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Conference Paper: Down-regulation of two novel genes by hypoxic-ischaemic encephalopathy in neonatal mouse

TitleDown-regulation of two novel genes by hypoxic-ischaemic encephalopathy in neonatal mouse
Authors
KeywordsHypoxia
Ischemia
Gene expression
Apoptosis
Issue Date2001
PublisherSociety for Neuroscience.
Citation
The 2001 Annual Meeting of the Society for Neuroscience (SfN) - Neuroscience 2001, San Diego, CA., 10-15 November 2001. How to Cite?
AbstractHypoxic-ischaemic encephalopathy (HIE) is a major cause of neurologic deficit in neonates. Apoptosis is a key event triggered by HIE. To elucidate the cellular and molecular basis of HI-induced apoptosis, we adopted differential gene expression studies in 7-day-old C57Bl/6 mice HIE model, with permanent unilateral common carotid artery ligation plus 30 minutes of 8% O2/92% N2 hypoxia. Subtractive hybridization carried out between ipsilateral (to ligation) and contralateral brain hemispheres led to isolation of 87 differentially expressed genes in response to the HIE insult (43 and 44 are up- and down-regulated, respectively). Sequences of these products revealed about a quarter of them were homologous to known mouse genes and one-third were homologous to mouse EST sequences only and the other share various degree of homologies with cDNA of other species. HIE-Down-regulated gene (HID)-44 and -1 were two with partial sequences homologous with EST sequences. Northern analysis showed that the expression of these two genes were inhibited by 3 hours after HIE insult. Analysis of HID-44 showed that its mRNA was a 6-kb brain-specific transcript. However, mRNA of HID-1 was a 2-kb transcript expressed in most tissues, highest in testis followed by thymus and brain. Full-length cDNA of HID-44 and HID-1 genes were isolated from a mouse brain cDNA library and characterization of the full-length genes and their alteration in expression by HIE are currently ongoing. . Supported by Hong Kong Research Grant Council Fund HKU7249/99M to PT Cheung, HK Yip and MH Sham
DescriptionPresentation no. 203.12
Persistent Identifierhttp://hdl.handle.net/10722/95159
ISSN

 

DC FieldValueLanguage
dc.contributor.authorLeung, TWCen_HK
dc.contributor.authorCheung, HWen_HK
dc.contributor.authorTse, LYen_HK
dc.contributor.authorYip, HKFen_HK
dc.contributor.authorSham, MHen_HK
dc.contributor.authorCheung, PTen_HK
dc.date.accessioned2010-09-25T15:53:29Z-
dc.date.available2010-09-25T15:53:29Z-
dc.date.issued2001en_HK
dc.identifier.citationThe 2001 Annual Meeting of the Society for Neuroscience (SfN) - Neuroscience 2001, San Diego, CA., 10-15 November 2001.-
dc.identifier.issn0190-5295-
dc.identifier.urihttp://hdl.handle.net/10722/95159-
dc.descriptionPresentation no. 203.12-
dc.description.abstractHypoxic-ischaemic encephalopathy (HIE) is a major cause of neurologic deficit in neonates. Apoptosis is a key event triggered by HIE. To elucidate the cellular and molecular basis of HI-induced apoptosis, we adopted differential gene expression studies in 7-day-old C57Bl/6 mice HIE model, with permanent unilateral common carotid artery ligation plus 30 minutes of 8% O2/92% N2 hypoxia. Subtractive hybridization carried out between ipsilateral (to ligation) and contralateral brain hemispheres led to isolation of 87 differentially expressed genes in response to the HIE insult (43 and 44 are up- and down-regulated, respectively). Sequences of these products revealed about a quarter of them were homologous to known mouse genes and one-third were homologous to mouse EST sequences only and the other share various degree of homologies with cDNA of other species. HIE-Down-regulated gene (HID)-44 and -1 were two with partial sequences homologous with EST sequences. Northern analysis showed that the expression of these two genes were inhibited by 3 hours after HIE insult. Analysis of HID-44 showed that its mRNA was a 6-kb brain-specific transcript. However, mRNA of HID-1 was a 2-kb transcript expressed in most tissues, highest in testis followed by thymus and brain. Full-length cDNA of HID-44 and HID-1 genes were isolated from a mouse brain cDNA library and characterization of the full-length genes and their alteration in expression by HIE are currently ongoing. . Supported by Hong Kong Research Grant Council Fund HKU7249/99M to PT Cheung, HK Yip and MH Sham-
dc.languageengen_HK
dc.publisherSociety for Neuroscience.-
dc.relation.ispartofNeuroscience 2001en_HK
dc.subjectHypoxia-
dc.subjectIschemia-
dc.subjectGene expression-
dc.subjectApoptosis-
dc.titleDown-regulation of two novel genes by hypoxic-ischaemic encephalopathy in neonatal mouseen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailTse, LY: ly_tse@yahoo.comen_HK
dc.identifier.emailYip, HKF: hkfyip@hku.hken_HK
dc.identifier.emailSham, MH: mhsham@hkucc.hku.hken_HK
dc.identifier.emailCheung, PT: ptcheung@hkucc.hku.hken_HK
dc.identifier.authoritySham, MH=rp00380en_HK
dc.identifier.authorityCheung, PT=rp00351en_HK
dc.identifier.hkuros109235en_HK

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