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ATP + KKVLTQMGSPSIRCS(P)SV(P)S
ADP + ?
-
Smad3-derived peptide substrate
-
-
?
ATP + KKVLTQMGSPSIRCS(P)SVA
ADP + ?
-
Smad3-derived peptide substrate
-
-
?
ATP + KKVLTQMGSPSIRCS(P)SVS
ADP + ?
-
Smad3-derived peptide substrate
-
-
?
ATP + KMGSPSVRCS(P)SMS
ADP + ?
TGF-beta-induced phosphorylation by TbetaRI receptor kinase of the Smad2-derived, phosphorylated peptide substrate containing Ser465 phosphorylation site, poor activity with nonphosphorylated peptide substrate
-
-
?
ATP + KVLTQMGSPSIRCS(P)SVS
ADP + ?
-
Smad3-derived peptide substrate
-
-
?
ATP + KVLTQMGSPSIRCSSV(P)S
ADP + ?
-
Smad3-derived peptide substrate
-
-
?
ATP + KVLTQMGSPSVRCS(P)SMS
ADP + ?
-
Smad2-derived peptide substrate
-
-
?
ATP + KVLTQMGSPSVRCSSMS
ADP + ?
-
Smad2-derived peptide substrate
-
-
?
ATP + KVLTQMGSPSVRCSSMS(P)S
ADP + ?
-
Smad2-derived peptide substrate
-
-
?
ATP + Smad
ADP + phosphorylated Smad
ATP + Smad1
ADP + phosphorylated Smad1
-
phosphorylation by ALK1
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
ATP + Smad3
ADP + phosphorylated Smad3
ATP + Smad5
ADP + phosphorylated Smad5
-
phosphorylation by ALK1
-
-
?
ATP + [actividin receptor]
ADP + [actividin receptor] phosphate
ATP + [receptor-protein]
ADP + [receptor-protein] phosphate
-
-
-
-
?
ATP + [TGF-beta receptor II]
ADP + [TGF-beta receptor II] phosphate
ATP + [TGF-beta receptor I]
ADP + [TGF-beta receptor I] phosphate
additional information
?
-
ATP + Smad
ADP + phosphorylated Smad
-
-
-
-
?
ATP + Smad
ADP + phosphorylated Smad
-
involved in ALK5 activation of p38 MAPK signaling and of GADDbeta45 and BGN expression induced by TGF-beta
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
step in the MAPK signaling pathway via JNK and p38
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
TGF-beta- or actividin-induced phosphorylation
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
TGF-beta-induced phosphorylation by TbetaRI receptor kinase at both phosphorylation sites Ser465 and Ser467 leads to release of Smad2 from membrane-anchored protein SARA and signaling co-mediator Smad4, translocation into the nucleus, and regulation of target gene expression
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
TGF-beta-mediated activation of Smad2 by the TGF-beta receptor
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
phosphorylation by ALK7
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
recombinant GST-fusion Smad2 substrate expressed in Escherichia coli, TGF-beta- or actividin-induced phosphorylation of the two C-terminal Ser residues in the Ser-Ser-Xaa-Ser motif
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
TGF-beta-induced phosphorylation by TbetaRI receptor kinase at two phosphorylation sites Ser465 and Ser467 within the MH2 domain, activity with Smad2 analogues, overview
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
the substrate is a tumor suppressor
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
-
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
phosphorylation by ALK5
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
TGF-beta-induced phosphorylation of Arg462 and Cys463 by TbetaR-I, no activity with Smad2 mutant R462I/C463A by TbetaR-I, Smad2 is no substrate of TbetaR-II and BMP type II receptor
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
ALK7
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
ALK7 is involved in regulation of cell proliferation and apoptosis, regulation, overview
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
GDF-9-induced phosphorylation
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
TGF-beta-mediated activation of Smad2 by the TGF-beta receptor
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
phosphorylation by the TGF-beta receptor
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
step in the MAPK signaling pathway via JNK and p38
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
TGF-beta-mediated activation of Smad3 by the TGF-beta receptor
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
phosphorylation by ALK7
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
the substrate is a tumor suppressor
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
-
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
phosphorylation by ALK5
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
TGF-beta-induced C-terminal phosphorylation
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
ALK7
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
GDF-9-induced phosphorylation
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
TGF-beta-mediated activation of Smad3 by the TGF-beta receptor
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
phosphorylation by the TGF-beta receptor
-
-
?
ATP + [actividin receptor]
ADP + [actividin receptor] phosphate
-
-
-
-
?
ATP + [actividin receptor]
ADP + [actividin receptor] phosphate
-
activins regulate pancreatic development, differentiation and insulin secretion, insulin gene is a target in activin receptor-like kinase 7 signaling pathway in pancreatic beta-cells, SBE and A/GG elements of the human insulin promoter are involved in the regulation of the ALK7 signal, regulation, overview
-
-
?
ATP + [TGF-beta receptor II]
ADP + [TGF-beta receptor II] phosphate
-
-
-
-
?
ATP + [TGF-beta receptor II]
ADP + [TGF-beta receptor II] phosphate
-
regulation and metabolism, overview
-
-
?
ATP + [TGF-beta receptor I]
ADP + [TGF-beta receptor I] phosphate
-
-
-
-
?
ATP + [TGF-beta receptor I]
ADP + [TGF-beta receptor I] phosphate
-
-
-
?
ATP + [TGF-beta receptor I]
ADP + [TGF-beta receptor I] phosphate
-
TGF-beta signalling pathway regulation, overview
-
-
?
additional information
?
-
-
TGF-beta signals via its receptor type I and type II, ALK5 mediates most of the TGF-beta signaling, misexpression of ALK2, being constitutively active, in nontransforming ventricular, endocardial cells causes epithelial-mesenchymal transformation, EMT, which can be inhibited by Smad6, since ALK2 alone is sufficient to cause EMT, overview
-
-
?
additional information
?
-
-
ALK2 and ALK5 are type I receptors
-
-
?
additional information
?
-
-
activin receptor-like kinase-7, ALK7, induces apoptosis through activation of MAPKs, e.g. SEK1, in a Smad3-dependent mechanism in hepatoma cells
-
-
?
additional information
?
-
-
ALK4 forms a complex with type II serine/threonine transmembrane receptor ActRIIB or ActRII and activin for initiation of signaling, ALK3 forms a complex with bone morphogenetic protein-2
-
-
?
additional information
?
