RET plays a crucial role in the development of peripheral nervous systems (PNS) and excretory system. Activating mutations of RET gene are responsible for familial multiple endocrine neoplasia and medullary thyroid carcinoma. On the other hand, inactivating mutations of RET gene cause PNS defects. Alternative splicing of sequence 3 of exon 19 of RET gene generates splicing variants. Translation of the 3 splicing variants generates several isoforms including RET9, RET43 and RET51. RET isoforms differ in their C-terminus and present distinct transforming activity in cell transfection. Differential expression of various RET isoforms were described in developing human kidney and in tumor cell lines. The mouse Ret gene was shown to contain only 20 exons and expression study of various 3 splicing variants of Ret gene in mouse is lacking. In order to study function of various Ret isoforms in mouse development, we identify the alternative spliced exon 21 in the mouse Ret gene and analyse the expression pattern of various splicing variants during mouse embryonic development. DNA sequencing of 3 end of the mouse Ret gene identified the presence of exon 21. The mouse exon 21 shares 71.7% similarity at the nucleotide level with the respective exon in human RET gene. Expression of various 3 splicing variants of Ret gene in developing mouse embryos was analysed using RT-PCR with primers specific for exons 19, 20 and 21. We showed that the Ret 3 splicing variant equivalent of human RET51 encoding variant was the only predominant Ret transcript in the developing mouse embryos from 9.5 to 14.5 d.p.c. Differential expression of different Ret isoforms during mouse embryonic development suggesting that splicing of Ret gene is developmentally regulated and different Ret isoforms may have specific function in embryonic development. EMBR-
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/cellbien_HK
dc.publisherAcademic Press.-
dc.relation.ispartofCell Biology Internationalen_HK
dc.titleIdentification of 3' splicing variants of receptor tyrosine kinase encoding gene RET in mouse and expression study of RET splicing variants in developing mouse embryoen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1065-6995&volume=24&issue=12&spage=968&epage=&date=2000&atitle=Identification+of+3%27+splicing+variants+of+receptor+tyrosine+kinase+encoding+gene+RET+in+mouse+and+expression+study+of+RET+splicing+variants+in+developing+mouse+embryoen_HK
dc.identifier.emailSham, MH: mhsham@hkucc.hku.hken_HK
dc.identifier.emailTam, PKH: paultam@hkucc.hku.hken_HK
dc.identifier.emailLui, VCH: vchlui@hkucc.hku.hken_HK
dc.identifier.authoritySham, MH=rp00380en_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.identifier.authorityLui, VCH=rp00363en_HK
dc.identifier.doi10.1006/cbir.2000.0671-
dc.identifier.hkuros59881en_HK
dc.identifier.volume24en_HK
dc.identifier.issue12en_HK
dc.identifier.spage968en_HK
dc.identifier.epage968-
dc.publisher.placeUnited Kingdom-

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