The Influence of the MAPK Pathway on T Cell Lineage Commitment

Sharp, Leslie L.; Schwarz, David; Bott, Cynthia M.; Marshall, Christopher J.; Hedrick, Stephen M.

doi:10.1016/s1074-7613(00)80382-9

Cited by 208 publications

(160 citation statements)

References 60 publications

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“…For example, in some systems the platelet-derived growth factor (PDGF) stimulates sustained ERK activity and results in S-phase entry or cell differentiation whereas epidermal growth factor (EGF) stimulates transient ERK activity that does not drive cells in to S-phase and does not promote cell differentiation [204][205][206][207]. Duration and strength dependent modulation of cell fate appear to operate in neuronal PC12 cells, NIH3T3 fibroblasts [208], macrophages [209] and lymphocytes [210,211]. It is becoming apparent that cell fates determined by different growth factors that activate the same MAPK components requires a spatiotemporal control of MAPK targeting, sequestration and activation.…”

Section: Multiple Erk Scaffolds Regulate the Diverse Functions Of Thementioning

confidence: 99%

Scaffold mediated regulation of MAPK signaling and cytoskeletal dynamics: A perspective

Pullikuth

Catling

2007

Cellular Signalling

136

107

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Cell migration is critical for many physiological processes and is often misregulated in developmental disorders and pathological conditions including cancer and neurodegeneration. MAPK signaling and the Rho family of proteins are known regulators of cell migration that exert their influence on cellular cytoskeleton during cell adhesion and migration. Here we review data supporting the view that localized ERK signaling mediated through recently identified scaffold proteins may regulate cell migration.

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Section: Multiple Erk Scaffolds Regulate the Diverse Functions Of Thementioning

confidence: 99%

Scaffold mediated regulation of MAPK signaling and cytoskeletal dynamics: A perspective

Pullikuth

Catling

2007

Cellular Signalling

136

107

View full text Add to dashboard Cite

show abstract

“…61 Similarly, other studies have suggested that increased or decreased MAPK signaling can influence T cell differentiation between either a CD4 or CD8 expressing cell lineage. 62 In nonleukemic cells, several groups have demonstrated that MAPK signaling can both promote and inhibit adipogenesis and myogenesis in pre-adipocytes and myoblasts, respectively, in a time and context-dependent manner. [63][64][65][66] Thus in some established cell systems, constitutive elevation of MAP kinase activity can stimulate proliferation, whereas in others it triggers increased p21 Cip-1/MDA6/WAF1 levels, cell cycle arrest, and cellular maturation.…”

Section: An Overview For the Role Of The Map Kinase Pathway In Prolifmentioning

confidence: 99%

The roles of signaling by the p42/p44 mitogen-activated protein (MAP) kinase pathway; a potential route to radio- and chemo-sensitization of tumor cells resulting in the induction of apoptosis and loss of clonogenicity

et al. 1998

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During the last 10 years, multiple signal transduction pathways within cells have been discovered. These pathways have been linked to the regulation of many diverse cellular events such as proliferation, senescence, differentiation and apoptosis. This review will focus upon the many roles of signaling by the p42/p44 mitogen-activated protein (MAP) kinase pathway. Recent evidence suggests that signaling by the MAP kinase pathway can both enhance proliferation by increased expression of molecules such as cyclin D1, but also cause growth arrest by increased expression of molecules such as the cyclin kinase inhibitor protein p21 Cip-1/MDA6/WAF1 . These differential effects on growth have been correlated to the amplitude and duration of the MAP kinase activity signal. Furthermore several laboratories are reporting data suggesting that inhibition of the MAP kinase pathway, as well as a family of upstream MAP kinase activators, the protein kinase C family, represent an important route to both radio-and chemo-sensitization of tumor cells. Herein, we describe the historical discovery and characterization of the MAP kinase pathway. In addition we describe potential mechanisms by which inhibition of protein kinase C, the MAP kinase pathway, and potentially of p21 Cip-1/MDA6/WAF1 expression, may alter the sensitivities of leukemic and carcinoma cells to cytotoxic insults, leading to increased apoptosis and loss of clonogenicity.

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“…How signals that induce positive selection trigger differentiation into the CD4 ϩ or CD8 ϩ mature cell type is not fully understood. Nonetheless, quantitative differences in MAPK and Lck activation appear to alter the CD4 ϩ / CD8 ϩ differentiation ratio (12,13).…”

mentioning

confidence: 99%

Phosphatidylinositol 3-Kinase Regulates the CD4/CD8 T Cell Differentiation Ratio

Rodrı́guez-Borlado

Barber

Hernández

et al. 2003

The Journal of Immunology

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The signaling pathways that control T cell differentiation have only begun to be elucidated. Using T cell lines, it has been shown that class IA phosphatidylinositol 3-kinase (PI3K), a heterodimer composed of a p85 regulatory and a p110 catalytic subunit, is activated after TCR stimulation. Nonetheless, the contribution of p85/p110 PI3K isoforms in T cell development has not been described. Mice deficient in the other family of class I PI3K, p110γ, which is regulated by G protein-coupled receptors, exhibit reduced thymus size. Here we examine T cell development in p110γ-deficient mice and in mice expressing an activating mutation of the p85 regulatory subunit, p65PI3K, in T cells. We show that p110γ-deficient mice have a partial defect in pre-TCR-dependent differentiation, which is restored after expression of the p65PI3K activating mutation. Genetic alteration of both PI3K isoforms also affects positive selection; p110γ deletion decreased and p65PI3K expression augmented the CD4+/CD8+ differentiation ratio. Finally, data are presented showing that both PI3K isoforms influenced mature thymocyte migration to the periphery. These observations underscore the contribution of PI3K in T cell development, as well as its implication in determining the CD4+/CD8+ T cell differentiation ratio in vivo.

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The Influence of the MAPK Pathway on T Cell Lineage Commitment

Cited by 208 publications

References 60 publications

Scaffold mediated regulation of MAPK signaling and cytoskeletal dynamics: A perspective

Scaffold mediated regulation of MAPK signaling and cytoskeletal dynamics: A perspective

The roles of signaling by the p42/p44 mitogen-activated protein (MAP) kinase pathway; a potential route to radio- and chemo-sensitization of tumor cells resulting in the induction of apoptosis and loss of clonogenicity

Phosphatidylinositol 3-Kinase Regulates the CD4/CD8 T Cell Differentiation Ratio

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