TC-PTP and PTP1B: Regulating JAK–STAT signaling, controlling lymphoid malignancies

Pike, Kelly A.; Tremblay, Michel L.

doi:10.1016/j.cyto.2015.12.025

Cited by 61 publications

(58 citation statements)

References 52 publications

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“…In this context, the collaborative pathways and genes are: (a) increased stem cell self-renewal conferred by the NHD13 + transgene, (b) impaired B cell differentiation caused by Pax5 deletion, and (c) hyperproliferation conferred by a Nup214-Abl1 fusion gene (Supplemental Figure 14B). Although the role of Ptpn1 deletion is unclear, it is interesting to note Ptpn1 deletion accelerates lymphoma onset in Trp53-deficient mice (51), conceivably by enforcing active kinase signaling (52), and deletions of the closely related PTPN2 are common in pre-T LBL patients with NUP214-ABL1 fusion. In both cases, the PTPN deletion is thought to be oncogenic through enforcing hyperactive kinase signaling (52,53).…”

Section: Discussionmentioning

confidence: 99%

“…Although the role of Ptpn1 deletion is unclear, it is interesting to note Ptpn1 deletion accelerates lymphoma onset in Trp53-deficient mice (51), conceivably by enforcing active kinase signaling (52), and deletions of the closely related PTPN2 are common in pre-T LBL patients with NUP214-ABL1 fusion. In both cases, the PTPN deletion is thought to be oncogenic through enforcing hyperactive kinase signaling (52,53).…”

Section: Discussionmentioning

confidence: 99%

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A unique mutator phenotype reveals complementary oncogenic lesions leading to acute leukemia

et al. 2019

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

A unique mutator phenotype reveals complementary oncogenic lesions leading to acute leukemia

et al. 2019

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“…Studies of IFN signaling in Shp2 ‐deficient MEFs demonstrated that it can inhibit IFN‐induced JAK1, STAT1, and STAT2 phosphorylation . Both overexpression and knockdown studies revealed that PTP1B can target TYK2 for dephosphorylation, while TC‐PTP can target JAK1 . Therefore, the expression of these phosphatases can suppress type I IFN‐induced STAT1 phosphorylation.…”

Section: Type I Ifn Response and Its Regulationmentioning

confidence: 99%

Negative regulation of type I IFN signaling

Arimoto

Miyauchi

Stoner

et al. 2018

Journal of Leukocyte Biology

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Type I IFNs (α, β, and others) are a family of cytokines that are produced in physiological conditions as well as in response to the activation of pattern recognition receptors. They are critically important in controlling the host innate and adaptive immune response to viral and some bacterial infections, cancer, and other inflammatory stimuli. However, dysregulation of type I IFN production or response can contribute to immune pathologies termed "interferonopathies", pointing to the importance of balanced activating signals with tightly regulated mechanisms of tuning this signaling. Here, we summarize the recent advances of how type I IFN production and response are controlled at multiple levels of the type I IFN signaling cascade.

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“…This tyrosine phosphatase negatively regulates TCR and JAK-STAT signalling, being an inhibitor of T cell activation [93,94]. The SNP rs1893217(C) in PTPN2 is associated with juvenile idiopathic arthritis and results in decreased gene expression [95].…”

Section: Tc-ptpmentioning

confidence: 99%

Physiology and Pathology of Autoimmune Diseases: Role of CD4+ T cells in Rheumatoid Arthritis

Castro-Sánchez¹,

Roda-Navarro²

2017

Physiology and Pathology of Immunology

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Rheumatoid arthritis (RA) is a chronic autoimmune disease characterised by synovial inlammation leading to bone erosion and to systemic manifestations in patients with long RA duration. Although the aetiology is unknown, several observations make currently clear that CD4 T cells play a key role in the pathogenesis: (1) RA associates with certain polymorphisms of HLA class II molecules, and (2) the repertoire and aging of CD4 T cells as well as the intracellular signalling mediating CD4 T cell activation are altered in RA patients. We describe herein the alterations found in CD4 T cells and the role of these cells in the development and progression of RA.

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TC-PTP and PTP1B: Regulating JAK–STAT signaling, controlling lymphoid malignancies

Cited by 61 publications

References 52 publications

A unique mutator phenotype reveals complementary oncogenic lesions leading to acute leukemia

A unique mutator phenotype reveals complementary oncogenic lesions leading to acute leukemia

Negative regulation of type I IFN signaling

Physiology and Pathology of Autoimmune Diseases: Role of CD4+ T cells in Rheumatoid Arthritis

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