Reference : The role of SHIP1 in T-lymphocyte life and death
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
http://hdl.handle.net/2268/21000
The role of SHIP1 in T-lymphocyte life and death
English
Gloire, Geoffrey mailto [Université de Liège - ULg > > Virologie - Immunologie >]
Erneux, Christophe [> > > >]
Piette, Jacques mailto [Université de Liège - ULg > Département des sciences de la vie > Virologie - Immunologie >]
Apr-2007
Biochemical Society Transactions
Portland Press Ltd
35
Pt 2
277-280
Yes (verified by ORBi)
International
0300-5127
London
[en] apoptosis ; cell proliferation ; nuclear factor kappa B (NF-kappa B) ; phosphoinosilide 3-kinase (PI3K) ; Src homology 2 domain-containing inositol phosphatase-1 (SHIP1) ; T-lymphocyte
[en] SHIP1 [SH2 (Src homology 2)-containing inositol phosphatase-1], an inositol 5-phosphatase expressed in haemopoietic cells, acts by hydrolysing the 5-phosphates from PtdIns(3,4,5)P(3) and Ins(1,3,4,5)P(4), thereby negatively regulating the PI3K (phosphoinositide 3-kinase) pathway. SHIP1 plays a major role in inhibiting proliferation of myeloid cells. As a result, SHIP1(-/-) mice have an increased number of neutrophils and monocytes/macrophages due to enhanced survival and proliferation of their progenitors. Although SHIP1 contributes to PtdIns(3,4,5)P(3) metabolism in T-lymphocytes, its exact role in this cell type is much less explored. Jurkat cells have recently emerged as an interesting tool to study SHIP1 function in T-cells because they do not express SHIP1 at the protein level, thereby allowing reintroduction experiments in a relatively easy-to-use system. Data obtained from SHIP1 reintroduction have revealed that SHIP1 not only acts as a negative player in T-cell lines proliferation, but also regulates critical pathways, such as NF-kappaB (nuclear factor kappaB) activation, and also appears to remarkably inhibit T-cell apoptosis. On the other hand, experiments using primary T-cells from SHIP1(-/-) mice have highlighted a new role for SHIP1 in regulatory T-cell development, but also emphasize that this protein is not required for T-cell proliferation. In support of these results, SHIP1(-/-) mice are lymphopenic, suggesting that SHIP1 function in T-cells differs from its role in the myeloid lineage.
http://hdl.handle.net/2268/21000
10.1042/BST0350277

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