Proteomic analysis identifies that 14-3-3ζ interacts with β-catenin and facilitates its activation by Akt

Tian, Qiang; Feetham, Megan C.; Tao, Wanyu; He, Xi; Li, Linheng; Aebersold, Ruedi; Hood, Leroy

doi:10.1073/pnas.0406499101

Cited by 145 publications

(158 citation statements)

References 37 publications

Supporting

Mentioning

144

Contrasting

Order By: Relevance

“…Endocytosis is regulated by phosphorylation (Shikano et al, 2006). 14-3-3 binds to specific phosphorylated (pSerine/pThreonine) motifs in its protein targets and occupancy protects the site from phosphatases (Petosa et al, 1998;Tian et al, 2004). It remains to be determined whether 14-3-3 may regulate α3*nAChR surface expression by this mechanism.…”

Section: Discussionmentioning

confidence: 99%

Adenomatous polyposis coli plays a key role, in vivo, in coordinating assembly of the neuronal nicotinic postsynaptic complex

Rosenberg

Yang

Giovanni

et al. 2008

Molecular and Cellular Neuroscience

View full text Add to dashboard Cite

The neuronal nicotinic synapse plays a central role in normal cognitive and autonomic function. Molecular mechanisms that direct the assembly of this synapse remain poorly defined, however. We show here that adenomatous polyposis coli (APC) organizes a multi-molecular complex that is essential for targeting α3*nAChRs to synapses. APC interaction with microtubule plus-end binding protein EB1 is required for α3*nAChR surface membrane insertion and stabilization. APC brings together EB1, the key cytoskeletal regulators macrophin and IQGAP1, and 14-3-3 adapter protein at nicotinic synapses. 14-3-3, in turn, links the α3-subunit to APC. This multi-molecular APC complex stabilizes the local microtubule and F-actin cytoskeleton and links postsynaptic components to the cytoskeleton-essential functions for controlling the molecular composition and stability of synapses. This work identifies macrophin, IQGAP1 and 14-3-3 as novel nicotinic synapse components and defines a new role for APC as an in vivo coordinator of nicotinic postsynaptic assembly in vertebrate neurons.

show abstract

Section: Discussionmentioning

confidence: 99%

Adenomatous polyposis coli plays a key role, in vivo, in coordinating assembly of the neuronal nicotinic postsynaptic complex

Rosenberg

Yang

Giovanni

et al. 2008

Molecular and Cellular Neuroscience

View full text Add to dashboard Cite

show abstract

“…4). The phosphorylated forms of PTEN and Akt, along with the adaptor protein 14-3-3ζ, have been found in ISCs 9,19 . Extending these findings, we found that cells in the ISC position, as well as a limited number of progenitor cells higher in the crypt, were highly positive for phosphorylated PTEN (p-PTEN), p-Akt, p-GSK3β, 14-3-3-ζ and Musashi ( Fig.…”

Section: Pten-akt Pathway Linked To Isc/p Cell Number and Behaviormentioning

confidence: 99%

“…We have proposed that Akt coordinates with Wnt signaling and assists in the activation of β-catenin in ISCs 9 , either through phosphorylation of GSK3β (ref. 37) or by phosphorylation of β-catenin itself 19 .…”

Section: Akt Phosphorylates the C Terminus Of β-Catenin At Ser552mentioning

confidence: 99%

“…5b,c). The phosphorylation of β-catenin by Akt can prime β-catenin for 14-3-3ζ binding and further stabilization 19 . The Arg-Arg-ThrSer sequence containing Ser552 forms a phosphoserine motif that serves as an optimal recognition site for 14-3-3ζ (ref.…”

Section: Akt Phosphorylates the C Terminus Of β-Catenin At Ser552mentioning

confidence: 99%

“…Mutation of BMPR1A can result in a Cowden-like syndrome resembling loss of PTEN 17 . BMP signaling may in part be mediated by inhibition of PI3K-Akt activity via positive regulation of PTEN 9,18,19 . In turn, PTEN inhibits, whereas Akt enhances, the nuclear localization of β-catenin 20,21 , consistent with our previous model in which Akt assists Wnt signaling in activation of β-catenin in ISCs 9,19 .…”

