File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Overexpression of epidermal growth factor induced hypospermatogenesis in transgenic mice

TitleOverexpression of epidermal growth factor induced hypospermatogenesis in transgenic mice
Authors
Issue Date2000
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 2000, v. 275 n. 24, p. 18297-18301 How to Cite?
AbstractThe in vivo role of epidermal growth factor (EGF) is not well defined even though its effects on culture cells were well studied. To understand the developmental, physiological, and pathological roles of EGF, we have generated transgenic mice widely expressing human EGF with the use of the β- actin promoter. EGF and transforming growth factor α (TGFα) bind with equal affinity to the EGF receptor, a transmembrane tyrosine kinase, to trigger various biological responses. EGF and TGFα signaling are implicated in the development of the reproductive system. EGF also plays a physiological role in reproduction. Removal of the salivary gland in rodents, which reduces circulating EGF, reduces spermatogenesis, which can be corrected by EGF replacement. Here we show that in our transgenic males, only few post-meiosis II gametes were found, and the mice were sterile. This resembles a common cause of infertility in humans. Furthermore, the transgenic males had reduced serum testosterone. Our findings contrast the previous report on transgenic mice overexpressing TGFα in testis, which showed normal spermatogenesis. These data suggest that EGF is the active ligand for EGF receptor reported in germ cells, and proper EGF expression is important for completion of spermatogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/68104
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, RWCen_HK
dc.contributor.authorKwan, RWPen_HK
dc.contributor.authorMak, PHSen_HK
dc.contributor.authorMak, KKLen_HK
dc.contributor.authorSham, MHen_HK
dc.contributor.authorChan, SYen_HK
dc.date.accessioned2010-09-06T06:01:22Z-
dc.date.available2010-09-06T06:01:22Z-
dc.date.issued2000en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2000, v. 275 n. 24, p. 18297-18301en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68104-
dc.description.abstractThe in vivo role of epidermal growth factor (EGF) is not well defined even though its effects on culture cells were well studied. To understand the developmental, physiological, and pathological roles of EGF, we have generated transgenic mice widely expressing human EGF with the use of the β- actin promoter. EGF and transforming growth factor α (TGFα) bind with equal affinity to the EGF receptor, a transmembrane tyrosine kinase, to trigger various biological responses. EGF and TGFα signaling are implicated in the development of the reproductive system. EGF also plays a physiological role in reproduction. Removal of the salivary gland in rodents, which reduces circulating EGF, reduces spermatogenesis, which can be corrected by EGF replacement. Here we show that in our transgenic males, only few post-meiosis II gametes were found, and the mice were sterile. This resembles a common cause of infertility in humans. Furthermore, the transgenic males had reduced serum testosterone. Our findings contrast the previous report on transgenic mice overexpressing TGFα in testis, which showed normal spermatogenesis. These data suggest that EGF is the active ligand for EGF receptor reported in germ cells, and proper EGF expression is important for completion of spermatogenesis.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_HK
dc.relation.ispartofJournal of Biological Chemistryen_HK
dc.rightsJournal of Biological Chemistry. Copyright © American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshDNA - administration & dosageen_HK
dc.subject.meshEpidermal Growth Factor - genetics - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshMicroinjectionsen_HK
dc.subject.meshOligospermia - etiologyen_HK
dc.subject.meshReceptor, Epidermal Growth Factor - physiologyen_HK
dc.subject.meshSpermatogenesis - physiologyen_HK
dc.subject.meshSubmandibular Gland - chemistryen_HK
dc.subject.meshTestis - chemistryen_HK
dc.subject.meshTestosterone - blooden_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTransforming Growth Factor alpha - physiologyen_HK
dc.titleOverexpression of epidermal growth factor induced hypospermatogenesis in transgenic miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9258&volume=275&issue=24&spage=18297&epage=18301&date=2000&atitle=Overexpression+of+Epidermal+Growth+Factor+Induced+Hypospermatogenesis+in+Transgenic+Miceen_HK
dc.identifier.emailWong, RWC:fyoung@hkucc.hku.hken_HK
dc.identifier.emailSham, MH:mhsham@hkucc.hku.hken_HK
dc.identifier.emailChan, SY:sychan@hkucc.hku.hken_HK
dc.identifier.authorityWong, RWC=rp00038en_HK
dc.identifier.authoritySham, MH=rp00380en_HK
dc.identifier.authorityChan, SY=rp00356en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1074/jbc.M001965200en_HK
dc.identifier.pmid10748057-
dc.identifier.scopuseid_2-s2.0-0034674581en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034674581&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume275en_HK
dc.identifier.issue24en_HK
dc.identifier.spage18297en_HK
dc.identifier.epage18301en_HK
dc.identifier.isiWOS:000087659400054-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, RWC=7402127170en_HK
dc.identifier.scopusauthoridKwan, RWP=7004066556en_HK
dc.identifier.scopusauthoridMak, PHS=36877626400en_HK
dc.identifier.scopusauthoridMak, KKL=7102679897en_HK
dc.identifier.scopusauthoridSham, MH=7003729109en_HK
dc.identifier.scopusauthoridChan, SY=7404255082en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats