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10.1182/blood-2006-06-031856

http://scihub22266oqcxt.onion/10.1182/blood-2006-06-031856
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17023580!1794048!17023580
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suck abstract from ncbi

pmid17023580      Blood 2007 ; 109 (4): 1568-73
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  • L-arginine availability regulates T-lymphocyte cell-cycle progression #MMPMID17023580
  • Rodriguez PC; Quiceno DG; Ochoa AC
  • Blood 2007[Feb]; 109 (4): 1568-73 PMID17023580show ga
  • L-arginine (L-Arg) plays a central role in several biologic systems including the regulation of T-cell function. L-Arg depletion by myeloid-derived suppressor cells producing arginase I is seen in patients with cancer inducing T-cell anergy. We studied how L-Arg starvation could regulate T-cell-cycle progression. Stimulated T cells cultured in the absence of L-Arg are arrested in the G0-G1phase of the cell cycle. This was associated with an inability of T cells to up-regulate cyclin D3 and cyclin-dependent kinase 4 (cdk4), but not cdk6, resulting in an impaired downstream signaling with a decreased phosphorylation of Rb protein and a low expression and binding of E2F1. Silencing of cyclin D3 reproduced the cell cycle arrest caused by L-Arg starvation. The regulation of cyclin D3 and cdk4 by L-Arg starvation occurs at transcriptional and posttranscriptional levels. Signaling through GCN2 kinase is triggered during amino acid starvation. Experiments demonstrated that T cells from GCN2 knock-out mice did not show a decreased proliferation and were able to up-regulate cyclin D3 when cultured in the absence of L-Arg. These results contribute to the understanding of a central mechanism by which cancer and other diseases characterized by high arginase I production may cause T-cell dysfunction.
  • |*Cell Cycle[MESH]
  • |*Clonal Anergy[MESH]
  • |Animals[MESH]
  • |Arginine/analysis/deficiency/*physiology[MESH]
  • |Cell Proliferation[MESH]
  • |Cyclin D3[MESH]
  • |Cyclin-Dependent Kinases/genetics[MESH]
  • |Cyclins/genetics[MESH]
  • |Gene Expression Regulation[MESH]
  • |Humans[MESH]
  • |Mice[MESH]
  • |Mice, Knockout[MESH]
  • |Neoplasms/immunology[MESH]
  • |Protein Serine-Threonine Kinases[MESH]


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