Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Gene Ontology annotation of human sequence-specific DNA binding transcription factors (DbTFs) based on the TFClass database
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
Identification and characterization of a PDZ protein that interacts with activin type II receptors.
Transforming growth factor beta -inducible independent binding of SMAD to the Smad7 promoter.
Inactivation of menin, a Smad3-interacting protein, blocks transforming growth factor type beta signaling.
Smurf1 interacts with transforming growth factor-beta type I receptor through Smad7 and induces receptor degradation.
Ski-interacting protein interacts with Smad proteins to augment transforming growth factor-beta-dependent transcription.
The adaptor molecule Disabled-2 links the transforming growth factor beta receptors to the Smad pathway.
Smad3 allostery links TGF-beta receptor kinase activation to transcriptional control.
Cellular response to hypoxia involves signaling via Smad proteins.
TGFbeta-Smad signalling in postoperative human lens epithelial cells.
Identification of three novel Smad binding proteins involved in cell polarity.
Features of a Smad3 MH1-DNA complex. Roles of water and zinc in DNA binding.
Direct interaction of Ski with either Smad3 or Smad4 is necessary and sufficient for Ski-mediated repression of transforming growth factor-beta signaling.
Requirement of the co-repressor homeodomain-interacting protein kinase 2 for ski-mediated inhibition of bone morphogenetic protein-induced transcriptional activation.
Identification of glucocorticoid receptor domains involved in transrepression of transforming growth factor-beta action.
DACH1 inhibits transforming growth factor-beta signaling through binding Smad4.
Differential regulation of TGF-beta signaling through Smad2, Smad3 and Smad4.
A novel E1A-like inhibitor of differentiation (EID) family member, EID-2, suppresses transforming growth factor (TGF)-beta signaling by blocking TGF-beta-induced formation of Smad3-Smad4 complexes.
Atrophin-1-interacting protein 4/human Itch is a ubiquitin E3 ligase for human enhancer of filamentation 1 in transforming growth factor-beta signaling pathways.
Integration of Smad and forkhead pathways in the control of neuroepithelial and glioblastoma cell proliferation.
Activin receptor-like kinase-7 induces apoptosis through activation of MAPKs in a Smad3-dependent mechanism in hepatoma cells.
Nodal and ALK7 inhibit proliferation and induce apoptosis in human trophoblast cells.
Functional proteomics mapping of a human signaling pathway.
Hepatitis C viral proteins interact with Smad3 and differentially regulate TGF-beta/Smad3-mediated transcriptional activation.
Structural basis of heteromeric smad protein assembly in TGF-beta signaling.
Proteomics-based identification of proteins interacting with Smad3: SREBP-2 forms a complex with Smad3 and inhibits its transcriptional activity.
The Smad3 linker region contains a transcriptional activation domain.
The integral inner nuclear membrane protein MAN1 physically interacts with the R-Smad proteins to repress signaling by the transforming growth factor-{beta} superfamily of cytokines.
CHIP controls the sensitivity of transforming growth factor-beta signaling by modulating the basal level of Smad3 through ubiquitin-mediated degradation.
Nuclear targeting of transforming growth factor-beta-activated Smad complexes.
Oligomerization of Evi-1 regulated by the PR domain contributes to recruitment of corepressor CtBP.
Hepatitis C virus core variants isolated from liver tumor but not from adjacent non-tumor tissue interact with Smad3 and inhibit the TGF-beta pathway.
Cloning and functional characterization of a new Ski homolog, Fussel-18, specifically expressed in neuronal tissues.
PPM1A functions as a Smad phosphatase to terminate TGFbeta signaling.
The novel PIAS-like protein hZimp10 enhances Smad transcriptional activity.
Association of polymorphisms of IGF1R and genes in the transforming growth factor- beta /bone morphogenetic protein pathway with bacteremia in sickle cell anemia.
Potentiation of Smad-mediated transcriptional activation by the RNA-binding protein RBPMS.
The MH1 domain of Smad3 interacts with Pax6 and represses autoregulation of the Pax6 P1 promoter.
Fussel-15, a novel Ski/Sno homolog protein, antagonizes BMP signaling.
