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Gene Review

Sfn  -  stratifin

Mus musculus

Synonyms: 14-3-3 protein sigma, 14-3-3 sigma, Er, MME1, Mkrn3, ...
 
 
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Disease relevance of Sfn

 

High impact information on Sfn

  • Our results indicate that Irf6 is a key determinant of the keratinocyte proliferation-differentiation switch and that Irf6 and Sfn interact genetically in this process [3].
  • We further demonstrate that mice that are compound heterozygotes for mutations in Irf6 and the gene encoding the cell cycle regulator protein stratifin (Sfn; also known as 14-3-3sigma) show similar defects of keratinizing epithelia [3].
  • Stratifin (Sfn, also called 14-3-3sigma) is highly expressed in differentiating epidermis and mediates cell cycle arrest [4].
  • A mutation in stratifin is responsible for the repeated epilation (Er) phenotype in mice [4].
  • Loss of Efp function in mouse embryonic fibroblasts results in an accumulation of 14-3-3 sigma, which is responsible for reduced cell growth [1].
 

Biological context of Sfn

 

Anatomical context of Sfn

  • Ectopic overexpression of WT 14-3-3sigma in Er/Er keratinocytes rescues defects in keratinocyte differentiation [6].
  • BRCA1 is a selective co-activator of 14-3-3 sigma gene transcription in mouse embryonic stem cells [9].
  • Hair follicles of the Er/+, but not the normal adult, were stained with this antiserum to RPB in the outer root sheath layer [10].
  • RBP contents in plasma and in liver microsomes were also similar in normal and Er/+ adults despite different retinol contents in the Er/+ tissues [10].
  • Tissue-specific regulation of junctional communication in the skin of mouse fetuses homozygous for the repeated epilation (Er) mutation [11].
 

Associations of Sfn with chemical compounds

 

Physical interactions of Sfn

 

Regulatory relationships of Sfn

  • Significantly, we show that 14-3-3 sigma inhibits Akt-mediated cell growth, transformation, and tumorigenesis [7].
  • The only p53 target gene down-regulated with the loss of BRCA1 was 14-3-3 sigma, a major G(2)/M checkpoint control gene [9].
 

Other interactions of Sfn

  • These results suggest that the pf and Er genes may be expressed systemically and that transfer of the mutant skin to a "normal" environment results in the recovery of a normal phenotype [5].
  • Plasma retinol binding protein (RBP) was tested as a possible candidate gene for the Er defect because of the importance of retinol as a modulator of epithelial morphogenesis and differentiation [13].
  • Here we show that Efp is a RING-finger-dependent ubiquitin ligase (E3) that targets proteolysis of 14-3-3 sigma, a negative cell cycle regulator that causes G2 arrest [1].
  • Distal chromosome 4 deletions occur in a significantly higher proportion of Erbb2 than PyMT tumors and encompass 14-3-3sigma (Stratifin), which is expressed at low or undetectable levels in the majority of NeuNT tumors [14].
  • Stratifin, a keratinocyte specific 14-3-3 protein, harbors a pleckstrin homology (PH) domain and enhances protein kinase C activity [15].
 

Analytical, diagnostic and therapeutic context of Sfn

  • We identified an insertion mutation in the gene Sfn in repeated epilation (Er) mutant mice by positional cloning [4].
  • The developmental abilities of skin fragments from these Er/Er mouse embryos were studied in organ culture and in grafts performed either under the renal capsule of young mouse hosts or under the skin of mouse fetuses [16].