-
-
in TGF-beta signaling, phosphorylated Smad2 and Smad3 form a complex with tumor suppressor Smad4, the complex is translocated to the nucleus, nuclear translocation of Smad2 and Smad3 in absence of Smad4 is not sufficient for TGF-beta-induced transcriptional responses, Smad4 mutations occur in some human cancers and inactivate the TGF-beta signaling, overview
-
-
?
additional information
?
-
-
TGF-beta is responsible for induction of growth arrest in cells via the transforming growth factor-beta receptor I, the inhibition can be blocked by cell treatment with SD-093overview
-
-
?
additional information
?
-
TGF-beta signaling is involved in a wide range of cellular processes and various disease states in humans, R-Smad phosphorylation plays a key role
-
-
?
additional information
?
-
-
TGF-beta signaling is involved in a wide range of cellular processes and various disease states in humans, R-Smad phosphorylation plays a key role
-
-
?
additional information
?
-
-
the enzyme is involved in p38 MAPK activation
-
-
?
additional information
?
-
-
the TGF-beta receptor kinase is involved in transforming growth in advanced carcinogenesis and in epithelial-to-mesenchymal cell transition, EMT, overview
-
-
?
additional information
?
-
-
the TGF-beta type I receptor/ALK5-dependent activation of the GADD45beta gene mediates the induction of biglycan expression by TGF-beta, th TGF-beta type II receptor is required for for TGF-beta binding and signaling induction activity, overview
-
-
?
additional information
?
-
-
ALK5 performs autophosphorylation, substrate specificities of recombinant wild-type and mutant T204D ALK5, ALK5 is the intracellular domain of the transforming growth factor beta type-I receptor
-
-
?
additional information
?
-
ALK1 mutations cause hereditary hemorrhagic telangiectasia in association with pulmonary arterial hypertension, PAH, in patients
-
-
?
additional information
?
-
-
ALK1 mutations cause hereditary hemorrhagic telangiectasia in association with pulmonary arterial hypertension, PAH, in patients
-
-
?
additional information
?
-
-
ALK7 is a receptor for nodal and activin AB and B, overview. The insulin promoter is activated by Smad2, Smad3 and the pancreatic and duodenal homeobox factor-1, PDX-1, in the ALK7 pathway, overview
-
-
?
additional information
?
-
-
cyclin G2 mRNA is strongly up-regulated by Nodal and ALK7, Nodal and ALK7 decrease the expression of Skp1 and Skp2 and increase cyclin G2 levels. The antiproliferative effect of Nodal/ALK7 on ovarian cancer cells is in part mediated by cyclin G2, regulation, overview
-
-
?
additional information
?
-
-
signaling by RON, a phosphotyrosine kinase receptor, cooperates with Smad4-independent TGF-beta signaling to promote cell motility and invasion, knocking down RON expression in Smad4-deficient cells suppresses TGF-beta-mediated motility and invasion. Functional inactivation by site-directed mutations of two Smad binding sites on the RON promoter inhibits TGF-beta-mediated repression of RON promoter activity, cross-talk of Smad4-independent TGF-beta signaling and the RON pathway promotes an invasive phenotype, overview
-
-
?
additional information
?
-
-
TGF-beta receptor kinase inhibitor LY2109761 reverses the anti-apoptotic effects of TGF-beta1 in myelo-monocytic leukaemic cells, overview
-
-
?
additional information
?
-
the TGF-beta pathway is overactivated in myelodysplastic syndrome, MDS, involving ineffective hematopoiesis leading to peripheral cytopenias. Suppression of the TGF-beta signaling leads to in vitro enhancement of hematopoiesis, overview. TBRi inhibition can improve anemia in a model of bone marrow failure, overview
-
-
?
additional information
?
-
-
TGF-beta regulates the activation state of endothelium via two opposing type I receptor/Smad pathways: ALK1 induces Smad1/5 phosphorylation leading to increased endothelial cell proliferation and migration, while ALK5 promotes Smad2/3 activation and inhibits both processes, regulation overview
-
-
?
additional information
?
-
-
the enzyme is involved in p38 MAPK activation
-
-
?
additional information
?
-
-
substrate specificity of transforming growth factor-beta receptor I
-
-
?
additional information
?
-
-
ALK6 modulates follicle-stimulating hormone secretion
-
-
?
additional information
?
-
-
ALK7 induces apoptosis of pancreatic beta cells and beta cell lines via Smad2-caspase3 pathways causing diabetes of type 1 and 2, ALK7 activation suppresses Akt activation
-
-
?
additional information
?
-
diverse ligand members of the TGF-beta family interact with a limited number of receptors in a combinatorial manner to activate two downstream Smad pathways
-
-
?
additional information
?
-
-
TGF-beta mediates activation of Smad2 and Smad3 in a differentiated way dependent on the developmental and activationstages of the cells, regulation, overview
-
-
?
additional information
?
-
GDF-9 does not induce phosphorylation of Smad1
-
-
?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
ATP + Smad
ADP + phosphorylated Smad
-
involved in ALK5 activation of p38 MAPK signaling and of GADDbeta45 and BGN expression induced by TGF-beta
-
-
?
ATP + Smad1
ADP + phosphorylated Smad1
-
phosphorylation by ALK1
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
ATP + Smad3
ADP + phosphorylated Smad3
ATP + Smad5
ADP + phosphorylated Smad5
-
phosphorylation by ALK1
-
-
?
ATP + [actividin receptor]
ADP + [actividin receptor] phosphate
ATP + [receptor-protein]
ADP + [receptor-protein] phosphate
-
-
-
-
?
ATP + [TGF-beta receptor II]
ADP + [TGF-beta receptor II] phosphate
-
regulation and metabolism, overview
-
-
?
ATP + [TGF-beta receptor I]
ADP + [TGF-beta receptor I] phosphate
additional information
?
-
ATP + Smad2
ADP + phosphorylated Smad2
-
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
step in the MAPK signaling pathway via JNK and p38
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
TGF-beta- or actividin-induced phosphorylation
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
TGF-beta-induced phosphorylation by TbetaRI receptor kinase at both phosphorylation sites Ser465 and Ser467 leads to release of Smad2 from membrane-anchored protein SARA and signaling co-mediator Smad4, translocation into the nucleus, and regulation of target gene expression
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
TGF-beta-mediated activation of Smad2 by the TGF-beta receptor
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
-
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
phosphorylation by ALK5
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
ALK7 is involved in regulation of cell proliferation and apoptosis, regulation, overview
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
GDF-9-induced phosphorylation
-
-
?
