Transforming Growth Factor 3 receptor

T, thymine T, threonine T3, triiodothyronine T4, tetraiodothyronine TBPS, ferft ary-butylbicyclophosphorothioate TGA, tricarboxylic acid TF, transcription factor TGI -fi, transforming growth factor (3 TGI -fi-Rs, transforming growth factor (3 receptors... 

Brandes, M.E., Mai, U.E.H., Ohura, K. and Wahl, S.M. (1991). Type I transforming growth factor-(3 receptors on human neutrophils mediate chemotaxis to transforming growth factor-(3. J. Immunol. 147, 1600-1606. 

Transforming growth factor receptor (TGFR) pathway.218... 

What do we know about receptor-mediated signalling pathways in parasitic platyhelminths Unfortunately, as a larger taxonomic group, we know very little. In-depth studies of the human blood fluke, 5. mansoni, have provided some of the most complete information on receptor-mediated signal transduction, and are summarized in the section on Transforming Growth Factor Receptor (TGFR) Pathway. ... 

Shah, P.K., Buslje, C.M. and Sowdhamini, R. (2001) Structural determinants of binding and specificity in transforming growth factor-receptor interactions. Proteins, 45, 408-420. 

Receptor Serine/Threonine Receptor Kinase Transforming Growth Factor- 3 Superfamily... 

Besides the cytokine receptors that lack intrinsic kinase activity but have associated JAK kinases, STAT proteins can be activated by a variety of G-protein coupled receptors and growth factor receptors with intrinsic tyrosine kinase activity (for example EGF, PDGF, CSF-1, and angiotensin receptor). Increasing evidence suggests a critical role for STAT family members in oncogenesis and aberrant cell proliferation. Constitutively activated STATs have been found in many transformed cell lines and a wide variety of human tumor entities. Numerous non-receptor tyrosine kinases and viral oncoproteins, such as v-Src, v-Abl, v-Sis, and v-Eyk, have been identified to induce DNA-binding activity of STAT proteins. 

In the interstitium, angiotensin II induces proliferation of mesangial cells and fibroblasts and the synthesis of collagen and other matrix molecules by these cells via the ATI receptor. Moreover, by the concomitant stimulation of chemoattractant cytokines, inflammation is induced. These processes are mediated by endothelin, transforming growth factor(3, and reactive oxygen species, and finally lead to interstitial fibrosis and glomerulosclerosis observed in hypertension and diabetes. 

Hyperphosphorylation of ERAK-1 by itself and ERAK-4 causes ERAK-1 to dissociate from the membrane-bound complex. Tumour necrosis factor (TNF) receptor-associated factor-6 ( TRAF-6), a cytoplasmic protein, is activated by ERAK-1 and with TAB-2, another cytoplasmic protein, activates transforming growth factor-P (TFG-P)-activating kinase (TAK-1). During this process both TRAF-6 and TAK-1 become ubiquitinated. TAK-1 then promotes activation of the IkB kinases, or the IKK family, EKKa and EKK 3 (found in a complex with NFicB-essential modulator [NEMO]), which phosphorylate the IkB family, notably IkB-u. IkB-u is an inhibitor of NFkB as it sequesters NFkB in an... 

Gharaee-Kermani M, Denholm EM, Phan SH. Costimulation of fibroblast collagen and transforming growth factor betal gene expression by monocyte chemoattractant protein-1 via specific receptors. J Biol Chem 1996 271(30) 17779-17784. 

Date M et al. Differential expression of transforming growth factor-/ and its receptors in hepatocytes and nonparenchy-mal cells of rat liver after CC14 administration. J Hepatol 1998 28 572-581. Frueh FW et al. Extent and character of Phenobarbital-mediated changes in gene expression in the liver. Mol Pharmacol 1997 51 363-369. 

Narayan, S., Thangasamy, T., and Balusu, R. 2005. Transforming growth factor beta receptor signaling in cancer. Frontiers in Bioscience 10, 1135-1145. 

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