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• W1988201205 abstract "Recent studies using SOCS family knock-out mice have suggested that SOCS proteins have multiple biological functions in addition to their role as negative regulators of JAK-STAT signaling. To explore these other functions of this family of proteins, we used yeast two-hybrid screening to find proteins interacting with human SOCS-3. We identified the transcriptional factor DP-1 as a SOCS-3-interacting protein involved in regulation of the cell cycle. Immunoprecipitation-Western blot assay showed that this interaction between these endogenous proteins occurred in cells both in vitro and in vivo. SOCS-3 interacted with the C-terminal region of DP-1, and amino acids 156-172 of SOCS-3 were required for this interaction. Confocal microscopy revealed that SOCS-3 and DP-1 were primarily colocalized in the cytoplasm. SOCS-3 inhibited E2F/DP-1 transcriptional activity under the cyclin-E promoter and actually inhibited cell cycle progression and cell growth under E2F/DP-1 control. In contrast, DP-1 almost completely eliminated the inhibitory action of SOCS-3 on LIF-stimulated STAT-3 transcriptional activity in JAK-STAT signaling. Interestingly, the alternative regulatory action of SOCS-3 and DP-1 was dramatically eliminated by each siRNA. Taken together, these findings demonstrate that SOCS-3 acts as a negative regulator of the cell cycle progression under E2F/DP-1 control by interfering with heterodimer formation between DP-1 and E2F and also that DP-1 plays an important role in controlling JAK-STAT signaling." @default.
• W1988201205 created "2016-06-24" @default.
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• W1988201205 date "2008-11-01" @default.
• W1988201205 modified "2023-09-30" @default.
• W1988201205 title "SOCS-3 Inhibits E2F/DP-1 Transcriptional Activity and Cell Cycle Progression via Interaction with DP-1" @default.
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• W1988201205 doi "https://doi.org/10.1074/jbc.m800328200" @default.
• W1988201205 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2581570" @default.
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