Smad Transcriptional Co-Activators and Co-Repressors

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[2]  R. Derynck,et al.  Repression of Bone Morphogenetic Protein and Activin-inducible Transcription by Evi-1* , 2005, Journal of Biological Chemistry.

[3]  Sylvia M. Wilson,et al.  SnoN Is a Cell Type-specific Mediator of Transforming Growth Factor-β Responses* , 2005, Journal of Biological Chemistry.

[4]  F. Verrecchia,et al.  The steroid receptor co-activator-1 (SRC-1) potentiates TGF-β/Smad signaling: role of p300/CBP , 2005, Oncogene.

[5]  I. Matsuura,et al.  The Smad3 linker region contains a transcriptional activation domain. , 2005, The Biochemical journal.

[6]  M. Barton,et al.  A Direct Intersection between p53 and Transforming Growth Factor β Pathways Targets Chromatin Modification and Transcription Repression of the α-Fetoprotein Gene , 2005, Molecular and Cellular Biology.

[7]  F. Lallemand,et al.  The novel E3 ubiquitin ligase Tiul1 associates with TGIF to target Smad2 for degradation , 2004, The EMBO journal.

[8]  Y. Maeda,et al.  Chick Dach1 interacts with the Smad complex and Sin3a to control AER formation and limb development along the proximodistal axis , 2004, Development.

[9]  F. Liu,et al.  Repression of Endogenous Smad7 by Ski* , 2004, Journal of Biological Chemistry.

[10]  R. Lechleider,et al.  Suv39h histone methyltransferases interact with Smads and cooperate in BMP-induced repression , 2004, Oncogene.

[11]  K. Miyazono,et al.  c-Ski inhibits the TGF-β signaling pathway through stabilization of inactive Smad complexes on Smad-binding elements , 2004, Oncogene.

[12]  C. Caldas,et al.  p300/CBP and cancer , 2004, Oncogene.

[13]  R. Derynck,et al.  TGF‐β‐activated Smad3 represses MEF2‐dependent transcription in myogenic differentiation , 2004, The EMBO journal.

[14]  M. Matsuoka,et al.  Aberrant expression of the MEL1S gene identified in association with hypomethylation in adult T-cell leukemia cells. , 2004, Blood.

[15]  K. Luo.  Ski and SnoN: negative regulators of TGF-β signaling , 2004 .

[16]  K. Miyazono,et al.  Regulation of transforming growth factor‐β and bone morphogenetic protein signalling by transcriptional coactivator GCN5 , 2004, Genes to cells : devoted to molecular & cellular mechanisms.

[17]  K. Miyazono,et al.  Interaction with Smad4 is indispensable for suppression of BMP signaling by c-Ski. , 2003, Molecular biology of the cell.

[18]  Anping Li,et al.  DACH1 Inhibits Transforming Growth Factor-β Signaling through Binding Smad4* , 2003, Journal of Biological Chemistry.

[19]  Xin-Hua Feng,et al.  Smad6 Recruits Transcription Corepressor CtBP To Repress Bone Morphogenetic Protein-Induced Transcription , 2003, Molecular and Cellular Biology.

[20]  N. Ueki,et al.  Direct Interaction of Ski with Either Smad3 or Smad4 Is Necessary and Sufficient for Ski-mediated Repression of Transforming Growth Factor-β Signaling* , 2003, Journal of Biological Chemistry.

[21]  L. Nelles,et al.  Interaction between Smad-interacting Protein-1 and the Corepressor C-terminal Binding Protein Is Dispensable for Transcriptional Repression of E-cadherin* , 2003, Journal of Biological Chemistry.

[22]  N. Ueki,et al.  Signal-dependent N-CoR Requirement for Repression by the Ski Oncoprotein* , 2003, Journal of Biological Chemistry.

[23]  Hyungtae Kim,et al.  The Ski-binding Protein C184M Negatively Regulates Tumor Growth Factor-β Signaling by Sequestering the Smad Proteins in the Cytoplasm* , 2003, Journal of Biological Chemistry.

[24]  E. Medrano.  Repression of TGF-β signaling by the oncogenic protein SKI in human melanomas: consequences for proliferation, survival, and metastasis , 2003, Oncogene.

[25]  A. Postigo,et al.  Regulation of Smad signaling through a differential recruitment of coactivators and corepressors by ZEB proteins , 2003, The EMBO journal.

[26]  K. Miyazono,et al.  Two Short Segments of Smad3 Are Important for Specific Interaction of Smad3 with c-Ski and SnoN* 210 , 2003, The Journal of Biological Chemistry.

[27]  Yigong Shi,et al.  Structural Mechanism of Smad4 Recognition by the Nuclear Oncoprotein Ski Insights on Ski-Mediated Repression of TGF-β Signaling , 2002, Cell.

[28]  K. Jeang,et al.  Human T-cell Lymphotropic Virus Type 1 Tax Inhibits Transforming Growth Factor-β Signaling by Blocking the Association of Smad Proteins with Smad-binding Element* , 2002, The Journal of Biological Chemistry.

[29]  F. Lallemand,et al.  c-Jun Associates with the Oncoprotein Ski and Suppresses Smad2 Transcriptional Activity* , 2002, The Journal of Biological Chemistry.

[30]  A. Näär,et al.  A component of the ARC/Mediator complex required for TGFβ/Nodal signalling , 2002, Nature.

