Efp targets 14-3-3σ for proteolysis and promotes breast tumour growth

[1]  A. Brice,et al.  MID1, mutated in Opitz syndrome, encodes a ubiquitin ligase that targets phosphatase 2A for degradation , 2002, Nature Genetics.

[2]  P. Freemont,et al.  PML protein isoforms and the RBCC/TRIM motif , 2001, Oncogene.

[3]  H. Ruffner,et al.  Cancer-predisposing mutations within the RING domain of BRCA1: Loss of ubiquitin protein ligase activity and protection from radiation hypersensitivity , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[4]  C. Pickart,et al.  Mechanisms underlying ubiquitination. , 2001, Annual review of biochemistry.

[5]  A. Weissman,et al.  RING Finger Proteins Mediators of Ubiquitin Ligase Activity , 2000, Cell.

[6]  Mong-Hong Lee,et al.  Association of the Cyclin-dependent Kinases and 14-3-3 Sigma Negatively Regulates Cell Cycle Progression* , 2000, The Journal of Biological Chemistry.

[7]  Shinsei Minoshima,et al.  Familial Parkinson disease gene product, parkin, is a ubiquitin-protein ligase , 2000, Nature Genetics.

[8]  E. Dellambra,et al.  Downregulation of 14-3-3σ Prevents Clonal Evolution and Leads to Immortalization of Primary Human Keratinocytes , 2000, The Journal of cell biology.

[9]  A Orimo,et al.  Efp as a primary estrogen‐responsive gene in human breast cancer , 2000, FEBS letters.

[10]  S. Inoue,et al.  Estrogen receptors: how do they control reproductive and nonreproductive functions? , 2000, Biochemical and biophysical research communications.

[11]  P. Freemont.  Ubiquitination: RING for destruction? , 2000, Current Biology.

[12]  S. Inoue,et al.  Underdeveloped uterus and reduced estrogen responsiveness in mice with disruption of the estrogen-responsive finger protein gene, which is a direct target of estrogen receptor alpha. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[13]  T. Hunter,et al.  The tyrosine kinase negative regulator c-Cbl as a RING-type, E2-dependent ubiquitin-protein ligase. , 1999, Science.

[14]  K. Kinzler,et al.  14-3-3σ is required to prevent mitotic catastrophe after DNA damage , 1999, Nature.

[15]  Y. Ouchi,et al.  p57Kip2 Is Degraded through the Proteasome in Osteoblasts Stimulated to Proliferation by Transforming Growth Factor β1* , 1999, The Journal of Biological Chemistry.

[16]  Mike Tyers,et al.  One Ring to Rule a Superfamily of E3 Ubiquitin Ligases , 1999, Science.

[17]  S. Elledge,et al.  Rbx1, a component of the VHL tumor suppressor complex and SCF ubiquitin ligase. , 1999, Science.

[18]  S. Elledge,et al.  Reconstitution of G1 cyclin ubiquitination with complexes containing SCFGrr1 and Rbx1. , 1999, Science.

[19]  R. Honda,et al.  Association of p19ARF with Mdm2 inhibits ubiquitin ligase activity of Mdm2 for tumor suppressor p53 , 1999, The EMBO journal.

[20]  Y. Ouchi,et al.  p57(Kip2) is degraded through the proteasome in osteoblasts stimulated to proliferation by transforming growth factor beta1. , 1999, The Journal of biological chemistry.

[21]  K. Kinzler,et al.  Requirement for p53 and p21 to sustain G2 arrest after DNA damage. , 1998, Science.

[22]  K. Kinzler,et al.  14-3-3σ Is a p53-Regulated Inhibitor of G2/M Progression , 1997 .

[23]  S. Inoue,et al.  Molecular Cloning, Structure, and Expression of Mouse Estrogen-responsive Finger Protein Efp , 1995, The Journal of Biological Chemistry.

[24]  P. Beer-Romero,et al.  Role of the ubiquitin-proteasome pathway in regulating abundance of the cyclin-dependent kinase inhibitor p27. , 1995, Science.

[25]  D. Lane,et al.  Tumour suppressors, kinases and clamps: How p53 regulates the cell cycle in response to DNA damage , 1995, BioEssays : news and reviews in molecular, cellular and developmental biology.

[26]  P. Chambon,et al.  The N‐terminal part of TIF1, a putative mediator of the ligand‐dependent activation function (AF‐2) of nuclear receptors, is fused to B‐raf in the oncogenic protein T18. , 1995, The EMBO journal.

[27]  P. Baeuerle,et al.  A proteasome inhibitor prevents activation of NF‐kappa B and stabilizes a newly phosphorylated form of I kappa B‐alpha that is still bound to NF‐kappa B. , 1994, The EMBO journal.

[28]  Y. Ouchi,et al.  Genomic binding-site cloning reveals an estrogen-responsive gene that encodes a RING finger protein. , 1993, Proceedings of the National Academy of Sciences of the United States of America.

[29]  B. Vogelstein,et al.  A mammalian cell cycle checkpoint pathway utilizing p53 and GADD45 is defective in ataxia-telangiectasia , 1992, Cell.

[30]  E. Valverius,et al.  Complementary DNA cloning of a novel epithelial cell marker protein, HME1, that may be down-regulated in neoplastic mammary cells. , 1992, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.

[31]  D. W. Kim,et al.  Use of the human elongation factor 1α promoter as a versatile and efficient expression system , 1990 .