A Dibromotyrosine Derivative from Pseudoceratina sp. Suppresses TGF-β Responsiveness by Inhibiting TGF-β type I Receptor Kinase Activity

2017 ◽  
Author(s):  
CL Chen ◽  
YC Kao ◽  
PJ Sung ◽  
ZH Wen
Keyword(s):  
Kinase Activity ◽  
Type I ◽  
Receptor Kinase

scholarly journals Cercosporamide inhibits bone morphogenetic protein receptor type I kinase activity in zebrafish

2020 ◽  
Author(s):  
Jelmer Hoeksma ◽  
Gerard C.M. van der Zon ◽  
Peter ten Dijke ◽  
Jeroen den Hertog
Keyword(s):  
Bone Morphogenetic Protein ◽  
Mammalian Cells ◽  
Kinase Activity ◽  
Fibrodysplasia Ossificans Progressiva ◽  
Type I ◽  
Receptor Kinase ◽  
Developmental Defects ◽  
Bmp Receptors ◽  
Morphogenetic Protein ◽  
Constitutively Active

AbstractZebrafish models are well established tools for investigating underlying mechanisms of diseases. Here, we identified cercosporamide, a metabolite from the fungus Ascochyta aquiliqiae, as a potent bone morphogenetic protein (BMP) type I receptor kinase inhibitor through a zebrafish embryo phenotypic screen. The developmental defects in zebrafish, including lack of the ventral fin induced by cercosporamide was strikingly similar as the phenotypes caused by renowned small molecule BMP type I receptor kinase inhibitors and inactivating mutations in zebrafish BMP receptors. In mammalian cell-based assays, cercosporamide blocked BMP/SMAD-dependent transcriptional reporter activity and BMP-induced SMAD1/5-phosphorylation. Biochemical assays with a panel of purified recombinant kinases demonstrated that cercosporamide directly inhibited kinase activity of BMP type I receptors (also called activin receptor-like kinases (ALKs)). In mammalian cells, cercosporamide selectively inhibited constitutively active BMP type I receptor-induced SMAD1/5 phosphorylation. Importantly, cercosporamide rescued the developmental defects caused by constitutively active Alk2 in zebrafish embryos. Taken together, we believe cercosporamide may be the first of a new class of molecules with potential to be developed further for clinical use against diseases that are causally linked to overactivation of BMP receptor signaling, including Fibrodysplasia ossificans progressiva and diffuse intrinsic pontine glioma.

Insulin-receptor kinase activity of adipose tissue from morbidly obese humans with and without NIDDM

Diabetes ◽  
1987 ◽  
Vol 36 (5) ◽  
pp. 620-625 ◽  
Author(s):  
M. K. Sinha ◽  
W. J. Pories ◽  
E. G. Flickinger ◽  
D. Meelheim ◽  
J. F. Caro
Keyword(s):  
Adipose Tissue ◽  
Insulin Receptor ◽  
Kinase Activity ◽  
Morbidly Obese ◽  
Receptor Kinase ◽  
Insulin Receptor Kinase ◽  
Insulin Receptor Kinase Activity

Alteration of insulin-receptor kinase activity by high-fat feeding

Diabetes ◽  
1988 ◽  
Vol 37 (10) ◽  
pp. 1397-1404 ◽  
Author(s):  
T. Watarai ◽  
M. Kobayashi ◽  
Y. Takata ◽  
T. Sasaoka ◽  
M. Iwasaki ◽  
...  
Keyword(s):  
Insulin Receptor ◽  
Kinase Activity ◽  
Receptor Kinase ◽  
High Fat ◽  
Insulin Receptor Kinase ◽  
Insulin Receptor Kinase Activity ◽  
Fat Feeding
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