ATP + Smad2
ADP + phosphorylated Smad2
-
TGF-beta-mediated activation of Smad2 by the TGF-beta receptor
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
step in the MAPK signaling pathway via JNK and p38
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
TGF-beta-mediated activation of Smad3 by the TGF-beta receptor
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
-
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
phosphorylation by ALK5
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
ALK7
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
GDF-9-induced phosphorylation
-
-
?
ATP + Smad3
ADP + phosphorylated Smad3
-
TGF-beta-mediated activation of Smad3 by the TGF-beta receptor
-
-
?
ATP + [actividin receptor]
ADP + [actividin receptor] phosphate
-
-
-
-
?
ATP + [actividin receptor]
ADP + [actividin receptor] phosphate
-
activins regulate pancreatic development, differentiation and insulin secretion, insulin gene is a target in activin receptor-like kinase 7 signaling pathway in pancreatic beta-cells, SBE and A/GG elements of the human insulin promoter are involved in the regulation of the ALK7 signal, regulation, overview
-
-
?
ATP + [TGF-beta receptor I]
ADP + [TGF-beta receptor I] phosphate
-
-
-
-
?
ATP + [TGF-beta receptor I]
ADP + [TGF-beta receptor I] phosphate
-
-
-
?
ATP + [TGF-beta receptor I]
ADP + [TGF-beta receptor I] phosphate
-
TGF-beta signalling pathway regulation, overview
-
-
?
additional information
?
-
-
TGF-beta signals via its receptor type I and type II, ALK5 mediates most of the TGF-beta signaling, misexpression of ALK2, being constitutively active, in nontransforming ventricular, endocardial cells causes epithelial-mesenchymal transformation, EMT, which can be inhibited by Smad6, since ALK2 alone is sufficient to cause EMT, overview
-
-
?
additional information
?
-
-
activin receptor-like kinase-7, ALK7, induces apoptosis through activation of MAPKs, e.g. SEK1, in a Smad3-dependent mechanism in hepatoma cells
-
-
?
additional information
?
-
-
ALK4 forms a complex with type II serine/threonine transmembrane receptor ActRIIB or ActRII and activin for initiation of signaling, ALK3 forms a complex with bone morphogenetic protein-2
-
-
?
additional information
?
-
-
in TGF-beta signaling, phosphorylated Smad2 and Smad3 form a complex with tumor suppressor Smad4, the complex is translocated to the nucleus, nuclear translocation of Smad2 and Smad3 in absence of Smad4 is not sufficient for TGF-beta-induced transcriptional responses, Smad4 mutations occur in some human cancers and inactivate the TGF-beta signaling, overview
-
-
?
additional information
?
-
-
TGF-beta is responsible for induction of growth arrest in cells via the transforming growth factor-beta receptor I, the inhibition can be blocked by cell treatment with SD-093overview
-
-
?
additional information
?
-
TGF-beta signaling is involved in a wide range of cellular processes and various disease states in humans, R-Smad phosphorylation plays a key role
-
-
?
additional information
?
-
-
TGF-beta signaling is involved in a wide range of cellular processes and various disease states in humans, R-Smad phosphorylation plays a key role
-
-
?
additional information
?
-
-
the enzyme is involved in p38 MAPK activation
-
-
?
additional information
?
-
-
the TGF-beta receptor kinase is involved in transforming growth in advanced carcinogenesis and in epithelial-to-mesenchymal cell transition, EMT, overview
-
-
?
additional information
?
-
-
the TGF-beta type I receptor/ALK5-dependent activation of the GADD45beta gene mediates the induction of biglycan expression by TGF-beta, th TGF-beta type II receptor is required for for TGF-beta binding and signaling induction activity, overview
-
-
?
additional information
?
-
ALK1 mutations cause hereditary hemorrhagic telangiectasia in association with pulmonary arterial hypertension, PAH, in patients
-
-
?
additional information
?
-
-
ALK1 mutations cause hereditary hemorrhagic telangiectasia in association with pulmonary arterial hypertension, PAH, in patients
-
-
?
additional information
?
-
-
ALK7 is a receptor for nodal and activin AB and B, overview. The insulin promoter is activated by Smad2, Smad3 and the pancreatic and duodenal homeobox factor-1, PDX-1, in the ALK7 pathway, overview
-
-
?
additional information
?
-
-
cyclin G2 mRNA is strongly up-regulated by Nodal and ALK7, Nodal and ALK7 decrease the expression of Skp1 and Skp2 and increase cyclin G2 levels. The antiproliferative effect of Nodal/ALK7 on ovarian cancer cells is in part mediated by cyclin G2, regulation, overview
-
-
?
additional information
?
-
-
signaling by RON, a phosphotyrosine kinase receptor, cooperates with Smad4-independent TGF-beta signaling to promote cell motility and invasion, knocking down RON expression in Smad4-deficient cells suppresses TGF-beta-mediated motility and invasion. Functional inactivation by site-directed mutations of two Smad binding sites on the RON promoter inhibits TGF-beta-mediated repression of RON promoter activity, cross-talk of Smad4-independent TGF-beta signaling and the RON pathway promotes an invasive phenotype, overview
-
-
?
additional information
?
-
-
TGF-beta receptor kinase inhibitor LY2109761 reverses the anti-apoptotic effects of TGF-beta1 in myelo-monocytic leukaemic cells, overview
-
-
?
additional information
?
-
the TGF-beta pathway is overactivated in myelodysplastic syndrome, MDS, involving ineffective hematopoiesis leading to peripheral cytopenias. Suppression of the TGF-beta signaling leads to in vitro enhancement of hematopoiesis, overview. TBRi inhibition can improve anemia in a model of bone marrow failure, overview
-
-
?
additional information
?
-
-
TGF-beta regulates the activation state of endothelium via two opposing type I receptor/Smad pathways: ALK1 induces Smad1/5 phosphorylation leading to increased endothelial cell proliferation and migration, while ALK5 promotes Smad2/3 activation and inhibits both processes, regulation overview
-
-
?
additional information
?
-
-
the enzyme is involved in p38 MAPK activation
-
-
?
additional information
?
