Associated Papers
The SOS1 Inhibitor MRTX0902 Blocks KRAS Activation and Demonstrates Antitumor Activity in Cancers Dependent on KRAS Nucleotide Loading.
Sudhakar N et al.
Molecular Cancer Therapeutics, 2024
A multiplexed time-resolved fluorescence resonance energy transfer ultrahigh-throughput screening assay for targeting the SMAD4-SMAD3-DNA complex.
Ouyang W et al.
Journal of Molecular Cell Biology, 2024
A multiplexed time-resolved fluorescence resonance energy transfer ultrahigh-throughput screening assay for targeting SMAD4-SMAD3-DNA complex.
Ouyang W et al.
Biorxiv : the Preprint Server for Biology, 2023
Consequences of Mutations and Abnormal Expression of SMAD4 in Tumors and T Cells.
Wan R et al.
Oncotargets and Therapy, 2021
SMAD4 rare variants in individuals and families with thoracic aortic aneurysms and dissections.
Duan XY et al.
European Journal of Human Genetics : Ejhg, 2019
Mutant KRAS-driven cancers depend on PTPN11/SHP2 phosphatase.
Ruess DA et al.
Nature Medicine, 2018
Digital next-generation sequencing identifies low-abundance mutations in pancreatic juice samples collected from the duodenum of patients with pancreatic cancer and intraductal papillary mucinous neoplasms.
Yu J et al.
Gut, 2017
Structural determinants of Smad function in TGF-β signaling.
Macias MJ et al.
Trends in Biochemical Sciences, 2015
Postnatal ablation of osteoblast Smad4 enhances proliferative responses to canonical Wnt signaling through interactions with β-catenin.
Salazar VS et al.
Journal of Cell Science, 2013
SMAD2, SMAD3 and SMAD4 mutations in colorectal cancer.
Fleming NI et al.
Cancer Research, 2013
A novel human Smad4 mutation is involved in papillary thyroid carcinoma progression.
D'Inzeo S et al.
Endocrine-related Cancer, 2012
SMURF1 amplification promotes invasiveness in pancreatic cancer.
Kwei KA et al.
Plos One, 2011
Phospho-control of TGF-beta superfamily signaling.
Wrighton KH et al.
Cell Research, 2009
To (TGF)beta or not to (TGF)beta: fine-tuning of Smad signaling via post-translational modifications.
Wrighton KH et al.
Cellular Signalling, 2008
Acute myelogenous leukemia-derived SMAD4 mutations target the protein to ubiquitin-proteasome degradation.
Yang L et al.
Human Mutation, 2006
DNA-binding domain mutations in SMAD genes yield dominant-negative proteins or a neomorphic protein that can activate WG target genes in Drosophila.
Takaesu NT et al.
Development (cambridge, England), 2005
Germ-layer specification and control of cell growth by Ectodermin, a Smad4 ubiquitin ligase.
Dupont S et al.
Cell, 2005
Two somatic biallelic lesions within and near SMAD4 in a human breast cancer cell line.
Jakob J et al.
Genes, Chromosomes & Cancer, 2005
Regulation of the TGFbeta signalling pathway by ubiquitin-mediated degradation.
Izzi L et al.
Oncogene, 2004
Regulation of large-scale chromatin unfolding by Smad4.
Yan J et al.
Biochemical and Biophysical Research Communications, 2004
Tumor-derived C-terminal mutations of Smad4 with decreased DNA binding activity and enhanced intramolecular interaction.
Kuang C et al.
Oncogene, 2004
Receptor-regulated Smads in TGF-beta signaling.
Liu F
Frontiers in Bioscience : a Journal and Virtual Library, 2003
Differential ubiquitination defines the functional status of the tumor suppressor Smad4.
Morén A et al.
The Journal of Biological Chemistry, 2003
SUMO-1/Ubc9 promotes nuclear accumulation and metabolic stability of tumor suppressor Smad4.
Lin X et al.
The Journal of Biological Chemistry, 2003
Sumoylation of Smad4, the common Smad mediator of transforming growth factor-beta family signaling.
Lee PS et al.
The Journal of Biological Chemistry, 2003
An extended bipartite nuclear localization signal in Smad4 is required for its nuclear import and transcriptional activity.
Xiao Z et al.
Oncogene, 2003
Loss of Smad4 function in pancreatic tumors: C-terminal truncation leads to decreased stability.
Maurice D et al.
The Journal of Biological Chemistry, 2001
Functional consequences of tumorigenic missense mutations in the amino-terminal domain of Smad4.
Morén A et al.
Oncogene, 2000
Functional mapping of the MH1 DNA-binding domain of DPC4/SMAD4.
Jones JB et al.
Nucleic Acids Research, 2000
Mutations in the tumor suppressors Smad2 and Smad4 inactivate transforming growth factor beta signaling by targeting Smads to the ubiquitin-proteasome pathway.
Xu J et al.
Proceedings of the National Academy of Sciences of the United States of America, 2000
Smad2 and Smad4 gene mutations in hepatocellular carcinoma.
Yakicier MC et al.
Oncogene, 1999
Cooperative binding of Smad proteins to two adjacent DNA elements in the plasminogen activator inhibitor-1 promoter mediates transforming growth factor beta-induced smad-dependent transcriptional activation.
Stroschein SL et al.
The Journal of Biological Chemistry, 1999
Smad4/DPC4 and Smad3 mediate transforming growth factor-beta (TGF-beta) signaling through direct binding to a novel TGF-beta-responsive element in the human plasminogen activator inhibitor-1 promoter.
Song CZ et al.
The Journal of Biological Chemistry, 1998
Crystal structure of a Smad MH1 domain bound to DNA: insights on DNA binding in TGF-beta signaling.
Shi Y et al.
Cell, 1998
TGF-beta signaling and cancer: structural and functional consequences of mutations in Smads.
Hata A et al.
Molecular Medicine Today, 1998
Alterations in components of the TGF-beta superfamily signaling pathways in human cancer.
Levy L et al.
Cytokine & Growth Factor Reviews, 0