mentioning

confidence: 99%

See 2 more Smart Citations

PTEN-deficient intestinal stem cells initiate intestinal polyposis

et al. 2007

Self Cite

View full text Add to dashboard Cite

Intestinal polyposis, a precancerous neoplasia, results primarily from an abnormal increase in the number of crypts, which contain intestinal stem cells (ISCs). In mice, widespread deletion of the tumor suppressor Phosphatase and tensin homolog (PTEN) generates hamartomatous intestinal polyps with epithelial and stromal involvement. Using this model, we have established the relationship between stem cells and polyp and tumor formation. PTEN helps govern the proliferation rate and number of ISCs and loss of PTEN results in an excess of ISCs. In PTENdeficient mice, excess ISCs initiate de novo crypt formation and crypt fission, recapitulating crypt production in fetal and neonatal intestine. The PTEN-Akt pathway probably governs stem cell activation by helping control nuclear localization of the Wnt pathway effector β-catenin. Akt phosphorylates β-catenin at Ser552, resulting in a nuclear-localized form in ISCs. Our observations show that intestinal polyposis is initiated by PTEN-deficient ISCs that undergo excessive proliferation driven by Akt activation and nuclear localization of β-catenin. Accession codes. Gene Expression Omnibus (GEO): GSE6078.URLs. GEO: http://www.ncbi.nlm.nih.gov/projects/geo/.Supplementary information is available on the Nature Genetics website. COMPETING INTERESTS STATEMENTThe authors declare that they have no competing financial interests. HHS Public AccessAuthor manuscript Nat Genet. Author manuscript; available in PMC 2015 December 16. Published in final edited form as:Nat Genet. 2007 February ; 39(2): 189-198. doi:10.1038/ng1928. Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptThe failure of most current therapies to cure cancer has led to the hypothesis that treatments targeted at malignant proliferation spare a more slowly cycling 'cancer stem cell' population that has the ability to regenerate the tumor 1 . Recently, cancer stem cells have been identified and shown to seed tumors upon transplantation into a secondary host [2][3][4] . However, little is known about the process by which mutation(s) in a stem cell result in primary tumor initiation.Although there are many 'causes' of intestinal cancer, it is well established that almost all cases begin with the development of benign polyps, mainly involving benign neoplastic proliferation of epithelium. The epithelium of the small intestine is composed of a proliferation compartment (crypt) and a differentiation compartment in the villus (Fig. 1a). ISCs, located near the crypt base and above Paneth cells 5,6 , give rise to enterocytes, goblet cells, enteroendocrine cells and Paneth cells [6][7][8] . Intestinal polyposis features a substantial increase in the number of crypts (crypt expansion) and a reduction in epithelial cell differentiation 6,7,9,10 . A key question 7,9,11 is whether stem cells are involved in the abnormal crypt expansion during polyp initiation.Studies of human hereditary intestinal polyposis syndromes (which typically, but not uniformly, predispose affected individuals to gastrointes...

show abstract

Synthesis and characterization of chelating resins with amino moieties and application on removal of copper(II) from EDTA complexes

Wang

2005

J of Applied Polymer Sci

View full text Add to dashboard Cite

Strong-field ligands (amino moieties) are introduced into a hydrogel resin to obtain a chelating resin via inversion suspension polymerization. The characteristics of chelating copolymers are measured by using Fourier transform IR spectroscopy (FTIR), elemental analysis (EA), and scanning electron microscopy (SEM). After chelating copolymers adsorb cupric ions, the absorption peak of stretch NOH is shifted to higher frequency because of a coordination reaction from the FTIR spectra. Furthermore, the mechanism of metal complex adsorption on the chelating copolymer is that the strong-field chelating ligand decomposes the bonding of the metal complexes and recoordinates the cupric ion to a chelating polymer, which is examined via FTIR, SEM with EA, and ionic chromatography analysis. The maximum adsorption capacity of cupric ions is 1.08 mmol/g and the adsorption capacity increases with the increase of the pH of the solution. The stability constant of the Cu chelating copolymer is 10 18.72 , and it can have competition adsorption with EDTA in aqueous solution. These amino chelating copolymers can be used not only to recover metal ions but also to move anion pollution in wastewater. It is interesting that parts of the cupric ions adsorbed on the chelating copolymer are reduced into cupreous ions and/or copper atoms after electron spectroscopy for chemical analysis measurement.

show abstract

Proteomic analysis identifies that 14-3-3ζ interacts with β-catenin and facilitates its activation by Akt

Cited by 145 publications

References 37 publications

Adenomatous polyposis coli plays a key role, in vivo, in coordinating assembly of the neuronal nicotinic postsynaptic complex

Adenomatous polyposis coli plays a key role, in vivo, in coordinating assembly of the neuronal nicotinic postsynaptic complex

PTEN-deficient intestinal stem cells initiate intestinal polyposis

Synthesis and characterization of chelating resins with amino moieties and application on removal of copper(II) from EDTA complexes

Contact Info

Product

Resources

About