-
-
ALK6 modulates follicle-stimulating hormone secretion
-
-
?
additional information
?
-
-
ALK7 induces apoptosis of pancreatic beta cells and beta cell lines via Smad2-caspase3 pathways causing diabetes of type 1 and 2, ALK7 activation suppresses Akt activation
-
-
?
additional information
?
-
diverse ligand members of the TGF-beta family interact with a limited number of receptors in a combinatorial manner to activate two downstream Smad pathways
-
-
?
additional information
?
-
-
TGF-beta mediates activation of Smad2 and Smad3 in a differentiated way dependent on the developmental and activationstages of the cells, regulation, overview
-
-
?
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
Please wait a moment until the data is sorted. This message will disappear when the data is sorted.
(1'R,5'S,6'S)-2-(3',5'-dibromo-1',6'-dihydroxy-4'-oxocyclohex-2'-enyl) acetonitrile
the small dibromotyrosine derivative purified from Pseudoceratina sp. suppresses TGF-beta responsiveness by inhibiting TGF-beta type I receptor serine/threonine kinase activity. The compound inhibits the TGF-beta-stimulated transcriptional activations of 3TP-Lux and decreases phosphorylated Smad2/3 levels and the nuclear translocation of Smad2/3 increased by TGF-beta. The compound inhibits TGF-beta-induced EMT and wound healing of A-549 cells and is a potential therapeutic agent for fibrotic disease and cancer treatment. The compound has no effects on TGF-beta receptor synthesis but attenuates TGF-beta-induced transcriptional activation in Mv1Lu cells and TGF-beta-induced expression of fibronectin and PAI-1 in A549 and NMuMG cells and TGF-beta-induced cell migration
1-(1,3-benzodioxol-5-yl)-2-(6-ethylpyridin-2-yl)ethanone
-
-
1-(1,3-benzodioxol-5-yl)-2-(6-methylpyridin-2-yl)ethanone
-
-
1-(1,3-benzodioxol-5-yl)-2-bromo-2-(6-ethylpyridin-2-yl)ethanone
-
-
1-(1,3-benzodioxol-5-yl)-2-bromo-2-(6-methylpyridin-2-yl)ethanone
-
-
1-(1,3-benzodioxol-5-yl)-2-bromo-2-pyridin-2-ylethanone
-
-
1-(1,3-benzodioxol-5-yl)-2-pyridin-2-ylethanone
-
-
2,6-lutidine
-
i.e. 2,6-dimethylpyridine
2-(6-ethylpyridin-2-yl)-1-quinoxalin-6-ylethanone
-
-
2-(6-methylpyridin-2-yl)-1-quinoxalin-6-ylethanone
-
-
2-bromo-2-(6-ethylpyridin-2-yl)-1-quinoxalin-6-ylethanone
-
-
2-bromo-2-(6-methylpyridin-2-yl)-1-quinoxalin-6-ylethanone
-
-
2-bromo-2-pyridin-2-yl-1-quinoxalin-6-ylethanone
-
-
2-pyridin-2-yl-1-quinoxalin-6-ylethanone
-
-
3-((4-(6-methylpyridin-2-yl)-5-(quinolin-6-yl)-1H-imidazol-2-yl)methyl)benzamide
-
IN-1233, inhibitor specifically inhibits TGF-beta signaling via ALK-5 by acting as a competitive inhibitor of the ATP-binding site, inhibition of activin receptor-like kinase-5 signaling in vivo with the selective small-molecule inhibitor prevents pulmonary arterial hypertension, right ventricular hypertrophy, and vascular remodeling after monocrotaline injection and inhibits the progression of established pulmonary arterial hypertension in this model
3-([[4-(1,3-benzodioxol-5-yl)-5-(6-ethylpyridin-2-yl)-1,3-thiazol-2-yl]amino]methyl)benzamide
-
-
3-([[4-(1,3-benzodioxol-5-yl)-5-(6-ethylpyridin-2-yl)-1,3-thiazol-2-yl]amino]methyl)benzonitrile
-
-
3-([[4-(1,3-benzodioxol-5-yl)-5-(6-methylpyridin-2-yl)-1,3-thiazol-2-yl]amino]methyl)benzamide
-
-
3-([[4-(1,3-benzodioxol-5-yl)-5-(6-methylpyridin-2-yl)-1,3-thiazol-2-yl]amino]methyl)benzonitrile
-
-
3-([[4-(1,3-benzodioxol-5-yl)-5-pyridin-2-yl-1,3-thiazol-2-yl]amino]methyl)benzamide
-
-
3-([[4-(1,3-benzodioxol-5-yl)-5-pyridin-2-yl-1,3-thiazol-2-yl]amino]methyl)benzonitrile
-
-
3-([[5-(6-ethylpyridin-2-yl)-4-quinoxalin-6-yl-1,3-thiazol-2-yl]amino]methyl)benzonitrile
-
-
3-([[5-(6-methylpyridin-2-yl)-4-quinoxalin-6-yl-1,3-thiazol-2-yl]amino]methyl)benzonitrile
-
-
3-[[(5-pyridin-2-yl-4-quinoxalin-6-yl-1,3-thiazol-2-yl)amino]methyl]benzamide
-
-
3-[[(5-pyridin-2-yl-4-quinoxalin-6-yl-1,3-thiazol-2-yl)amino]methyl]benzonitrile
-
-
3-[[5-(6-ethylpyridin-2-yl)-4-(quinoxalin-6-yl)thiazol-2-ylamino]methyl]benzamide
-
-
3-[[5-(6-methylpyridin-2-yl)-4-(quinoxalin-6-yl)thiazol-2-ylamino]methyl]benzamide
-
-
4(quinolin-4-yl)-substituted 5,6-dihydro-4H-pyrrolo[1,2-b]pyrazole derivatives
4-(1,3-benzodioxol-5-yl)-5-(6-ethylpyridin-2-yl)-1,3-thiazol-2-amine
-
-
4-(1,3-benzodioxol-5-yl)-5-(6-methylpyridin-2-yl)-1,3-thiazol-2-amine
-
-
4-(1,3-benzodioxol-5-yl)-5-pyridin-2-yl-1,3-thiazol-2-amine
-
-
4-([[4-(1,3-benzodioxol-5-yl)-5-(6-ethylpyridin-2-yl)-1,3-thiazol-2-yl]amino]methyl)benzonitrile
-
-
4-([[4-(1,3-benzodioxol-5-yl)-5-(6-methylpyridin-2-yl)-1,3-thiazol-2-yl]amino]methyl)benzonitrile
-
-
4-([[4-(1,3-benzodioxol-5-yl)-5-pyridin-2-yl-1,3-thiazol-2-yl]amino]methyl)benzonitrile
-
-
4-([[5-(6-ethylpyridin-2-yl)-4-quinoxalin-6-yl-1,3-thiazol-2-yl]amino]methyl)benzamide
-
-
4-([[5-(6-ethylpyridin-2-yl)-4-quinoxalin-6-yl-1,3-thiazol-2-yl]amino]methyl)benzonitrile
-
-
4-([[5-(6-methylpyridin-2-yl)-4-quinoxalin-6-yl-1,3-thiazol-2-yl]amino]methyl)benzamide
-
-
4-([[5-(6-methylpyridin-2-yl)-4-quinoxalin-6-yl-1,3-thiazol-2-yl]amino]methyl)benzonitrile
-
-
4-phenyl substituted pyrazole inhibitors
-
inhibitory potency of 4-phenyl substituted pyrazole derivatives, IC50 of 30-555 nM, overview
-
4-phenyl-substituted 5,6-dihydro-4H-pyrrolo[1,2-b]pyrazole derivatives
