Genomes and Genes
14 3 3gamma
Gene Symbol: 14 3 3gamma
Description: tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, gamma polypeptide
Alias: 14-3-3gamma, D7Bwg1348e, 14-3-3 protein gamma, 14-3-3 gamma, 14-3-3 protein gamma subtype, 3-monooxgenase/tryptophan 5-monooxgenase activation protein, gamma polypeptide, 3-monooxgenase/tryptophan 5-monooxygenase activation protein, gamma polypeptide, 3-monooxygenase/tryptophan 5-monooxygenase activation protein, gamma polypeptide
Products: 14 3 3gamma
- Sadik G, Tanaka T, Kato K, Yamamori H, Nessa B, Morihara T, et al. Phosphorylation of tau at Ser214 mediates its interaction with 14-3-3 protein: implications for the mechanism of tau aggregation. J Neurochem. 2009;108:33-43 pubmed publisher..Also as the phosphorylation at Ser214 is up-regulated in Alzheimer's disease brain, tau's interaction with 14-3-3 might be involved in the pathology of this disease. ..
- Ye S, Zhou X, Lai X, Zheng L, Chen X. Silencing neuroglobin enhances neuronal vulnerability to oxidative injury by down-regulating 14-3-3gamma. Acta Pharmacol Sin. 2009;30:913-8 pubmed publisher..Ngb contributes to neuronal defensive machinery against oxidative injuries by regulating 14-3-3gamma expression.Acta Pharmacologica Sinica (2009) 30: 913-918; doi: 10.1038/aps.2009.70. ..
- Radhakrishnan V, Martinez J. 14-3-3gamma induces oncogenic transformation by stimulating MAP kinase and PI3K signaling. PLoS ONE. 2010;5:e11433 pubmed publisher..Overall, our studies establish 14-3-3gamma as an oncogene and implicate MAPK and PI3K signaling as important for 14-3-3gamma induced transformation. ..
- Kosaka Y, Cieslik K, Li L, Lezin G, Maguire C, Saijoh Y, et al. 14-3-3? plays a role in cardiac ventricular compaction by regulating the cardiomyocyte cell cycle. Mol Cell Biol. 2012;32:5089-102 pubmed publisher..These data are consistent with the long-held view that human LVNC may result from compaction arrest, and they implicate 14-3-3? as a new candidate gene in congenital human cardiomyopathies. ..
- Aghazadeh Y, Rone M, Blonder J, Ye X, Veenstra T, Hales D, et al. Hormone-induced 14-3-3? adaptor protein regulates steroidogenic acute regulatory protein activity and steroid biosynthesis in MA-10 Leydig cells. J Biol Chem. 2012;287:15380-94 pubmed publisher..Over time 14-3-3? homodimerizes and dissociates from STAR, allowing this protein to induce maximal mitochondrial steroid formation...
- Chen X, Yu A. The association of 14-3-3gamma and actin plays a role in cell division and apoptosis in astrocytes. Biochem Biophys Res Commun. 2002;296:657-63 pubmed
- Eilers A, Sundwall E, Lin M, Sullivan A, Ayer D. A novel heterodimerization domain, CRM1, and 14-3-3 control subcellular localization of the MondoA-Mlx heterocomplex. Mol Cell Biol. 2002;22:8514-26 pubmed..Second, an extracellular signal(s) must overcome the cytoplasmic localization function imparted by CRM1 and 14-3-3 binding to the N terminus of MondoA. ..
- Challen G, Gardiner B, Caruana G, Kostoulias X, Martinez G, Crowe M, et al. Temporal and spatial transcriptional programs in murine kidney development. Physiol Genomics. 2005;23:159-71 pubmed
- Li H, Guo Y, Teng J, Ding M, Yu A, Chen J. 14-3-3gamma affects dynamics and integrity of glial filaments by binding to phosphorylated GFAP. J Cell Sci. 2006;119:4452-61 pubmed..This data demonstrates that 14-3-3gamma contributes to the regulation of dynamics of GFAP filaments, which may contribute to the stability of the cytoskeleton and the mechanisms of central nervous system neurodegenerative disease. ..
- Lee J, Jin Y, He G, Zeng S, Wang Y, Wahl G, et al. Hypoxia activates tumor suppressor p53 by inducing ATR-Chk1 kinase cascade-mediated phosphorylation and consequent 14-3-3? inactivation of MDMX protein. J Biol Chem. 2012;287:20898-903 pubmed publisher..These results demonstrate that hypoxia can activate p53 through inactivation of MDMX by the ATR-Chk1-MDMX-14-3-3? pathway. ..
- Sehgal L, Mukhopadhyay A, Rajan A, Khapare N, Sawant M, Vishal S, et al. 14-3-3?-Mediated transport of plakoglobin to the cell border is required for the initiation of desmosome assembly in vitro and in vivo. J Cell Sci. 2014;127:2174-88 pubmed publisher..Our results suggest that loss of 14-3-3? leads to decreased desmosome formation and a decrease in cell-cell adhesion in vitro, and in the mouse testis in vivo, leading to defects in testis organization and spermatogenesis. ..
