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Conference Paper: Over-expression of a Dominant Negative Form of OREBP in the Lens Causes Congenital Cataract

TitleOver-expression of a Dominant Negative Form of OREBP in the Lens Causes Congenital Cataract
Authors
Issue Date2002
PublisherAssociation for Research in Vision and Ophthalmology
Citation
Association for Research in Vision and Ophthalmology Annual Meeting, Fort Lauderdale, FL, 5-10 May 2002. In Investigative Ophthalmology & Visual Science, 2002, v. 43 n. 13, Abstract no. 3585 How to Cite?
AbstractPurpose:To determine the role of a newly discovered osmotic response element binding protein (OREBP) in lens development and lens osmoregulation. OREBP is a transcription factor that regulates the expression of genes involved in osmoregulation. Methods:A dominant-negative form of OREBP that lacks the C-terminal transactivation domain was placed under the transcriptional control of the aA crystalline promoter. The transgene construct was used to create transgenic mouse lines. Lens morphology was determined by slit lamp examination, tissue sectioning and microscopy. Levels of mRNA of the lens were analyzed by real-time quantitative PCR. Results:Several lines of transgenic mice over-expressing the dominant negative form of OREBP lens-specifically at various levels have been generated. In transgenic lines with moderate transgene expression, morphological analysis showed that their lenses developed congenital pulverulent cataract. The higher expressing transgenic mouse lines showed liquefication of lens fibers. Analysis of aldose reductase mRNA indicates that lens osmoregulatory mechanism is down regulated in the transgenic mice. Conclusion:OREBP appeared to be important for lens development although the role is not clear at present.
Persistent Identifierhttp://hdl.handle.net/10722/108788
ISSN

 

DC FieldValueLanguage
dc.contributor.authorYang, JYen_HK
dc.contributor.authorKo, CBen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorChung, SSMen_HK
dc.date.accessioned2010-09-26T00:54:28Z-
dc.date.available2010-09-26T00:54:28Z-
dc.date.issued2002en_HK
dc.identifier.citationAssociation for Research in Vision and Ophthalmology Annual Meeting, Fort Lauderdale, FL, 5-10 May 2002. In Investigative Ophthalmology & Visual Science, 2002, v. 43 n. 13, Abstract no. 3585-
dc.identifier.issn1552-5783-
dc.identifier.urihttp://hdl.handle.net/10722/108788-
dc.description.abstractPurpose:To determine the role of a newly discovered osmotic response element binding protein (OREBP) in lens development and lens osmoregulation. OREBP is a transcription factor that regulates the expression of genes involved in osmoregulation. Methods:A dominant-negative form of OREBP that lacks the C-terminal transactivation domain was placed under the transcriptional control of the aA crystalline promoter. The transgene construct was used to create transgenic mouse lines. Lens morphology was determined by slit lamp examination, tissue sectioning and microscopy. Levels of mRNA of the lens were analyzed by real-time quantitative PCR. Results:Several lines of transgenic mice over-expressing the dominant negative form of OREBP lens-specifically at various levels have been generated. In transgenic lines with moderate transgene expression, morphological analysis showed that their lenses developed congenital pulverulent cataract. The higher expressing transgenic mouse lines showed liquefication of lens fibers. Analysis of aldose reductase mRNA indicates that lens osmoregulatory mechanism is down regulated in the transgenic mice. Conclusion:OREBP appeared to be important for lens development although the role is not clear at present.-
dc.languageengen_HK
dc.publisherAssociation for Research in Vision and Ophthalmology-
dc.relation.ispartofInvestigative Ophthalmology & Visual Scienceen_HK
dc.titleOver-expression of a Dominant Negative Form of OREBP in the Lens Causes Congenital Cataracten_HK
dc.typeConference_Paperen_HK
dc.identifier.emailKo, CB: cbko@hkucc.hku.hken_HK
dc.identifier.emailWang, Y: ywang3@hkucc.hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.hkuros68669en_HK

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