4-[[(5-pyridin-2-yl-4-quinoxalin-6-yl-1,3-thiazol-2-yl)amino]methyl]benzamide
-
-
4-[[(5-pyridin-2-yl-4-quinoxalin-6-yl-1,3-thiazol-2-yl)amino]methyl]benzonitrile
-
-
5-(6-ethylpyridin-2-yl)-4-quinoxalin-6-yl-1,3-thiazol-2-amine
-
-
5-(6-methylpyridin-2-yl)-4-quinoxalin-6-yl-1,3-thiazol-2-amine
-
-
5-pyridin-2-yl-4-quinoxalin-6-yl-1,3-thiazol-2-amine
-
-
6-ethyl-2-methylpyridine
-
i.e. 2-ethyl-6-methylpyridine
LY-2157299
LY-2157299 inhibits TGF-beta mediated SMAD2 activation and hematopoietic suppression in primary hematopoietic stem cells. In vivo administration of LY-2157299 ameliorates anemia in a TGF-beta overexpressing transgenic mouse model of bone marrow failure. Treatment with LY-2157199 stimulates hematopoiesis from primary myelodysplastic syndrome bone marrow specimens
LY2109761
-
TGF-beta receptor kinase inhibitor LY2109761 reverses the anti-apoptotic effects of TGF-beta1 in myelo-monocytic leukaemic cells, it LY2109761 enhanced apoptosis only in the presence of exogenously added TGF-beta1
LY2157299
-
inhibits Smad3 and Smad3 phosphorylation and antagonizes TGF-beta receptor I kinase activity in vivo in human cancer cells implanted into nude mice, pharmacokinetic model, overview
LY566578
-
competitive to ATP, noncompetitive to the peptide substrate, IC50 is 70 nM, mechanism
PEG10
-
ancient retroviral/retrotransposon element intergrated as a single copy gene in to human chromosome 7q21, encodes two splicing varaiants PEG10-RF1 and PEG10-RF1/2, gag- and gag-pol-like proteins that interact with TGF-beta family proteins, DNA and amino acid sequence deteramination and analysis of PEG10-RF1, PEG10-RF1 inhibits ALK1 and ALK5 signaling by direct interaction, overview
Smad7
inhibits induction of receptor activation/signaling by GDF-9 in vivo
-
4(quinolin-4-yl)-substituted 5,6-dihydro-4H-pyrrolo[1,2-b]pyrazole derivatives
-
IC50 of 0.00005-0.0013 mM
4(quinolin-4-yl)-substituted 5,6-dihydro-4H-pyrrolo[1,2-b]pyrazole derivatives
-
IC50 of 0.00015-0.0051 mM, overview
4-phenyl-substituted 5,6-dihydro-4H-pyrrolo[1,2-b]pyrazole derivatives
-
IC50 of 0.000005-0.0195 mM
4-phenyl-substituted 5,6-dihydro-4H-pyrrolo[1,2-b]pyrazole derivatives
-
IC50 of 0.00011-0.020 mM, overview
LY364947
-
competitive to ATP, noncompetitive to the peptide substrate, IC50 is 175 nM, mechanism
LY580276
-
competitive to ATP, noncompetitive to the peptide substrate, IC50 is 580 nM, mechanism
SB-431542
-
specific TGF-beta receptor kinase inhibitor, a potent antitumor agent for human cancers, induces anchorage-independent cell growth in TGF-beta growth-inhibited cells, and colony formation in growth-induced cells, overview
SD-208
inhibition of the TBRI kinase inhibits TGF-beta-mediated smad2 activation in hematopoietic progenitors, alleviates anemia, and stimulates hematopoiesis in vivo in bone marrow
SD-208
-
selektive ALK5 kinase inhibitor
SD-208
-
inhibitor reduces the monocrotaline-induced increase in RV systolic pressure, but the effects on established pulmonary arterial hypertension are modest, and no convincing evidence for in vivo inhibition of TGF-beta-driven target genes is presented
additional information
-
a dominant negative SEK1 mutant abolishes the ALK7-induced apoptosis
-
additional information
-
LY294002 completely abolishes the ALK7 mutant T194D/Smad3-induced synergistic effect by inhibiting interaction between the Smad3-Linker and PDX-1
-
additional information
-
ALK1 mediates inhibition of the ALK5/Smad2/3 pathway
-
additional information
no inhibition of GDF-9-induced receptor activation by Smad6
-
additional information
-
inhibitory potency of 5-(pyridin-2-yl)thiazole inhibitors, overview
-
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A78G
-
site-directed mutagenesis, the mutation affects binding of actividin
D89A
-
site-directed mutagenesis, the mutation does not affect binding of actividin
E74A
-
site-directed mutagenesis, the mutation affects binding of actividin
E88A
-
site-directed mutagenesis, the mutation does not affect binding of actividin
F82A
-
site-directed mutagenesis, the mutation slightly affects binding of actividin
G79A
-
site-directed mutagenesis, the mutation affects binding of actividin
H312Q
naturally occuring mutation in Japanese pulmonary arterial hypertension patients
I70A
-
site-directed mutagenesis, the mutation of a residue from the ALK4 extracellular domain affects the binding of activin and the substantial effects of the dominant negative truncated ALK4 mutant
K72A
-
site-directed mutagenesis, the mutation does not affect binding of actividin
K80A
-
site-directed mutagenesis, the mutation affects binding of actividin
L381P
naturally occuring mutation in Japanese pulmonary arterial hypertension patients
L40A
-
site-directed mutagenesis, the mutation of a residue from the ALK4 extracellular domain affects the binding of activin and the substantial effects of the dominant negative truncated ALK4 mutant
L75A
-
site-directed mutagenesis, the mutation of a residue from the ALK4 extracellular domain affects the binding of activin and the substantial effects of the dominant negative truncated ALK4 mutant
L85A
-
site-directed mutagenesis, the mutation affects binding of actividin
L90A
-
site-directed mutagenesis, the mutation does not affect binding of actividin
