title: Expression of OASIS, a CREB/ATF family transcription factor, in CNS lesion and its transcriptional activity.
abstract: We reported the expression patterns of a novel member of the CREB/ATF family, OASIS, in central nervous system (CNS) lesions and its transcriptional activity. OASIS gene expression was upregulated in the stab-injured spinal cord. Double labeling experiments revealed that the distribution of OASIS mRNA-positive cells overlapped with a population of GFAP-immunoreactive cells. This finding suggested that OASIS might regulate expression of important downstream molecules in certain subset of the reactive astrocytes (e.g. inhibitory substances in injured brain). In gel shift assays, OASIS was able to specifically bind to CRE as CREB family members were. We then examined transcriptional activity of full-length OASIS with GAL4-UAS-luciferase reporter assay in COS7 cells. OASIS protein activated transcription, but did not inhibit basal transcription driven by AdML promoter. To determine critical portion(s) of the OASIS protein in transcriptional activation, we examined the activity of various deletion constructs of OASIS gene. The assay revealed that a strong transcriptional activation domain lay in the N-terminal region where acidic amino acids clustered and a possible repression domain, which had not been reported for other CREB/ATF family members, lay in the more C-terminal region. We therefore proposed that OASIS protein positively regulated gene transcription in a subset of reactive astrocytes, and thereby influenced the reaction of injured CNS tissues.
authors.affiliation: Department of Cell Science, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, Japan.
authors.forename: Takuya
authors.initials: T
authors.lastname: Nikaido
authors.forename: Ken
authors.initials: K
authors.lastname: Iseki
authors.forename: Tetsuji
authors.initials: T
authors.lastname: Mori
authors.forename: Hiromi
authors.initials: H
authors.lastname: Takaki
authors.forename: Sachihiko
authors.initials: S
authors.lastname: Yokoya
authors.forename: Seita
authors.initials: S
authors.lastname: Hagino
authors.forename: Junko
authors.initials: J
authors.lastname: Takeda
authors.forename: Yuxiang
authors.initials: Y
authors.lastname: Zhang
authors.forename: Mayumi
authors.initials: M
authors.lastname: Takeuchi
authors.forename: Shin-ichi
authors.initials: S
authors.lastname: Kikuchi
authors.forename: Akio
authors.initials: A
authors.lastname: Wanaka
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000502:physiology; D002490:Central Nervous System / Q000473:pathology* / Q000502:physiology*; D016384:Consensus Sequence; D017362:Cyclic AMP Response Element-Binding Protein; D005786:Gene Expression Regulation; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D011485:Protein Binding; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D013116:Spinal Cord / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*; D014158:Transcription, Genetic
chemical_list: C119923:Creb3l1 protein, mouse; D017362:Cyclic AMP Response Element-Binding Protein; D005904:Glial Fibrillary Acidic Protein; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger; D011993:Recombinant Fusion Proteins; D014157:Transcription Factors