Differential proteome profiles in E2F2-deficient T lymphocytes.
E2F transcription factors are important regulators of proliferation, differentiation and apoptosis. We have previously shown that E2F2-/- mice develop late-onset autoimmune features, similar to systemic lupus erythematosus. E2F2-deficient T lymphocytes exhibit enhanced T cell receptor (TCR)-stimulated proliferation, which is presumably responsible for causing autoimmunity in E2F2-deficient mice. The comparison of E2F2-/- and wild-type T lymphocyte expression profiles by 2-DE followed by MS identification has revealed a set of deregulated proteins involved in TCR-mediated signaling, cell survival and stress responses. The deregulation of these proteins may account for the hyperproliferative phenotype that characterizes E2F2-/- T cells. Our work shows that proteomic analysis of gene-knockout strains can be a useful methodology to study the functional role of specific genes.
Department of Biochemistry and Molecular Biology, University of the Basque Country, Leioa, Spain.
Mikel
M
Azkargorta
Jesus M
JM
Arizmendi
Felix
F
Elortza
Nere
N
Alkorta
Ana M
AM
Zubiaga
Asier
A
Fullaondo
D000595:Amino Acid Sequence; D000818:Animals; D050703:E2F2 Transcription Factor / Q000032:analysis* / Q000172:deficiency / Q000235:genetics*; D015180:Electrophoresis, Gel, Two-Dimensional; D051379:Mice; D018345:Mice, Knockout; D008969:Molecular Sequence Data; D020543:Proteome / Q000032:analysis / Q000096:biosynthesis*; D016176:T-Lymphocyte Subsets / Q000737:chemistry / Q000378:metabolism*
D050703:E2F2 Transcription Factor; C484940:E2f2 protein, mouse; D020543:Proteome