M53A
-
site-directed mutagenesis, the mutation slightly affects binding of actividin
P71A
-
site-directed mutagenesis, the mutation affects binding of actividin
P77A
-
site-directed mutagenesis, the mutation of a residue from the ALK4 extracellular domain affects the binding of activin and the substantial effects of the dominant negative truncated ALK4 mutant
P81A
-
site-directed mutagenesis, the mutation does not affect binding of actividin
Q201D
-
constitutively active ALK1 mutant
R479Q
naturally occuring mutation in Japanese pulmonary arterial hypertension patients
R484Q
naturally occuring mutation in Japanese pulmonary arterial hypertension patients
R91A
-
site-directed mutagenesis, the mutation affects binding of actividin
S38A
-
site-directed mutagenesis, the mutation slightly affects binding of actividin
S55A
-
site-directed mutagenesis, the mutation affects binding of actividin
S86A
-
site-directed mutagenesis, the mutation affects binding of actividin
S87A
-
site-directed mutagenesis, the mutation affects binding of actividin
T202D
site-directed mutagenesis
T204D
-
constitutively active ALK5 mutant
T93A
-
site-directed mutagenesis, the mutation affects binding of actividin
V73A
-
site-directed mutagenesis, the mutation of a residue from the ALK4 extracellular domain affects the binding of activin and the substantial effects of the dominant negative truncated ALK4 mutant
V76A
-
site-directed mutagenesis, the mutation affects binding of actividin
Y83A
-
site-directed mutagenesis, the mutation affects binding of actividin
T194D
-
constitutive active ALK7 mutant
T194D
-
site-directed mutagenesis of ALK7
additional information
-
misexpression of ALK2 in nontransforming ventricular, endocardial cells causes epithelial-mesenchymal transformation, EMT, which can be decreased by overexpression of inhibitor Smad6
additional information
-
construction of a truncated dominant negative ALK4 mutant
additional information
construction of a truncated mutant ALK7
additional information
-
construction of a truncated mutant ALK7
additional information
-
expression of HA-tagged wild-type ALK7 in rat FaO hepatoma cells and transiently of HA-tagged ALK mutant T194D in human Hep3B hepatoma cells using the adenovirus infection method, expression leads in both cases to an apoptosis-positive phenotype, expression of inactive ALK7 mutant K222R dos not cause an altered phenotype
additional information
-
functional co-expression of TGF-beta and the soluble intracellular domain of the TGF-beta type I receptor in murine mammary gland epithelial cells induces transdifferentiation of epithelial cells to mesenchymal cells, overview
additional information
ALK1 mutations cause hereditary hemorrhagic telangiectasia in association with pulmonary arterial hypertension, PAH, in patients, determination of polymorphisms in Japanese pulmonary arterial hypertension patients, phenotypes, overview
additional information
-
ALK1 mutations cause hereditary hemorrhagic telangiectasia in association with pulmonary arterial hypertension, PAH, in patients, determination of polymorphisms in Japanese pulmonary arterial hypertension patients, phenotypes, overview
additional information
knockout of TBRI by shRNA suppression using a lentiviral construct leads to decreased smad2 activtaion and reverses the suppressive effects of TGF-beta on hematopoiesis, overview
additional information
-
knockdown of ALK5 expression in embryonic endothelial cells by antisense oligonucleotides results in inhibition of both TGF-beta-induced Smad 2 and Smad1/5 phosphorylation, an ALk5mutant defective in Smad activation rescues TGF-beta/ALK1-induced signaling in ALK5 null mutant endothelial cells
additional information
-
activin receptor-like kinase 6 Booroola mutation enhances suppressive effects of bone morphogenetic protein 2, BMP2, BMP4, BMP6 and growth and differentiation factor-9 on FSH release from ovine primary pituitary cell cultures
additional information
conferring of responsiveness to GDF-9-mediated stimulation of ALK5 and Smad3 phosphorylation in normally unresponsive COS-7 cells by overexpression of the three proteins, no responsiveness by co-expression with BMPRII receptor, expression of GDF-9 in a CAGA-luciferase reporter construct in P19 cells reveals that GDF-9 binds to BMP-activated type II receptors but its downstream actions are mediated by the type I receptor ALK5, overview, expression of ALK5 siRNA inhibits GDF-9-induced stimulation in granulosa cells
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Ge, R.; Rajeev, V.; Subramanian, G.; Reiss, K.A.; Liu, D.; Higgins, L.; Joly, A.; Dugar, S.; Chakravarty, J.; Henson, M.; McEnroe, G.; Schreiner, G.; Reiss, M.
Selective inhibitors of type I receptor kinase block cellular transforming growth factor-beta signaling
Biochem. Pharmacol.
68
41-50
2004
Homo sapiens
brenda
Ottesen, J.J.; Huse, M.; Sekedat, M.D.; Muir, T.W.
Semisynthesis of phosphovariants of Smad2 reveals a substrate preference of the activated TbetaRI kinase
Biochemistry
43
5698-5706
2004
Homo sapiens (P36897), Homo sapiens
brenda
Peng, S.B.; Yan, L.; Xia, X.; Watkins, S.A.; Brooks, H.B.; Beight, D.; Herron, D.K.; Jones, M.L.; Lampe, J.W.; McMillen, W.T.; Mort, N.; Sawyer, J.S.; Yingling, J.M.
