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10.4049/jimmunol.1501896

http://scihub22266oqcxt.onion/10.4049/jimmunol.1501896
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C4868629!4868629 !27001958
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suck abstract from ncbi


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pmid27001958
      J+Immunol 2016 ; 196 (9 ): 3537-41
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  • Cutting Edge: Foxp1 Controls Naive CD8+ T Cell Quiescence by Simultaneously Repressing Key Pathways in Cellular Metabolism and Cell Cycle Progression #MMPMID27001958
  • Wei H ; Geng J ; Shi B ; Liu Z ; Wang YH ; Stevens AC ; Sprout SL ; Yao M ; Wang H ; Hu H
  • J Immunol 2016[May]; 196 (9 ): 3537-41 PMID27001958 show ga
  • Previously we have shown that transcription factor Foxp1 plays an essential role in maintaining naive T cell quiescence; in the absence of Foxp1, mature naive CD8(+) T cells proliferate in direct response to homeostatic cytokine IL-7. In this study, we report that the deletion of Foxp1 in naive CD8(+) T cells leads to enhanced activation of the PI3K/Akt/mammalian target of rapamycin signaling pathway and its downstream cell growth and metabolism targets in response to IL-7. We found that Foxp1 directly regulates PI3K interacting protein 1, a negative regulator of PI3K. Additionally, we found that deletion of Foxp1 in naive CD8(+) T cells results in increased expression levels of E2fs, the critical components for cell cycle progression and proliferation, in a manner that is not associated with increased phosphorylation of retinoblastoma protein. Taken together, our studies suggest that Foxp1 enforces naive CD8(+) T cell quiescence by simultaneously repressing key pathways in both cellular metabolism and cell cycle progression.
  • |*Cell Cycle/physiology [MESH]
  • |*Gene Expression Regulation [MESH]
  • |Animals [MESH]
  • |CD8-Positive T-Lymphocytes/cytology/drug effects/*immunology/metabolism [MESH]
  • |Carrier Proteins/genetics/metabolism [MESH]
  • |Cell Proliferation [MESH]
  • |Forkhead Transcription Factors/deficiency/genetics/*metabolism [MESH]
  • |Homeostasis [MESH]
  • |Interleukin-7/immunology/*metabolism/pharmacology [MESH]
  • |Intracellular Signaling Peptides and Proteins [MESH]
  • |Membrane Proteins [MESH]
  • |Phosphatidylinositol 3-Kinases/genetics/metabolism [MESH]
  • |Phosphorylation [MESH]
  • |Repressor Proteins/deficiency/genetics/*metabolism [MESH]
  • |Retinoblastoma Protein/immunology/metabolism [MESH]
  • |Signal Transduction [MESH]


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