- Li G, White C, Lam T, Pone E, Tran D, Hayama K, et al. Combinatorial H3K9acS10ph histone modification in IgH locus S regions targets 14-3-3 adaptors and AID to specify antibody class-switch DNA recombination. Cell Rep. 2013;5:702-714 pubmed publisher..Thus, H3K9acS10ph is a histone code that is "written" specifically in S regions and is "read" by 14-3-3 adaptors to target AID for CSR as an important biological outcome. ..
- Lonic A, Barry E, Quach C, Kobe B, Saunders N, Guthridge M. Fibroblast growth factor receptor 2 phosphorylation on serine 779 couples to 14-3-3 and regulates cell survival and proliferation. Mol Cell Biol. 2008;28:3372-85 pubmed publisher..In this regard, we have identified conserved putative phosphotyrosine/phosphoserine motifs in the cytoplasmic domains of diverse cell surface receptors, suggesting that they may perform important functional roles beyond the FGFRs. ..
- Ajjappala B, Kim Y, Kim M, Lee M, Lee K, Ki H, et al. 14-3-3 gamma is stimulated by IL-3 and promotes cell proliferation. J Immunol. 2009;182:1050-60 pubmed..These results indicate that deregulated expression of 14-3-3gamma may contribute to malignant transformation, possibly providing a new target for therapeutic intervention in hematopoietic neoplasms...
- Czirják G, Enyedi P. TRESK background K(+) channel is inhibited by phosphorylation via two distinct pathways. J Biol Chem. 2010;285:14549-57 pubmed publisher..In conclusion, two distinct inhibitory kinase pathways converge on TRESK, and their effect on the calcineurin-dependent regulation is differentially modulated by the functional availability of 14-3-3. ..
- Lee J, Lu H. 14-3-3Gamma inhibition of MDMX-mediated p21 turnover independent of p53. J Biol Chem. 2011;286:5136-42 pubmed publisher..Hence, our study as presented here unravels a new role for 14-3-3? in protecting p21 from MDMX-mediated proteasomal turnover, which may partially account for DNA damage-induced elevation of p21 levels independent of p53. ..
- Li X, Wang Q, Pan N, Lee S, Zhao Y, Chait B, et al. Phosphorylation-dependent 14-3-3 binding to LRRK2 is impaired by common mutations of familial Parkinson's disease. PLoS ONE. 2011;6:e17153 pubmed publisher..Furthermore, the reduction of phosphorylation/14-3-3 binding of LRRK2 due to the common familial PD-related mutations provides novel insight into the pathogenic mechanism of LRRK2-linked PD. ..
- Xu Z, Fulop Z, Wu G, Pone E, Zhang J, Mai T, et al. 14-3-3 adaptor proteins recruit AID to 5'-AGCT-3'-rich switch regions for class switch recombination. Nat Struct Mol Biol. 2010;17:1124-35 pubmed publisher..Finally, 14-3-3 proteins interacted directly with AID and enhanced AID-mediated in vitro DNA deamination, further emphasizing the important role of these adaptors in CSR. ..
- Challen G, Martinez G, Davis M, Taylor D, Crowe M, Teasdale R, et al. Identifying the molecular phenotype of renal progenitor cells. J Am Soc Nephrol. 2004;15:2344-57 pubmed..These findings may assist in the isolation and characterization of potential renal stem cells for use in cellular therapies for kidney disease. ..
- Yam P, Kent C, Morin S, Farmer W, Alchini R, Lepelletier L, et al. 14-3-3 proteins regulate a cell-intrinsic switch from sonic hedgehog-mediated commissural axon attraction to repulsion after midline crossing. Neuron. 2012;76:735-49 pubmed publisher..Therefore, we identify a 14-3-3 protein-dependent mechanism for a cell-intrinsic temporal switch in the polarity of axon turning responses. ..
- He G, Zhang Y, Lee J, Zeng S, Wang Y, Luo Z, et al. AMP-activated protein kinase induces p53 by phosphorylating MDMX and inhibiting its activity. Mol Cell Biol. 2014;34:148-57 pubmed publisher..Together, the results unveil a mechanism by which metabolic stresses activate AMPK, which, in turn, phosphorylates and inactivates MDMX, resulting in p53 stabilization and activation. ..
- Satchell M, Zhang X, Kochanek P, Dixon C, Jenkins L, Melick J, et al. A dual role for poly-ADP-ribosylation in spatial memory acquisition after traumatic brain injury in mice involving NAD+ depletion and ribosylation of 14-3-3gamma. J Neurochem. 2003;85:697-708 pubmed
- Herrmann D, Straubinger M, Hashemolhosseini S. Protein kinase CK2 interacts at the neuromuscular synapse with Rapsyn, Rac1, 14-3-3Î³, and Dok-7 proteins and phosphorylates the latter two. J Biol Chem. 2015;290:22370-84 pubmed publisher..Additionally, we mapped the interacting epitopes of all four binding partners to CK2 and thereby gained insights into the potential role of the CK2/Rapsyn interaction. ..
- Kathiresan T, Harvey M, Orchard S, Sakai Y, Sokolowski B. A protein interaction network for the large conductance Ca(2+)-activated K(+) channel in the mouse cochlea. Mol Cell Proteomics. 2009;8:1972-87 pubmed publisher..The studies described herein provide insights into BK-related functions that include not only cell excitation, but also cell signaling and apoptosis, and involve proteins concerned with Ca(2+) regulation, structure, and hearing loss. ..