Kinetic characterization of novel pyrazole TGF-beta receptor I kinase inhibitors and their blockade of the epithelial-mesenchymal transition
Biochemistry
44
2293-2304
2005
Homo sapiens
brenda
Roberts, H.J.; Hu, S.; Qiu, Q.; Leung, P.C.; Caniggia, I.; Gruslin, A.; Tsang, B.; Peng, C.
Identification of novel isoforms of activin receptor-like kinase 7 (ALK7) generated by alternative splicing and expression of ALK7 and its ligand, Nodal, in human placenta
Biol. Reprod.
68
1719-1726
2003
Homo sapiens (Q8NER5), Homo sapiens
brenda
Sawyer, J.S.; Beight, D.W.; Britt, K.S.; Anderson, B.D.; Campbell, R.M.; Goodson, T.Jr.; Herron, D.K.; Li, H.Y.; McMillen, W.T.; Mort, N.; Parsons, S.; Smith, E.C.; Wagner, J.R.; Yan, L.; Zhang, F.; Yingling, J.M.
Synthesis and activity of new aryl- and heteroaryl-substituted 5,6-dihydro-4H-pyrrolo[1,2-b]pyrazole inhibitors of the transforming growth factor-beta type I receptor kinase domain
Bioorg. Med. Chem. Lett.
14
3581-3584
2004
Homo sapiens, Mus musculus
brenda
Desgrosellier, J.S.; Mundell, N.A.; McDonnell, M.A.; Moses, H.L.; Barnett, J.V.
Activin receptor-like kinase 2 and Smad6 regulate epithelial-mesenchymal transformation during cardiac valve formation
Dev. Biol.
280
201-210
2005
Gallus gallus
brenda
Zhang, N.; Kumar, M.; Xu, G.; Ju, W.; Yoon, T.; Xu, E.; Huang, X.; Gaisano, H.; Peng, C.; Wang, Q.
Activin receptor-like kinase 7 induces apoptosis of pancreatic beta cells and beta cell lines
Diabetologia
49
506-518
2006
Rattus norvegicus
brenda
Liu, C.; Gaca, M.D.; Swenson, E.S.; Vellucci, V.F.; Reiss, M.; Wells, R.G.
Smads 2 and 3 are differentially activated by transforming growth factor-beta (TGF-beta) in quiescent and activated hepatic stellate cells. Constitutive nuclear localization of Smads in activated cells is TGF-beta-independent
J. Biol. Chem.
278
11721-11728
2003
Rattus norvegicus
brenda
Harrison, C.A.; Gray, P.C.; Koerber, S.C.; Fischer, W.; Vale, W.
Identification of a functional binding site for activin on the type I receptor ALK4
J. Biol. Chem.
278
21129-21135
2003
Homo sapiens
brenda
Kim, B.C.; van Gelder, H.; Kim, T.A.; Lee, H.J.; Baik, K.G.; Chun, H.H.; Lee, D.A.; Choi, K.S.; Kim, S.J.
Activin receptor-like kinase-7 induces apoptosis through activation of MAPKs in a Smad3-dependent mechanism in hepatoma cells
J. Biol. Chem.
279
28458-28465
2004
Homo sapiens
brenda
Yakymovych, I.; Heldin, C.H.; Souchelnytskyi, S.
Smad2 phosphorylation by type I receptor. Contribution of arginine 462 and cysteine 463 In the C terminus of Smad2 for specificity
J. Biol. Chem.
279
35781-35787
2004
Mus musculus
brenda
Ungefroren, H.; Groth, S.; Ruhnke, M.; Kalthoff, H.; Fandrich, F.
Transforming growth factor-beta (TGF-beta) type I receptor/ALK5-dependent activation of the GADD45beta gene mediates the induction of biglycan expression by TGF-beta
J. Biol. Chem.
280
2644-2652
2005
Homo sapiens
brenda
Lux, A.; Beil, C.; Majety, M.; Barron, S.; Gallione, C.J.; Kuhn, H.M.; Berg, J.N.; Kioschis, P.; Marchuk, D.A.; Hafner, M.
Human retroviral gag- and gag-pol-like proteins interact with the transforming growth factor-beta receptor activin receptor-like kinase 1
J. Biol. Chem.
280
8482-8493
2005
Homo sapiens
brenda
Forrester, S.G.; Warfel, P.W.; Pearce, E.J.
Tegumental expression of a novel type II receptor serine/threonine kinase (SmRK2) in Schistosoma mansoni
Mol. Biochem. Parasitol.
136
149-156
2004
Schistosoma mansoni (Q6GZL5), Schistosoma mansoni
brenda
Goumans, M.J.; Valdimarsdottir, G.; Itoh, S.; Lebrin, F.; Larsson, J.; Mummery, C.; Karlsson, S.; ten Dijke, P.
Activin receptor-like kinase (ALK)1 is an antagonistic mediator of lateral TGFbeta/ALK5 signaling
Mol. Cell
12
817-828
2003
Mus musculus
brenda
Mazerbourg, S.; Klein, C.; Roh, J.; Kaivo-Oja, N.; Mottershead, D.G.; Korchynskyi, O.; Ritvos, O.; Hsueh, A.J.
Growth differentiation factor-9 signaling is mediated by the type I receptor, activin receptor-like kinase 5
Mol. Endocrinol.
18
653-665
2004
Rattus norvegicus (P80204)
brenda
Halder, S.K.; Beauchamp, R.D.; Datta, P.K.
A specific inhibitor of TGF-beta receptor kinase, SB-431542, as a potent antitumor agent for human cancers
Neoplasia
7
509-521
2005
Homo sapiens
brenda
Fink, S.P.; Mikkola, D.; Willson, J.K.V.; Markowitz, S.
TGF-beta-induced nuclear localization of Smad2 and Smad3 in Smad4 null cancer cell lines
Oncogene
22
1317-1323
2003
Homo sapiens
brenda
Watanabe, R.; Shen, Z.P.; Tsuda, K.; Yamada, Y.
Insulin gene is a target in activin receptor-like kinase 7 signaling pathway in pancreatic beta-cells
Biochem. Biophys. Res. Commun.
377
867-872
2008
Homo sapiens
brenda
Kim, D.K.; Choi, J.H.; An, Y.J.; Lee, H.S.
Synthesis and biological evaluation of 5-(pyridin-2-yl)thiazoles as transforming growth factor-beta type1 receptor kinase inhibitors
Bioorg. Med. Chem. Lett.
