Article thumbnail

Phosphorylation-Dependent 14-3-3 Binding to LRRK2 Is Impaired by Common Mutations of Familial Parkinson's Disease

By Xianting Li, Qing Jun Wang, Nina Pan, Sangkyu Lee, Yingming Zhao, Brian T. Chait and Zhenyu Yue
Topics: Research Article
Publisher: Public Library of Science
OAI identifier:
Provided by: PubMed Central

To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.

Suggested articles


  1. (2019S) Enhanced striatal dopamine transmission and motor performance with LRRK2 overexpression in mice is eliminated by familial Parkinson’s disease mutation G2019S.
  2. (1997). 14-3-3 (epsilon) interacts with the insulin-like growth factor I receptor and insulin receptor substrate I in a phosphoserine-dependent manner.
  3. 14-3-3 binding to LRRK2 is disrupted by multiple Parkinson’s disease-associated mutations and regulates cytoplasmic localization.
  4. (1997). 14-3-3 is phosphorylated by casein kinase I on residue 233. Phosphorylation at this site in vivo regulates Raf/14-3-3 interaction.
  5. (2000). 14-3-3 proteins: structure, function, and regulation.
  6. (2006). 14-3-3gamma binds to MDMX that is phosphorylated by UV-activated Chk1, resulting in p53 activation.
  7. (2005). A
  8. (1995). Bcr and Raf form a complex in vivo via 14-3-3 proteins.
  9. (2004). Cloning of the gene containing mutations that cause PARK8-linked Parkinson’s disease.
  10. (2004). DARPP32: an integrator of neurotransmission.
  11. (2009). Dependence of leucine-rich repeat kinase 2 (LRRK2) kinase activity on dimerization.
  12. (1996). Direct interaction between protein kinase C theta (PKC theta) and 14-3-3 tau in T cells: 14-3-3 overexpression results in inhibition of PKC theta translocation and function.
  13. (2007). GTP binding is essential to the protein kinase activity of LRRK2, a causative gene product for familial Parkinson’s disease.
  14. Impaired dopaminergic neurotransmission and microtubule-associated protein tau alterations in human LRRK2 transgenic mice.
  15. (2006). Induction of autophagy in axonal dystrophy and degeneration.
  16. Inhibition of LRRK2 kinase activity leads to dephosphorylation of Ser(910)/Ser(935), disruption of 14-3-3 binding and altered cytoplasmic localization.
  17. Inhibitors of leucine-rich repeat kinase-2 protect against models of Parkinson’s disease.
  18. (2005). Integrated approach for manual evaluation of peptides identified by searching protein sequence databases with tandem mass spectra.
  19. (1997). Interaction of the ligandactivated glucocorticoid receptor with the 14-3-3 eta protein.
  20. (2007). Leucine-rich repeat kinase 2 (LRRK2)/PARK8 possesses GTPase activity that is altered in familial Parkinson’s disease R1441C/G mutants.
  21. (2003). Mechanisms by which dopamine receptors may influence synaptic plasticity.
  22. (2009). Molecular characterization of propionyllysines in non-histone proteins.
  23. (2009). Mutant LRRK2(R1441G) BAC transgenic mice recapitulate cardinal features of Parkinson’s disease.
  24. (2004). Mutations in LRRK2 cause autosomal-dominant parkinsonism with pleomorphic pathology.
  25. (1998). Mutations in the hydrophobic surface of an amphipathic groove of 14-3-3zeta disrupt its interaction with Raf-1 kinase.
  26. (2005). Parkinson’s disease-associated mutations in leucine-rich repeat kinase 2 augment kinase activity.
  27. (2005). Parts per million mass accuracy on an Orbitrap mass spectrometer via lock mass injection into a C-trap. Mol Cell Proteomics
  28. (2009). Phosphorylation of ezrin/radixin/moesin proteins by LRRK2 promotes the rearrangement of actin cytoskeleton in neuronal morphogenesis.
  29. (2003). Phosphorylation of RIM1alpha by PKA triggers presynaptic long-term potentiation at cerebellar parallel fiber synapses.
  30. (2004). PKA phosphorylation and 14-3-3 interaction regulate the function of neurofibromatosis type I tumor suppressor, neurofibromin.
  31. (2007). Protein kinase A phosphorylation of human phosphodiesterase 3B promotes 14-3-3 protein binding and inhibits phosphatase-catalyzed inactivation.
  32. (2009). R1441C mutation in LRRK2 impairs dopaminergic neurotransmission in mice.
  33. (2000). Regulation of BAD by cAMPdependent protein kinase is mediated via phosphorylation of a novel site,
  34. (2008). RIM1alpha phosphorylation at serine-413 by protein kinase A is not required for presynaptic long-term plasticity or learning.
  35. (2008). Role of autophagy in G2019S-LRRK2-associated neurite shortening in differentiated SH-SY5Y cells.
  36. SmithWW,PeiZ,Jiang H,DawsonVL,Dawson TM,etal.(2006) Kinase activity of mutant LRRK2 mediates neuronal toxicity.
  37. (2008). Structure of the ROC domain from the Parkinson’s disease-associated leucine-rich repeat kinase 2 reveals a dimeric GTPase.
  38. (1997). Switching of the coupling of the beta2-adrenergic receptor to different G proteins by protein kinase A.
  39. (2006). The familial Parkinsonism gene LRRK2 regulates neurite process morphology.
  40. (2008). The Parkinson disease-associated leucine-rich repeat kinase 2 (LRRK2) is a dimer that undergoes intramolecular autophosphorylation.
  41. (2007). The Parkinson’s disease-associated protein, leucine-rich repeat kinase 2 (LRRK2), is an authentic GTPase that stimulates kinase activity.
  42. (1997). The structural basis for 14-3-3:phosphopeptide binding specificity.
  43. (2005). Wynshaw-Boris A