Involvement of the constitutive complex formation of c-Ski/SnoN with Smads in the impaired negative feedback regulation of transforming growth factor beta signaling in scleroderma fibroblasts.
Msk is required for nuclear import of TGF-{beta}/BMP-activated Smads.
Transforming growth factor-beta1, transforming growth factor-beta2, and transforming growth factor-beta3 enhance ovarian cancer metastatic potential by inducing a Smad3-dependent epithelial-to-mesenchymal transition.
SMAD proteins control DROSHA-mediated microRNA maturation.
TAZ controls Smad nucleocytoplasmic shuttling and regulates human embryonic stem-cell self-renewal.
Identification of novel Smad2 and Smad3 associated proteins in response to TGF-beta1.
Ligand-dependent ubiquitination of Smad3 is regulated by casein kinase 1 gamma 2, an inhibitor of TGF-beta signaling.
HMGA2 and Smads co-regulate SNAIL1 expression during induction of epithelial-to-mesenchymal transition.
Holding their own: the noncanonical roles of Smad proteins.
Ski co-repressor complexes maintain the basal repressed state of the TGF-beta target gene, SMAD7, via HDAC3 and PRMT5.
SKI and MEL1 cooperate to inhibit transforming growth factor-beta signal in gastric cancer cells.
Pin1 down-regulates transforming growth factor-beta (TGF-beta) signaling by inducing degradation of Smad proteins.
FAM/USP9x, a deubiquitinating enzyme essential for TGFbeta signaling, controls Smad4 monoubiquitination.
Nuclear export of Smad2 and Smad3 by RanBP3 facilitates termination of TGF-beta signaling.
MiR-21 regulates adipogenic differentiation through the modulation of TGF-beta signaling in mesenchymal stem cells derived from human adipose tissue.
MTMR4 attenuates transforming growth factor beta (TGFbeta) signaling by dephosphorylating R-Smads in endosomes.
TMEPAI, a transmembrane TGF-beta-inducible protein, sequesters Smad proteins from active participation in TGF-beta signaling.
An atlas of combinatorial transcriptional regulation in mouse and man.
IL-37 is a fundamental inhibitor of innate immunity.
The Crumbs complex couples cell density sensing to Hippo-dependent control of the TGF-β-SMAD pathway.
Selective targeting of activating and inhibitory Smads by distinct WWP2 ubiquitin ligase isoforms differentially modulates TGFβ signalling and EMT.
Homeodomain protein DLX4 counteracts key transcriptional control mechanisms of the TGF-β cytostatic program and blocks the antiproliferative effect of TGF-β.
Response gene to complement 32 interacts with Smad3 to promote epithelial-mesenchymal transition of human renal tubular cells.
Nodal enhances the activity of FoxO3a and its synergistic interaction with Smads to regulate cyclin G2 transcription in ovarian cancer cells.
Antagonistic regulation of EMT by TIF1γ and Smad4 in mammary epithelial cells.
HEB and E2A function as SMAD/FOXH1 cofactors.
USP15 is a deubiquitylating enzyme for receptor-activated SMADs.
Toward an understanding of the protein interaction network of the human liver.
Ablation of Smurf2 reveals an inhibition in TGF-β signalling through multiple mono-ubiquitination of Smad3.
Bone morphogenetic protein-3b (BMP-3b) inhibits osteoblast differentiation via Smad2/3 pathway by counteracting Smad1/5/8 signaling.
Intercellular variation in signaling through the TGF-β pathway and its relation to cell density and cell cycle phase.
CSMD1 exhibits antitumor activity in A375 melanoma cells through activation of the Smad pathway.
Kindlin-2 mediates activation of TGF-β/Smad signaling and renal fibrosis.
Crosstalk between TGF-β/Smad3 and BMP/BMPR2 signaling pathways via miR-17-92 cluster in carotid artery restenosis.
Hsp70 and Hsp90 oppositely regulate TGF-β signaling through CHIP/Stub1.
C18 ORF1, a novel negative regulator of transforming growth factor-β signaling.
Pin1 promotes degradation of Smad proteins and their interaction with phosphorylated tau in Alzheimer's disease.
A Smad3 and TTF-1/NKX2-1 complex regulates Smad4-independent gene expression.
A proteome-scale map of the human interactome network.
