
IndraLab
Statements
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"Notably, we found that these cellular responses described above did not require persistent TGF-beta1 stimulation (XREF_FIG), indicating that one possible mechanism by which TGF-beta1 triggered down-regulation of ALK5 protein and mRNA expression, leads to the desensitization of the leukocytes toward TGF-beta1 stimulation."
"In Tgfbr2fl/fl control MEPM cells, radioactive TGF-β2 ligands (12.5 kDa) bind to TβRI (53 kDa), TβRII (70 kDa), and TβRIII (100–200 kDa, highly glycosylated molecule) and form the ligand-receptor complexes of TβRI::TGF-β2 (65.5 kDa), TβRII::TGF-β2 (82.5 kDa), and TβRIII::TGF-β2 (112.5–212.5 kDa)"
"TGFbeta signals are transmitted via a cell surface receptor complex consisting of the TGFbeta type I receptor (TbetaRI) and TGFbeta type II receptor (TbetaRII). To initiate signal transduction, TGFbeta binds to TbetaRII, which in turn recruits TbetaRI, leading to the formation of a tetrameric receptor complex."
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"Further, PAI-1, which is induced by TGF-beta1 activation of the Alk5 and SMAD2/3 pathway, contributes to vessel stabilization by preventing degradation of the provisional matrix deposited around new vessels and favoring the establishment of new basal lamina, again consistently with our finding that PAI-1 was specifically and robustly induced in the low VEGF conditions, leading to the fastest stabilization."
"TGF-beta signaling mediates a wide range of biological activities in development and disease. TGF-beta ligands signal through heterodimeric type I and type II receptors (TGF-beta receptor type I [TbetaRI, also known as ALK5 and TGFBR1] and TbetaRII) that are members of the serine/threonine kinase family."