INT140794
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Immunohistochemistry (Smad3 And p-Smad2/3) | |||||||||||||||
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Expression of Smad3 and Sox17 inputs was assessed by immunoblot using cell lysates from transfections done in parallel to chromatin immunoprecipitations.
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Overexpression of both Smad2 and Smad3 blocked spontaneous maturation in Smad3-deficient chondrocytes [70,71]. | |||||||||||||||
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on chondrocyte maturation is mediated by the Smad2/3 pathway, as has been shown by overexpression of dominant negative Smad2 and Smad3 in chondrocytes. | |||||||||||||||
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In articular chondrocytes treated with azacytidine, reduced Smad2 and Smad3 expression and signaling and increased Smad1/5 expression correlated with elevated synthesis of type X collagen and alkaline phosphatase. | |||||||||||||||
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SMA expression is not Smad3-dependent in that Smad3 deficient mice can develop small ASC plaques that are ? | |||||||||||||||
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1 model to the Smad3 deficient mice confirmed our earlier findings demonstrating that while Smad3 is sufficient for, it is not necessary for the EMT of LECs during ASC formation in vivo. | |||||||||||||||
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SMA expression is not Smad3-dependent in that Smad3 deficient mice can develop small ASC plaques that are ? | |||||||||||||||
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Levels of prolyl 4-hydroxylase beta (P4Hbeta), cytoglobin/stellate cell activation-associated protein (Cygb/STAP), transgelin, tissue inhibitors of metalloproteinases, serum response factor, transforming growth factor beta (TGFbeta), Smad3, and pancreatitis-associated protein 1 (PAP-1) were determined by immunohistochemistry. | |||||||||||||||
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Rik Derynck (UCSF) [64], and the FLAG-tagged Smad3 expression vectors were generated by Dr. | |||||||||||||||
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Sox17-V5 and FLAG-Smad3 constructs were expressed in MLE-15 cells. | |||||||||||||||
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The GST-Sox17 and GST-Smad3 fusion proteins (and GST only) were expressed in BL21 cells induced with 1 mM isopropyl ? | |||||||||||||||
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1 and Smad3, consistent with an antagonistic effect of Sox17 on the TGF-? | |||||||||||||||
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/Smad3 Signaling to Initiate Progenitor Cell Behavior in the Respiratory Epithelium
The Sry-related high mobility group box transcription factor Sox17 is required for diverse developmental processes including endoderm formation, vascular development, and fetal hematopoietic stem cell maintenance. | |||||||||||||||
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Phosphorylated Smad2 and Smad3, the effectors of the TGF-? | |||||||||||||||
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Overexpression of dominant negative Smad3 causes neurodegeneration in cell cultures, indicating that loss of Smad2/3 signaling is involved. | |||||||||||||||
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Interaction of Runx2 with Smad1 facilitates the function of Runx2 in stimulating terminal differentiation, while Smad3 blocks Runx2 function [81-83]. | |||||||||||||||
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The ALK1 (Smad1/5/8) and ALK5 (Smad3) signaling balance in chondrocytes apparently determines MMP-13 expression. | |||||||||||||||
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A previous study demonstrated that Smad3, signal transducers of the TGF-? | |||||||||||||||
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Genes monitored were smad2, smad3, TGF-? | |||||||||||||||
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General Comments
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