Transient expression of Nxf, a bHLH–PAS transactivator induced by neuronal preconditioning, confers neuroprotection in cultured cells

Hester, Ian; McKee, Sarah; Pelletier, Phillip; Thompson, C. S.; Storbeck, Christopher J.; Mears, Alan J.; Schulz, Jörg B.; Hakim, Antoine A.; Sabourin, Luc A.

doi:10.1016/j.brainres.2006.11.083

Cited by 26 publications

(37 citation statements)

References 42 publications

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“…Consequently, Dys/Tgo should bind an NCGTG sequence. This is consistent with known Nxf/Arnt/Arnt2 binding sites of ACGTG, CGGTG, GCGTG, and TCGTG (7,9,10). The Drosophila Dys basic region (NKSTKGASKMRR) has three amino acid substitutions compared with human Nxf (YRSTK-GASKARR; differences are underlined), which could cause changes in DNA binding specificities between the two proteins.…”

Section: Dys/tgo Activates Transcription and Bindssupporting

confidence: 60%

“…This is particularly evident in the embryonic leading edge cells, in which no other bHLH-PAS protein besides Dys is known to be present. Second, the Nxf protein, which is the mammalian Dys ortholog, dimerizes with Arnt and Arnt2, the mammalian Tgo orthologs (7,10). To determine whether Drosophila Dys/Tgo heterodimerization occurs, biochemical protein binding assays, in vivo genetic and misexpression experiments, and cell culture-based molecular assays were performed.…”

Section: Dys Forms a Heterodimer With Tgo Inmentioning

confidence: 99%

“…Section 1734 solely to indicate this fact. 1 To whom correspondence should be addressed: Fordham Hall CB# 3280, Chapel Hill, NC 27599-3280. aromatic hydrocarbon nuclear translocator (Arnt) protein, the mammalian Tgo ortholog, and bound ACGTG, GCGTG, and TCGTG sequences (7,9,10). Which of these sequences is utilized in vivo to control gene expression by Nxf is unknown.…”

mentioning

confidence: 99%

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Transcriptional Specificity of Drosophila Dysfusion and the Control of Tracheal Fusion Cell Gene Expression

Jiang

Crews

2007

Journal of Biological Chemistry

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The Drosophila Dysfusion basic-helix-loop-helix-PAS (bHLH-PAS) protein controls the transcription of genes that mediate tracheal fusion. Dysfusion is highly related to the mammalian Nxf protein that has been implicated in nervous system gene regulation. Toward the goal of understanding how Dysfusion controls fusion cell gene expression, the biochemical properties of Dysfusion were investigated using protein interaction experiments, cell culture-based transcription assays, and in vivo transgenic analyses. Dysfusion dimerizes with the Tango bHLH-PAS protein, and together they act as a DNA binding transcriptional activator. Dysfusion/Tango binds multiple NCGTG binding sites, with the following preference: TCGTG > GCGTG > ACGTG > CCGTG. This binding site promiscuity differs from the restricted binding site preferences of other bHLH-PAS/Tango heterodimers. However, it is identical to the binding site preferences of mammalian Nxf/Arnt, indicating that the specificity is evolutionarily conserved. Germ line transformation experiments using a fragment of the CG13196 Dysfusion target gene allowed identification of a fusion cell enhancer. Experiments in which NCGTG sites were mutated individually and in combination revealed that TCGTG sites were required for fusion cell expression but that the single ACGTG and GCGTG sites present were not. Finally, a reporter transgene containing four tandemly arranged TCGTG elements has strong expression in tracheal fusion cells. Transgenic misexpression of dysfusion further revealed that Dysfusion has the ability to activate transcription in multiple cell types, although it does this most effectively in tracheal cells and can only function at midembryogenesis and later.

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Section: Dys/tgo Activates Transcription and Bindssupporting

confidence: 60%

Section: Dys Forms a Heterodimer With Tgo Inmentioning

confidence: 99%

mentioning

confidence: 99%

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Transcriptional Specificity of Drosophila Dysfusion and the Control of Tracheal Fusion Cell Gene Expression

Jiang

Crews

2007

Journal of Biological Chemistry

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“…This group included netrin-1, which plays a role in axon guidance. The second group included genes related to networks involved in cytoplasmic extension, enervation, and Schwann cell function (Table S3) (30)(31)(32)(33)(34)(35). TNF is more tightly connected with the first group at the more fundamental level of transcriptional control related to NF-B, compared with the cellular effectors represented in the second group, suggesting that TNF is a network node that intersects with these 2 groups.…”

Section: Tnf Is a Network Hub In Peripheral Nerve Development That Linksmentioning

confidence: 99%

Maximum-entropy network analysis reveals a role for tumor necrosis factor in peripheral nerve development and function

Dhadialla

Ohiorhenuan²,

Cohen³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

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Gene regulatory interactions that shape developmental processes can often can be inferred from microarray analysis of gene expression, but most computational methods used require extensive datasets that can be difficult to generate. Here, we show that maximum-entropy network analysis allows extraction of genetic interactions from limited microarray datasets. Maximum-entropy networks indicated that the inflammatory cytokine TNF-α plays a pivotal role in Schwann cell–axon interactions, and these data suggested that TNF mediates its effects by orchestrating cytoplasmic movement and axon guidance. In vivo and in vitro experiments confirmed these predictions, showing that Schwann cells in TNF −/− peripheral sensory bundles fail to envelop axons efficiently, and that recombinant TNF can partially correct these defects. These data demonstrate the power of maximum-entropy network-based methods for analysis of microarray data, and they indicate that TNF-α plays a direct role in Schwann cell–axon communication.

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“…Grabb and Choi (1999) and Grabb et al (2002) produced a mixed neuronal and glial cortical culture, induced preconditioning with a 15-min exposure to 45 mM KCl, and this treatment protected the cells against a subsequent insult (10-min application of 1 mM glutamate) applied 24 h later. Hester et al (2007) preconditioned the DRG/neuroblastoma hybrid cell line F-11 and cerebellar granule neurones (isolated from 7-to 9-day-old mice) with a 90 min exposure to 50 mM KCl, and assessed the cellular viability to an acute insult (3-h application of 1 mM potassium cyanide) 24 h later.…”

Section: Introductionmentioning

confidence: 99%

A new model for the study of high-K+-induced preconditioning in cultured neurones: Role of N-methyl-d-aspartate and α7-nicotinic acetylcholine receptors

Rensburg

Errington

Ennaceur

et al. 2009

Journal of Neuroscience Methods

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Transient expression of Nxf, a bHLH–PAS transactivator induced by neuronal preconditioning, confers neuroprotection in cultured cells

Cited by 26 publications

References 42 publications

Transcriptional Specificity of Drosophila Dysfusion and the Control of Tracheal Fusion Cell Gene Expression

Transcriptional Specificity of Drosophila Dysfusion and the Control of Tracheal Fusion Cell Gene Expression

Maximum-entropy network analysis reveals a role for tumor necrosis factor in peripheral nerve development and function

A new model for the study of high-K+-induced preconditioning in cultured neurones: Role of N-methyl-d-aspartate and α7-nicotinic acetylcholine receptors

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