14-3-3 Proteins

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  Subject Areas on Research

  • 14-3-3 Proteins regulate mutant LRRK2 kinase activity and neurite shortening. 
  • 14-3-3 proteins are part of an abscisic acid-VIVIPAROUS1 (VP1) response complex in the Em promoter and interact with VP1 and EmBP1. 
  • A biotin switch-based proteomics approach identifies 14-3-3ζ as a target of Sirt1 in the metabolic regulation of caspase-2. 
  • A role for PP1 in the Cdc2/Cyclin B-mediated positive feedback activation of Cdc25. 
  • A word of caution in the use of neuron-specific enolase expression in tumor diagnosis. 
  • Acute in vivo genetic rescue demonstrates that phosphorylation of RIM1alpha serine 413 is not required for mossy fiber long-term potentiation. 
  • Association of the protein kinases c-Bcr and Bcr-Abl with proteins of the 14-3-3 family. 
  • Calmodulin-dependent protein kinase IV regulates nuclear export of Cabin1 during T-cell activation. 
  • High frequency of hypermethylation at the 14-3-3 sigma locus leads to gene silencing in breast cancer. 
  • Histone deacetylase 6 (HDAC6) promotes the pro-survival activity of 14-3-3ζ via deacetylation of lysines within the 14-3-3ζ binding pocket. 
  • Hypermethylation of 14-3-3 sigma (stratifin) is an early event in breast cancer. 
  • Implications for proteasome nuclear localization revealed by the structure of the nuclear proteasome tether protein Cut8. 
  • LRRK2 activation in idiopathic Parkinson's disease. 
  • LRRK2 secretion in exosomes is regulated by 14-3-3. 
  • Maintenance of G2 arrest in the Xenopus oocyte: a role for 14-3-3-mediated inhibition of Cdc25 nuclear import. 
  • Metabolic control of oocyte apoptosis mediated by 14-3-3zeta-regulated dephosphorylation of caspase-2. 
  • Metabolic-stress-induced rearrangement of the 14-3-3ζ interactome promotes autophagy via a ULK1- and AMPK-regulated 14-3-3ζ interaction with phosphorylated Atg9. 
  • Nuclear pore component Nup98 is a potential tumor suppressor and regulates posttranscriptional expression of select p53 target genes. 
  • PP1 control of M phase entry exerted through 14-3-3-regulated Cdc25 dephosphorylation. 
  • Parathyroid hormone-related peptide represses chondrocyte hypertrophy through a protein phosphatase 2A/histone deacetylase 4/MEF2 pathway. 
  • Platelet-derived growth factor (PDGF) regulates Slingshot phosphatase activity via Nox1-dependent auto-dephosphorylation of serine 834 in vascular smooth muscle cells. 
  • Protein phosphatase 2A activates the proapoptotic function of BAD in interleukin- 3-dependent lymphoid cells by a mechanism requiring 14-3-3 dissociation. 
  • Protein phosphatase 2A dephosphorylation of phosphoserine 112 plays the gatekeeper role for BAD-mediated apoptosis. 
  • Role for the PP2A/B56delta phosphatase in regulating 14-3-3 release from Cdc25 to control mitosis. 
  • Rsk-mediated phosphorylation and 14-3-3ɛ binding of Apaf-1 suppresses cytochrome c-induced apoptosis. 
  • Signaling from the RNA sensor RIG-I is regulated by ufmylation. 
  • Stress and death: breaking up the c-Abl/14-3-3 complex in apoptosis. 
  • Structural basis of O-GlcNAc recognition by mammalian 14-3-3 proteins. 
  • TNK1 is a ubiquitin-binding and 14-3-3-regulated kinase that can be targeted to block tumor growth. 
  • The bacterial effector HopM1 suppresses PAMP-triggered oxidative burst and stomatal immunity. 
  • The mitochondrial targeting chaperone 14-3-3ε regulates a RIG-I translocon that mediates membrane association and innate antiviral immunity. 
  • The modular nature of histone deacetylase HDAC4 confers phosphorylation-dependent intracellular trafficking. 
  • The roles of 14-3-3 proteins in signal transduction. 
  • When the checkpoints have gone: insights into Cdc25 functional activation.