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Article: CREB3 subfamily transcription factors are not created equal: Recent insights from global analyses and animal models

TitleCREB3 subfamily transcription factors are not created equal: Recent insights from global analyses and animal models
Authors
Issue Date2011
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.cellandbioscience.com
Citation
Cell And Bioscience, 2011, v. 1 n. 1 How to Cite?
AbstractThe CREB3 subfamily of membrane-bound bZIP transcription factors has five members in mammals known as CREB3 and CREB3L1-L4. One current model suggests that CREB3 subfamily transcription factors are similar to ATF6 in regulated intramembrane proteolysis and transcriptional activation. Particularly, they were all thought to be proteolytically activated in response to endoplasmic reticulum (ER) stress to stimulate genes that are involved in unfolded protein response (UPR). Although the physiological inducers of their proteolytic activation remain to be identified, recent findings from microarray analyses, RNAi screens and gene knockouts not only demonstrated their critical roles in regulating development, metabolism, secretion, survival and tumorigenesis, but also revealed cell type-specific patterns in the activation of their target genes. Members of the CREB3 subfamily show differential activity despite their structural similarity. The spectrum of their biological function expands beyond ER stress and UPR. Further analyses are required to elucidate the mechanism of their proteolytic activation and the molecular basis of their target recognition. © 2011 Chan et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/138963
ISSN
2015 Impact Factor: 2.883
2015 SCImago Journal Rankings: 1.593
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, CPen_HK
dc.contributor.authorKok, KHen_HK
dc.contributor.authorJin, DYen_HK
dc.date.accessioned2011-09-23T05:43:11Z-
dc.date.available2011-09-23T05:43:11Z-
dc.date.issued2011en_HK
dc.identifier.citationCell And Bioscience, 2011, v. 1 n. 1en_HK
dc.identifier.issn2045-3701en_HK
dc.identifier.urihttp://hdl.handle.net/10722/138963-
dc.description.abstractThe CREB3 subfamily of membrane-bound bZIP transcription factors has five members in mammals known as CREB3 and CREB3L1-L4. One current model suggests that CREB3 subfamily transcription factors are similar to ATF6 in regulated intramembrane proteolysis and transcriptional activation. Particularly, they were all thought to be proteolytically activated in response to endoplasmic reticulum (ER) stress to stimulate genes that are involved in unfolded protein response (UPR). Although the physiological inducers of their proteolytic activation remain to be identified, recent findings from microarray analyses, RNAi screens and gene knockouts not only demonstrated their critical roles in regulating development, metabolism, secretion, survival and tumorigenesis, but also revealed cell type-specific patterns in the activation of their target genes. Members of the CREB3 subfamily show differential activity despite their structural similarity. The spectrum of their biological function expands beyond ER stress and UPR. Further analyses are required to elucidate the mechanism of their proteolytic activation and the molecular basis of their target recognition. © 2011 Chan et al; licensee BioMed Central Ltd.en_HK
dc.languageengen_US
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.cellandbioscience.comen_HK
dc.relation.ispartofCell and Bioscienceen_HK
dc.rightsCell & Bioscience. Copyright © BioMed Central Ltd.-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleCREB3 subfamily transcription factors are not created equal: Recent insights from global analyses and animal modelsen_HK
dc.typeArticleen_HK
dc.identifier.emailKok, KH:khkok@hku.hken_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.authorityKok, KH=rp01455en_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/2045-3701-1-6en_HK
dc.identifier.pmid21711675-
dc.identifier.pmcidPMC3116243-
dc.identifier.scopuseid_2-s2.0-80052899920en_HK
dc.identifier.hkuros193195en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80052899920&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume1en_HK
dc.identifier.issue1en_HK
dc.identifier.isiWOS:000307052200001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, CP=36193690700en_HK
dc.identifier.scopusauthoridKok, KH=7006862631en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.citeulike10010940-

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