Regulation of TSC2 by 14-3-3 Binding
Copyright policy )Regulation of TSC2 by 14-3-3 Binding
Mutation in either the TSC1 or TSC2 tumor suppressor gene is responsible for the inherited genetic disease of tuberous sclerosis complex. TSC1 and TSC2 form a physical and functional complex to regulate cell growth. Recently, it has been demonstrated that TSC1.TSC2 functions to inhibit ribosomal S6 kinase and negatively regulate cell size. TSC2 is negatively regulated by Akt phosphorylation. Here, we report that TSC2, but not TSC1, associates with 14-3-3 in vivo. Phosphorylation of Ser(1210) in TSC2 is required for its association with 14-3-3. Our data indicate that 14-3-3 association may inhibit the function of TSC2 and represents a possible mechanism of TSC2 regulation.
- University of Mary United States
- University of Michigan–Flint United States
- University of Michigan–Ann Arbor United States
- University of Washington United States
Binding Sites, Recombinant Fusion Proteins, Proteins, Cell Cycle Proteins, Protein Serine-Threonine Kinases, Phosphoproteins, Ribosomal Protein S6 Kinases, 90-kDa, Cell Line, Repressor Proteins, 14-3-3 Proteins, Proto-Oncogene Proteins, Mutation, Animals, Humans, Genes, Tumor Suppressor, Phosphorylation, Carrier Proteins, Proto-Oncogene Proteins c-akt, Adaptor Proteins, Signal Transducing, Protein Binding
Binding Sites, Recombinant Fusion Proteins, Proteins, Cell Cycle Proteins, Protein Serine-Threonine Kinases, Phosphoproteins, Ribosomal Protein S6 Kinases, 90-kDa, Cell Line, Repressor Proteins, 14-3-3 Proteins, Proto-Oncogene Proteins, Mutation, Animals, Humans, Genes, Tumor Suppressor, Phosphorylation, Carrier Proteins, Proto-Oncogene Proteins c-akt, Adaptor Proteins, Signal Transducing, Protein Binding
selected citations These citations are derived from selected sources.This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).103 popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.Top 10% influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).Top 10% impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.Top 1%
Citations provided by BIP!Popularity provided by BIP!