18
2122-2127
2008
Rattus norvegicus
brenda
Zhou, L.; Nguyen, A.N.; Sohal, D.; Ying Ma, J.; Pahanish, P.; Gundabolu, K.; Hayman, J.; Chubak, A.; Mo, Y.; Bhagat, T.D.; Das, B.; Kapoun, A.M.; Navas, T.A.; Parmar, S.; Kambhampati, S.; Pellagatti, A.; Braunchweig, I.; Zhang, Y.; Wickrema, A.; Medicherla, S.; Boultwood, J.; Platanias, L.C.; Higgins, L.S.
Inhibition of the TGF-beta receptor I kinase promotes hematopoiesis in MDS
Blood
112
3434-3443
2008
Homo sapiens (P36897)
brenda
Xu, Y.; Tabe, Y.; Jin, L.; Watt, J.; McQueen, T.; Ohsaka, A.; Andreeff, M.; Konopleva, M.
TGF-beta receptor kinase inhibitor LY2109761 reverses the anti-apoptotic effects of TGF-beta1 in myelo-monocytic leukaemic cells co-cultured with stromal cells
Br. J. Haematol.
142
192-201
2008
Homo sapiens
brenda
Fujiwara, M.; Yagi, H.; Matsuoka, R.; Akimoto, K.; Furutani, M.; Imamura, S.; Uehara, R.; Nakayama, T.; Takao, A.; Nakazawa, M.; Saji, T.
Implications of mutations of activin receptor-like kinase 1 gene (ALK1) in addition to bone morphogenetic protein receptor II gene (BMPR2) in children with pulmonary arterial hypertension
Circ. J.
72
127-133
2008
Homo sapiens (P37023), Homo sapiens
brenda
Bueno, L.; de Alwis, D.P.; Pitou, C.; Yingling, J.; Lahn, M.; Glatt, S.; Troconiz, I.F.
Semi-mechanistic modelling of the tumour growth inhibitory effects of LY2157299, a new type I receptor TGF-beta kinase antagonist, in mice
Eur. J. Cancer
44
142-150
2008
Homo sapiens
brenda
Zhao, S.; Ammanamanchi, S.; Brattain, M.; Cao, L.; Thangasamy, A.; Wang, J.; Freeman, J.W.
Smad4-dependent TGF-beta signaling suppresses RON receptor tyrosine kinase-dependent motility and invasion of pancreatic cancer cells
J. Biol. Chem.
283
11293-11301
2008
Homo sapiens
brenda
Young, J.M.; Juengel, J.L.; Dodds, K.G.; Laird, M.; Dearden, P.K.; McNeilly, A.S.; McNatty, K.P.; Wilson, T.
The activin receptor-like kinase 6 Booroola mutation enhances suppressive effects of bone morphogenetic protein 2 (BMP2), BMP4, BMP6 and growth and differentiation factor-9 on FSH release from ovine primary pituitary cell cultures
J. Endocrinol.
196
251-261
2008
Ovis aries
brenda
Xu, G.; Bernaudo, S.; Fu, G.; Lee, D.Y.; Yang, B.B.; Peng, C.
Cyclin G2 is degraded through the ubiquitin-proteasome pathway and mediates the antiproliferative effect of activin receptor-like kinase 7
Mol. Biol. Cell
19
4968-4979
2008
Homo sapiens
brenda
Haneen, S.; Johanna, H.; Ulrich, G.; Jens, S.S.; Frank, R.; Karl, H.; Peter, B.
Mutation analysis of "Endoglin" and "Activin receptor-like kinase" genes in German patients with hereditary hemorrhagic telangiectasia and the value of rapid genotyping using an allele-specific PCR-technique
BMC Med. Genet.
10
53
2009
Homo sapiens (P37023), Homo sapiens
brenda
Long, L.; Crosby, A.; Yang, X.; Southwood, M.; Upton, P.D.; Kim, D.K.; Morrell, N.W.
Altered bone morphogenetic protein and transforming growth factor-beta signaling in rat models of pulmonary hypertension: potential for activin receptor-like kinase-5 inhibition in prevention and progression of disease
Circulation
119
566-576
2009
Rattus norvegicus
brenda
Upton, P.D.; Davies, R.J.; Trembath, R.C.; Morrell, N.W.
Bone morphogenetic protein (BMP) and activin type II receptors balance BMP9 signals mediated by activin receptor-like kinase-1 in human pulmonary artery endothelial cells
J. Biol. Chem.
284
15794-15804
2009
Homo sapiens
brenda
Mahmoud, M.; Borthwick, G.M.; Hislop, A.A.; Arthur, H.M.
Endoglin and activin receptor-like-kinase 1 are co-expressed in the distal vessels of the lung: implications for two familial vascular dysplasias, HHT and PAH
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89
15-25
2009
Mus musculus
brenda
Li, L.; Zhao, X.Y.; Wang, B.E.
Down-regulation of transforming growth factor beta 1/activin receptor-like kinase 1 pathway gene expression by herbal compound 861 is related to deactivation of LX-2 cells
World J. Gastroenterol.
14
2894-2899
2008
Homo sapiens
brenda
Zhou, L.; McMahon, C.; Bhagat, T.; Alencar, C.; Yu, Y.; Fazzari, M.; Sohal, D.; Heuck, C.; Gundabolu, K.; Ng, C.; Mo, Y.; Shen, W.; Wickrema, A.; Kong, G.; Friedman, E.; Sokol, L.; Mantzaris, I.; Mantzaris, G.; Pellagatti, A.; Boultwood, J.; Platanias, L.C.; Steidl, U.; Yan, L.; Yingling, J.M.; Lahn, M.M.
Reduced SMAD7 leads to overactivation of TGF-beta signaling in MDS that can be reversed by a specific inhibitor of TGF-beta receptor I kinase
Cancer Res.
71
955-963
2011
Homo sapiens (P36897)
brenda
Chen, C.L.; Kao, Y.C.; Yang, P.H.; Sung, P.J.; Wen, Z.H.; Chen, J.J.; Huang, Y.B.; Chen, P.Y.
A small dibromotyrosine derivative purified from Pseudoceratina sp. suppresses TGF-beta responsiveness by inhibiting TGF-beta type I receptor serine/threonine kinase activity
J. Cell. Biochem.
117
2800-2814
2016
Homo sapiens (P36897)
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