[31]  B. Qin,et al.  Smad3 allostery links TGF-beta receptor kinase activation to transcriptional control. , 2002, Genes & development.

[32]  J. Massagué,et al.  E2F4/5 and p107 as Smad Cofactors Linking the TGFβ Receptor to c-myc Repression , 2002, Cell.

[33]  S. Ishii,et al.  Increased susceptibility to tumorigenesis of ski-deficient heterozygous mice , 2001, Oncogene.

[34]  M. Kirschner,et al.  The anaphase-promoting complex mediates TGF-beta signaling by targeting SnoN for destruction. , 2001, Molecular cell.

[35]  E. Medrano,et al.  Cytoplasmic localization of the oncogenic protein Ski in human cutaneous melanomas in vivo: functional implications for transforming growth factor beta signaling. , 2001, Cancer research.

[36]  J. Wrana,et al.  Smad3 recruits the anaphase-promoting complex for ubiquitination and degradation of SnoN. , 2001, Genes & development.

[37]  J. Massagué,et al.  The Smad transcriptional corepressor TGIF recruits mSin3. , 2001, Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research.

[38]  M. Crossley,et al.  Evi-1 Transforming and Repressor Activities Are Mediated by CtBP Co-repressor Proteins* , 2001, The Journal of Biological Chemistry.

[39]  J. Wrana,et al.  TGF-β induces assembly of a Smad2–Smurf2 ubiquitin ligase complex that targets SnoN for degradation , 2001, Nature Cell Biology.

[40]  Yuetsu Tanaka,et al.  Human T-cell leukemia virus type I oncoprotein Tax represses Smad-dependent transforming growth factor beta signaling through interaction with CREB-binding protein/p300. , 2001, Blood.

[41]  Xu Cao,et al.  Transcriptional Mechanisms of Bone Morphogenetic Protein-induced Osteoprotegrin Gene Expression* , 2001, The Journal of Biological Chemistry.

[42]  J. Massagué,et al.  Epidermal growth factor signaling via Ras controls the Smad transcriptional co‐repressor TGIF , 2001, The EMBO journal.

[43]  C. Heldin,et al.  The transcriptional co-activator P/CAF potentiates TGF-β/Smad signaling , 2000 .

[44]  K. Ozato,et al.  Distinct but overlapping roles of histone acetylase PCAF and of the closely related PCAF-B/GCN5 in mouse embryogenesis. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[45]  M. Gimbrone,et al.  Inhibition of E-Selectin Gene Expression by Transforming Growth Factor β in Endothelial Cells Involves Coactivator Integration of Smad and Nuclear Factor κB–Mediated Signals , 2000, The Journal of experimental medicine.

[46]  E. Zackai,et al.  Mutations in TGIF cause holoprosencephaly and link NODAL signalling to human neural axis determination , 2000, Nature Genetics.

[47]  S. Ishii,et al.  The sno gene, which encodes a component of the histone deacetylase complex, acts as a tumor suppressor in mice , 2000, The EMBO journal.

[48]  T. Shioda,et al.  The Smad4 Activation Domain (SAD) Is a Proline-rich, p300-dependent Transcriptional Activation Domain* , 2000, The Journal of Biological Chemistry.

[49]  K. Miyazono,et al.  c-Ski Acts as a Transcriptional Co-repressor in Transforming Growth Factor-β Signaling through Interaction with Smads* , 1999, The Journal of Biological Chemistry.

[50]  K. Luo,et al.  Negative Feedback Regulation of TGF-β Signaling by the SnoN Oncoprotein , 1999 .

[51]  K. Miyazono,et al.  E1A Inhibits Transforming Growth Factor-β Signaling through Binding to Smad Proteins* 210 , 1999, The Journal of Biological Chemistry.

[52]  L. Nelles,et al.  SIP1, a Novel Zinc Finger/Homeodomain Repressor, Interacts with Smad Proteins and Binds to 5′-CACCT Sequences in Candidate Target Genes* , 1999, The Journal of Biological Chemistry.

[53]  K. Miyazono,et al.  Synergistic signaling in fetal brain by STAT3-Smad1 complex bridged by p300. , 1999, Science.

[54]  J. Massagué,et al.  A Smad Transcriptional Corepressor , 1999, Cell.

[55]  K. Miyazono,et al.  Convergence of transforming growth factor-beta and vitamin D signaling pathways on SMAD transcriptional coactivators. , 1999, Science.

[56]  S. Ishii,et al.  Ski is a component of the histone deacetylase complex required for transcriptional repression by Mad and thyroid hormone receptor. , 1999, Genes & development.

[57]  R. Derynck,et al.  The tumor suppressor Smad4/DPC4 and transcriptional adaptor CBP/p300 are coactivators for smad3 in TGF-beta-induced transcriptional activation. , 1998, Genes & development.

[58]  K. Irie,et al.  The oncoprotein Evi-1 represses TGF-β signalling by inhibiting Smad3 , 1998, Nature.

[59]  David Newsome,et al.  Gene Dosage–Dependent Embryonic Development and Proliferation Defects in Mice Lacking the Transcriptional Integrator p300 , 1998, Cell.

[60]  H. Masuya,et al.  Abnormal skeletal patterning in embryos lacking a single Cbp allele: a partial similarity with Rubinstein-Taybi syndrome. , 1997, Proceedings of the National Academy of Sciences of the United States of America.