References

  1. Efp targets 14-3-3 sigma for proteolysis and promotes breast tumour growth. Urano, T., Saito, T., Tsukui, T., Fujita, M., Hosoi, T., Muramatsu, M., Ouchi, Y., Inoue, S. Nature (2002) [Pubmed]
  2. Multiple cutaneous papillomas and carcinomas that develop spontaneously in a mouse mutant, the repeated epilation heterozygote Er/+. Lutzner, M.A., Guenet, J.L., Breitburd, F. J. Natl. Cancer Inst. (1985) [Pubmed]
  3. Irf6 is a key determinant of the keratinocyte proliferation-differentiation switch. Richardson, R.J., Dixon, J., Malhotra, S., Hardman, M.J., Knowles, L., Boot-Handford, R.P., Shore, P., Whitmarsh, A., Dixon, M.J. Nat. Genet. (2006) [Pubmed]
  4. A mutation in stratifin is responsible for the repeated epilation (Er) phenotype in mice. Herron, B.J., Liddell, R.A., Parker, A., Grant, S., Kinne, J., Fisher, J.K., Siracusa, L.D. Nat. Genet. (2005) [Pubmed]
  5. Abnormal expression and processing of keratins in pupoid fetus (pf/pf) and repeated epilation (Er/Er) mutant mice. Fisher, C., Jones, A., Roop, D.R. J. Cell Biol. (1987) [Pubmed]
  6. Identification of 14-3-3sigma mutation causing cutaneous abnormality in repeated-epilation mutant mouse. Li, Q., Lu, Q., Estepa, G., Verma, I.M. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  7. DNA damage-induced protein 14-3-3 sigma inhibits protein kinase B/Akt activation and suppresses Akt-activated cancer. Yang, H., Wen, Y.Y., Zhao, R., Lin, Y.L., Fournier, K., Yang, H.Y., Qiu, Y., Diaz, J., Laronga, C., Lee, M.H. Cancer Res. (2006) [Pubmed]
  8. Association of the cyclin-dependent kinases and 14-3-3 sigma negatively regulates cell cycle progression. Laronga, C., Yang, H.Y., Neal, C., Lee, M.H. J. Biol. Chem. (2000) [Pubmed]
  9. BRCA1 is a selective co-activator of 14-3-3 sigma gene transcription in mouse embryonic stem cells. Aprelikova, O., Pace, A.J., Fang, B., Koller, B.H., Liu, E.T. J. Biol. Chem. (2001) [Pubmed]
  10. Altered retinoid distribution in the repeated epilation (Er) mutant mouse. Jones, A.H., Lehman, P., Dale, B.A. J. Craniofac. Genet. Dev. Biol. (1992) [Pubmed]
  11. Tissue-specific regulation of junctional communication in the skin of mouse fetuses homozygous for the repeated epilation (Er) mutation. Kam, E., Pitts, J.D. Development (1989) [Pubmed]
  12. 14-3-3 sigma positively regulates p53 and suppresses tumor growth. Yang, H.Y., Wen, Y.Y., Chen, C.H., Lozano, G., Lee, M.H. Mol. Cell. Biol. (2003) [Pubmed]
  13. Chromosomal localization of the retinol binding protein gene and its elimination as a candidate gene for the repeated epilation (Er) mutation in mice. Dale, B.A., Jones, A.H., Presland, R., Adler, D.A., Disteche, C.M. J. Craniofac. Genet. Dev. Biol. (1992) [Pubmed]
  14. Copy number aberrations in mouse breast tumors reveal loci and genes important in tumorigenic receptor tyrosine kinase signaling. Hodgson, J.G., Malek, T., Bornstein, S., Hariono, S., Ginzinger, D.G., Muller, W.J., Gray, J.W. Cancer Res. (2005) [Pubmed]
  15. Stratifin, a keratinocyte specific 14-3-3 protein, harbors a pleckstrin homology (PH) domain and enhances protein kinase C activity. Dellambra, E., Patrone, M., Sparatore, B., Negri, A., Ceciliani, F., Bondanza, S., Molina, F., Cancedda, F.D., De Luca, M. J. Cell. Sci. (1995) [Pubmed]
  16. The differentiation of repeated epilation (Er/Er) mouse mutant skin in organ culture and in grafts. Salaün, J., Salzgeber, B., Guénet, J.L. Anat. Embryol. (1986) [Pubmed]
 
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