The c-Jun transcription factor – bipotential mediator of neuronal death, survival and regeneration

Herdegen, Thomas; Skene, J. H. Pate; Bähr, Mathias

doi:10.1016/s0166-2236(96)01000-4

Cited by 479 publications

(354 citation statements)

References 66 publications

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“…Indeed, certain members of the Jun and Fos families may exert suppressive effects on viral transcription, as previously described with cAMP-responsive element (CRE)/ATF in Jurkat and HeLa cells (70). In support of this interpretation, it has been shown that a balance between ATF2 and c-Jun governs the choice between neuronal cell differentiation and triggering of an apoptotic program (71,72). Homo-or heterodimers of ATF2 can bind different DNA sites; in particular, ATF2 binds the CRE motif (73), whereas heterodimerization alters its binding, with remarkable differences in affinity among different CRE (74).…”

Section: Discussionmentioning

confidence: 62%

Pertussis Toxin B-Oligomer Suppresses IL-6 Induced HIV-1 and Chemokine Expression in Chronically Infected U1 Cells via Inhibition of Activator Protein 1

Rizzi

Crippa²,

Jeeninga

et al. 2006

The Journal of Immunology

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Pertussis toxin B-oligomer (PTX-B) inhibits HIV replication in T lymphocytes and monocyte-derived macrophages by interfering with multiple steps of the HIV life cycle. PTX-B prevents CCR5-dependent (R5) virus entry in a noncompetitive manner, and it also exerts suppressive effects on both R5- and CXCR4-dependent HIV expression at a less-characterized postentry level. We demonstrate in this study that PTX-B profoundly inhibits HIV expression in chronically infected promonocytic U1 cells stimulated with several cytokines and, particularly, the IL-6-mediated effect, a cytokine that triggers viral production in these cells independently of NF-κB activation. From U1 cells we have subcloned a cell line, named U1-CR1, with increased responsiveness to IL-6. In these cells, PTX-B neither down-regulated the IL-6R nor prevented IL-6 induced signaling in terms of STAT3 phosphorylation and DNA binding. In contrast, PTX-B inhibited AP-1 binding to target DNA and modified its composition with a proportional increases in FosB, Fra2, and ATF2. PTX-B inhibited IL-6-induced HIV-1 long-terminal repeat-driven transcription from A, C, E, and F viral subtypes, which contain functional AP-1 binding sites, but failed to inhibit transcription from subtypes B and D LTR devoid of these sites. In addition, PTX-B inhibited the secretion of IL-6-induced, AP-1-dependent genes, including urokinase-type plasminogen activator, CXCL8/IL-8, and CCL2/monocyte chemotactic protein-1. Thus, PTX-B suppression of IL-6 induced expression of HIV and cellular genes in chronically infected promonocytic cells is strongly correlated to inhibition of AP-1.

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Section: Discussionmentioning

confidence: 62%

Pertussis Toxin B-Oligomer Suppresses IL-6 Induced HIV-1 and Chemokine Expression in Chronically Infected U1 Cells via Inhibition of Activator Protein 1

Rizzi

Crippa²,

Jeeninga

et al. 2006

The Journal of Immunology

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“…Indeed, spontaneous neuronal death has been observed in other B-50/GAP-43-overexpressing transgenic mouse lines (Aigner et al, 1995). In addition, in several neuronal systems injury conditions leading to stronger B-50/ GAP-43 expression and regenerative processes are also associated with a more severe neuronal degeneration (Richardson et al, 1982;Misantone et al, 1984;Villegas-Perez et al, 1988;Bray and Aguayo, 1989;Doster et al, 1991;Tetzlaff et al, 1991Tetzlaff et al, , 1994Herdegen et al, 1997). This suggests that some relationship may link regenerative processes and degenerative phenomena in injured neurons.…”

Section: Transgenic Purkinje Cells Degenerate After Axotomy But Theymentioning

confidence: 98%

“…Although axon growth in the adult mammalian brain is primarily hampered by adverse environmental conditions, the success of regenerative processes is also dependent on the capability of injured neurons to express the intrinsic molecular machinery required for neurite elongation (for review, see Fawcett, 1992;Schwab and Bartholdi, 1996;Herdegen et al, 1997). The axon growth-associated gene program is thought to be inhibited in mature intact neurons, most likely through retrograde extrinsic influences (Skene, 1989(Skene, , 1992Smith and Skene, 1997).…”

Section: Abstract: Transgenic Mice; Axon Growth-associated Genes; L7mentioning

confidence: 99%

Targeted Overexpression of the Neurite Growth-Associated Protein B-50/GAP-43 in Cerebellar Purkinje Cells Induces Sprouting after Axotomy But Not Axon Regeneration into Growth-Permissive Transplants

et al. 1997

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B-50/GAP-43 is a nervous tissue-specific protein, the expression of which is associated with axon growth and regeneration. Its overexpression in transgenic mice produces spontaneous axonal sprouting and enhances induced remodeling in several neuron populations (Aigner et al., 1995;Holtmaat et al., 1995). We examined the capacity of this protein to increase the regenerative potential of injured adult central axons, by inducing targeted B-50/GAP-43 overexpression in Purkinje cells, which normally show poor regenerative capabilities. Thus, transgenic mice were produced in which B-50/GAP-43 overexpression was driven by the Purkinje cell-specific L7 promoter. Uninjured transgenic Purkinje cells displayed normal morphology, indicating that transgene expression does not modify the normal phenotype of these neurons. By contrast, after axotomy numerous transgenic Purkinje cells exhibited profuse sprouting along the axon and at its severed end. Nevertheless, despite these growth phenomena, which never occurred in wild-type mice, the severed transgenic axons were not able to regenerate, either spontaneously or into embryonic neural or Schwann cell grafts placed into the lesion site. Finally, although only a moderate Purkinje cell loss occurred in wild-type cerebella after axotomy, a considerable number of injured transgenic neurons degenerated, but they could be partially rescued by the different transplants placed into the lesion site. Thus, B-50/GAP-43 overexpression substantially modifies Purkinje cell response to axotomy, by inducing growth processes and decreasing their resistance to injury. However, the presence of this protein is not sufficient to enable these neurons to accomplish a full program of axon regeneration.

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“…C-Jun may play a role in a wide variety of phenomena including survival, differentiation, and neuronal regeneration (Herdegen et al, 1997). Recent evidence, wherein blocking c-Jun function has protected neurons from apoptosis, both in vitro (Estus et al, 1994;Ham et al, 1995) and in vivo (Behrens et al, 1999;Crocker et al, 2001), has specifically implicated c-Jun in apoptosis.…”

mentioning

confidence: 99%

C-jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis

Willaime‐Morawek¹,

Brami‐Cherrier²,

Mariani³

et al. 2003

Neuroscience

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The c-Jun transcription factor – bipotential mediator of neuronal death, survival and regeneration

Cited by 479 publications

References 66 publications

Pertussis Toxin B-Oligomer Suppresses IL-6 Induced HIV-1 and Chemokine Expression in Chronically Infected U1 Cells via Inhibition of Activator Protein 1

Pertussis Toxin B-Oligomer Suppresses IL-6 Induced HIV-1 and Chemokine Expression in Chronically Infected U1 Cells via Inhibition of Activator Protein 1

Targeted Overexpression of the Neurite Growth-Associated Protein B-50/GAP-43 in Cerebellar Purkinje Cells Induces Sprouting after Axotomy But Not Axon Regeneration into Growth-Permissive Transplants

C-jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis

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