A massively parallel pipeline to clone DNA variants and examine molecular phenotypes of human disease mutations.
New host factors important for respiratory syncytial virus (RSV) replication revealed by a novel microfluidics screen for interactors of matrix (M) protein.
Reduction of miR-29c enhances pancreatic cancer cell migration and stem cell-like phenotype.
Proteomic analyses reveal distinct chromatin-associated and soluble transcription factor complexes.
14-3-3ζ turns TGF-β's function from tumor suppressor to metastasis promoter in breast cancer by contextual changes of Smad partners from p53 to Gli2.
Syntenin regulates TGF-β1-induced Smad activation and the epithelial-to-mesenchymal transition by inhibiting caveolin-mediated TGF-β type I receptor internalization.
Widespread macromolecular interaction perturbations in human genetic disorders.
MicroRNA-143 Activation Regulates Smooth Muscle and Endothelial Cell Crosstalk in Pulmonary Arterial Hypertension.
ShcA Protects against Epithelial-Mesenchymal Transition through Compartmentalized Inhibition of TGF-β-Induced Smad Activation.
MiRNA-199a-5p influences pulmonary artery hypertension via downregulating Smad3.
Suppression of innate inflammation and immunity by interleukin-37.
Pooled-matrix protein interaction screens using Barcode Fusion Genetics.
PPARγ Links BMP2 and TGFβ1 Pathways in Vascular Smooth Muscle Cells, Regulating Cell Proliferation and Glucose Metabolism.
MiR-1 suppresses tumor cell proliferation in colorectal cancer by inhibition of Smad3-mediated tumor glycolysis.
IL-37 isoform D downregulates pro-inflammatory cytokines expression in a Smad3-dependent manner.
An interactome perturbation framework prioritizes damaging missense mutations for developmental disorders.
NEDD9 targets COL3A1 to promote endothelial fibrosis and pulmonary arterial hypertension.
LuTHy: a double-readout bioluminescence-based two-hybrid technology for quantitative mapping of protein-protein interactions in mammalian cells.
Novel role of the clustered miR-23b-3p and miR-27b-3p in enhanced expression of fibrosis-associated genes by targeting TGFBR3 in atrial fibroblasts.
LRP1 Deficiency in Vascular SMC Leads to Pulmonary Arterial Hypertension That Is Reversed by PPARγ Activation.
Extensive disruption of protein interactions by genetic variants across the allele frequency spectrum in human populations.
Structural basis for distinct roles of SMAD2 and SMAD3 in FOXH1 pioneer-directed TGF-β signaling.
miR-4286/TGF-β1/Smad3-Negative Feedback Loop Ameliorated Vascular Endothelial Cell Damage by Attenuating Apoptosis and Inflammatory Response.
A reference map of the human binary protein interactome.
Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.
Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.
GDF-8 stimulates trophoblast cell invasion by inducing ALK5-SMAD2/3-mediated MMP2 expression.
The Interplay Between TGF-β Signaling and Cell Metabolism.
Systematic discovery of mutation-directed neo-protein-protein interactions in cancer.
Gain-of-function variants in SMAD4 compromise respiratory epithelial function.
Receptor-associated Mad homologues synergize as effectors of the TGF-beta response.
Heteromeric and homomeric interactions correlate with signaling activity and functional cooperativity of Smad3 and Smad4/DPC4.
TGF-beta receptor-mediated signalling through Smad2, Smad3 and Smad4.
Smad3 and Smad4 cooperate with c-Jun/c-Fos to mediate TGF-beta-induced transcription.
SARA, a FYVE domain protein that recruits Smad2 to the TGFbeta receptor.
Roles of pathway-specific and inhibitory Smads in activin receptor signaling.
