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GADD45γ Mediates the Activation of the p38 and JNK MAP Kinase Pathways and Cytokine Production in Effector TH1 Cells
Abstract
The p38 and JNK stress-activated MAPK signal transduction pathways are activated by T cell receptor (TCR) signaling and are required for IFN-gamma production by TH1 effector cells. Here, we show that the expression of GADD45gamma is induced during T cell activation and that the level of expression is higher in TH1 cells than in TH2 cells. TH1 cells from GADD45gamma(-/-) mice are severely compromised in their abilities to activate p38 and JNK in response to TCR signaling, produce much less IFN-gamma upon restimulation, and are deficient in activation-induced cell death (AICD). Additionally, GADD45gamma deficiencies caused reduced contact hypersensitivity in mice. Thus, GADD45gamma mediates activation of the p38 and JNK pathways and effector function of TH1 cells.
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“and that dominant negative Rac1N17 almost completely suppresses cytokine release by activated Th1 cells.”
From The Hematopoiesis-Specific GTP-Binding Protein RhoH Is GTPase Deficient and Modulates Activities of Other Rho GTPases by an Inhibitory Function (2002) · cites this paper as [36]
In the citing paper
“The authors also showed that Rac2 is required for the production and release of IFN𝛄”
From The Hematopoiesis-Specific GTP-Binding Protein RhoH Is GTPase Deficient and Modulates Activities of Other Rho GTPases by an Inhibitory Function (2002) · cites this paper as [36]
In the citing paper
“Significantly, it was shown that this function of Rac2 depends on its ability to activate NF𝛋 B and p38”
From The Hematopoiesis-Specific GTP-Binding Protein RhoH Is GTPase Deficient and Modulates Activities of Other Rho GTPases by an Inhibitory Function (2002) · cites this paper as [36]
In the citing paper
“and that the activation of each alone is not sufficient to induce IFN𝛄 release.”
From The Hematopoiesis-Specific GTP-Binding Protein RhoH Is GTPase Deficient and Modulates Activities of Other Rho GTPases by an Inhibitory Function (2002) · cites this paper as [36]
In the citing paper
“Li et al. (34, 36) have shown that Rac2 is preferentially expressed in the Th1 subset of T cells.”
From The Hematopoiesis-Specific GTP-Binding Protein RhoH Is GTPase Deficient and Modulates Activities of Other Rho GTPases by an Inhibitory Function (2002) · cites this paper as [36]
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Cited by
Induction of gadd45β by NF-κB downregulates pro-apoptotic JNK signalling
De Smaele, E., Zazzeroni, F., Papa, S., Nguyen, D. U., Jin, R., Jones, J., Cong, R., & Franzoso, G. (2001) · Nature · doi:10.1038/35104560 · Cited by 732
Bulavin, D. V., Kovalsky, O., Hollander, M. C., & Fornace, A. J. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.11.3859-3871.2003 · Cited by 161
Li, X., Bu, X., Lu, B., Avraham, H., Flavell, R. A., & Lim, B. (2002) · Molecular and Cellular Biology · doi:10.1128/mcb.22.4.1158-1171.2002 · Cited by 153
Self-citation
Metadata
- Authors
- Lu, B., Yu, H., Chow, C.-W., Li, B., Zheng, W.-P., Davis, R. J., & Flavell, R. A.
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2001-05
- Volume
- 14
- Issue
- 5
- Pages
- 583-590
- ISSN
- 1074-7613
- Cited by
- 134
- References
- 1
- Language
- en
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- Lu, B., Yu, H., Chow, C.-W., Li, B., Zheng, W.-P., Davis, R. J., & Flavell, R. A. (2001). GADD45γ Mediates the Activation of the p38 and JNK MAP Kinase Pathways and Cytokine Production in Effector TH1 Cells. Immunity. https://doi.org/10.1016/s1074-7613(01)00141-8