Smad3 and Smad4 cooperate with c-Jun/c-Fos to mediate TGF-β-induced transcription

TGF-β signalling from cell membrane to nucleus through SMAD proteins

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Human Smad3 and Smad4 Are Sequence-Specific Transcription Activators

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Partnership between DPC4 and SMAD proteins in TGF-β signalling pathways

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Opposing BMP and EGF signalling pathways converge on the TGF-β family mediator Smad1

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Receptor-associated Mad homologues synergize as effectors of the TGF-β response

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A human Mad protein acting as a BMP-regulated transcriptional activator

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The tumor suppressor Smad4/DPC4 and transcriptional adaptor CBP/p300 are coactivators for Smad3 in TGF-β-induced transcriptional activationPreprint

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Mutations increasing autoinhibition inactivate tumour suppressors Smad2 and Smad4

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Identification of regulatory sequences in the type 1 plasminogen activator inhibitor gene responsive to transforming growth factor beta.

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The tumor suppressor Smad4/DPC 4 as a central mediator of Smad function

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Smad2 transduces common signals from receptor serine–threonine and tyrosine kinasesPreprint

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Tumor Suppressor Smad4 Is a Transforming Growth Factor β-Inducible DNA Binding Protein

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Human Transforming Growth Factor- β3: Recombinant Expression, Purification, and Biological Activities in Comparison with Transforming Growth Factors-β 1 and -β2

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Heteromeric and Homomeric Interactions Correlate with Signaling Activity and Functional Cooperativity of Smad3 and Smad4/DPC4

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Transformation suppressor activity of a Jun transcription factor lacking its activation domain

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Transforming Growth Factor-β (TGF-β)-induced Down-regulation of Cyclin A Expression Requires a Functional TGF-β Receptor Complex

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Ligand-independent Activation of Transforming Growth Factor (TGF) β Signaling Pathways by Heteromeric Cytoplasmic Domains of TGF-β Receptors

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Regulation of Clusterin Gene Expression by Transforming Growth Factor β

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Elevation of AP1 activity during F9 cell differentiation is due to increased c-jun transcription.

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The Human Leukemia Oncogene bcr-abl Abrogates the Anchorage Requirement but Not the Growth Factor Requirement for Proliferation

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Down-regulation of the Cyclin A Promoter by Transforming Growth Factor-β1 Is Associated with a Reduction in Phosphorylated Activating Transcription Factor-1 and Cyclic AMP-responsive Element-binding Protein

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Transcriptional activation by TGFβ1 mediated by the dyad symmetry element (DSE) and the TPA responsive element (TRE)

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Tissue factor gene transcription in serum-stimulated fibroblasts is mediated by recruitment of c-Fos into specific AP-1 DNA-binding complexes

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TGF-β Signaling in Tumor Suppression and Cancer Progression

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Intrinsic Disorder in Cell-signaling and Cancer-associated Proteins

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Reversible and adaptive resistance to BRAF(V600E) inhibition in melanoma

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TGF-β1 Signaling and Tissue Fibrosis

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Specificity, versatility, and control of TGF-β family signaling

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Transforming Growth Factor-β1 to the Bone

Janssens, K., ten Dijke, P., Janssens, S., & Van Hul, W. (2005) · Endocrine Reviews · doi:10.1210/er.2004-0001 · Cited by 710 · see citing works

TGF‐β‐induced repression of CBFA1 by Smad3 decreases cbfa1 and osteocalcin expression and inhibits osteoblast differentiation

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TGF-β inhibits muscle differentiation through functional repression of myogenic transcription factors by Smad3

Liu, D., Black, B. L., & Derynck, R. (2001) · Genes & Development · doi:10.1101/gad.925901 · Cited by 399 · see citing works

Transforming Growth Factor-β Inhibits Adipocyte Differentiation by Smad3 Interacting with CCAAT/Enhancer-binding Protein (C/EBP) and Repressing C/EBP Transactivation Function

Choy, L., & Derynck, R. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m212259200 · Cited by 343 · see citing works

The TGF-β/Smad4 Signaling Pathway in Pancreatic Carcinogenesis and Its Clinical Significance

Ahmed, S., Bradshaw, A.-D., Gera, S., Dewan, M., & Xu, R. (2017) · Journal of Clinical Medicine · doi:10.3390/jcm6010005 · Cited by 174 · see citing works

Occult polyclonality of preclinical pancreatic cancer models drives in vitro evolution

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A Strong Anti-Inflammatory Signature Revealed by Liver Transcription Profiling of Tmprss6-/- Mice

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Positive and negative feedback regulation of the TGF-β1 explains two equilibrium states in skin aging

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E1A dependent up-regulation of c-jun/AP-1 activity

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Differential display of human marrow stromal cells reveals unique mRNA expression patterns in response to dexamethasone

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AP1 Transcription Factors in Epidermal Differentiation and Skin Cancer

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Stepwise Transformation of Rat Embryo Fibroblasts: c-Jun, JunB, or JunD Can Cooperate with Ras for Focus Formation, but a c-Jun-Containing Heterodimer Is Required for Immortalization

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Stable induction of c-jun mRNA expression in normal human keratinocytes by agents that induce predifferentiation growth arrest.

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