Phospho R-SMAD(SMAD2/3):CO-SMAD(SMAD4):FOXO3 binds FoxO3a-binding elements
Phosphorylation of SMAD2,3 by Activin:Activin Receptor
An anchoring protein, ZFYVE9 (SARA), recruits SMAD2/3
Phosphorylated SMAD2 and SMAD3 form a complex with SMAD4
Phosphorylated SMAD2/3 dissociates from TGFBR
Activated type I receptor phosphorylates SMAD2/3 directly
SKI/SKIL binds SMAD complex, suppressing TGF-beta signaling
The SMAD2/3:SMAD4 complex transfers to the nucleus
Ubiquitin-dependent degradation of the SMAD complex terminates TGF-beta signaling
WWTR1 binds SMAD2/3:SMAD4 heterotrimer
PPM1A dephosphorylates nuclear SMAD2/3
WWTR1:SMAD translocates to the nucleus
SMAD2/3:SMAD4 heterotrimer forms a complex with RBL1, E2F4/5 and DP1/2
Phosphorylation of SMAD2 and SMAD3 linker regions by CDK8 or CDK9
NEDD4L binds phosphorylated linker region of SMAD2/3
NEDD4L ubiquitinates SMAD2/3
Degradation of SMAD2/3:SMAD4 complex
SMURF2 binds SMAD3 phosphorylated in the linker region
SMURF2 monoubiquitinates SMAD3
TGIF recruits HDAC1 to SMAD2/3:SMAD4 heterotrimer
MEN1 binds SMAD2/3:SMAD4 heterotrimer
SMAD2/3:SMAD4 heterotrimer binds SP1
PARP1 ADP-ribosylates SMAD3 and SMAD4
PARP1 binds SMAD2/3:SMAD4 heterotrimer
PMEPA1 sequesters phosphorylated SMAD2/3
PMEPA1 sequesters unphosphorylated SMAD2/3
STUB1 (CHIP) ubiquitinates SMAD3
Degradation of ubiquitinated SMAD3
PPM1A protein phosphatase binds phosphorylated SMAD2/3
Dephosphorylated SMAD2/3 translocates to the cytosol
MTMR4 dephosphorylates SMAD2/3
MTMR4 binds phosphorylated SMAD2/3
SMAD4 MH2 Domain Mutants do not bind phosphorylated SMAD2 and SMAD3
Phosphorylated SMAD2/3 MH2 Domain Mutants do not bind SMAD4
An anchoring protein ZFYVE9 (SARA) does not recruit SMAD2/3 to TGFB1:TGFBR2:p-TGFBR1 KD Mutants
USP15 deubiquitinates SMAD1,SMAD2,SMAD3, SMAD7:SMURF,KEAP1
TRIM33 monoubiquitinates SMAD4
TRIM33 (Ectodermin) binds SMAD heterotrimer in the nucleus
RUNX3 binds SMAD3 and SMAD4
The complex of RUNX3, SMAD3 and SMAD4 binds the CDKN1A gene promoter
RUNX3 binds the BCL2L11 (BIM) gene
IL37(?-218):p-S423,S425-SMAD3 translocates to the nucleus
IL37(?-218) binds p-S423,S425-SMAD3
FOXO1,FOXO3,FOXO4 bind p-2S-SMAD2/3:SMAD4
FOXO:SMAD complex binds CDKN1A gene promoter
FOXG1 binds FOXO:SMAD complexes
SARS-CoV-1 SUMO1-K62-p-S177-N dimer binds to SMAD3
MAPK1 and MAPK3 phosphorylate SMAD2 and SMAD3
p-2S-SMAD3:p-2S-SMAD3:SMAD4 forms a complex with SP1 and EP300 at the COL1A2 gene promoter
YBX1 binds COL1A2 gene promoter
WWTR1:p-2S-SMAD2,3:SMAD4 binds SERPINE1 gene promoter
WWTR1:p-2S-SMAD2,3:SMAD4 binds SMAD7 gene promoter
p-2S-SMAD2,3:SMAD4:SP1 binds CDKN2B gene promoter
p-2S-SMAD2,3:SMAD4:RBL1:E2F4,5:DP1,2 binds MYC gene promoter
p-2S-SMAD2,3:SMAD4 binds JUNB gene promoter
SARS-CoV-1 N binds SMAD3 and EP300 at the SERPINE1 gene promoter
EOMES, SMAD2,3, and GATA6 bind the CXCR4 gene
SMAD2,3 and GATA6-AS1 lncRNA bind the GATA6 gene
Rnf111 binds SKI/SKIL in complex with SMAD2/3:SMAD4 upon TGF-beta stimulation
Ubiquitination of SKI/SKIL by Rnf111
FOXO1,FOXO3 and SMAD3 bind Trim63 gene promoter