Words similar to tgfβ-dependent
Example sentences for: tgfβ-dependent
How can you use “tgfβ-dependent” in a sentence? Here are some example sentences to help you improve your vocabulary:
The altered kinetic of TGFβ-dependent Smad3 nuclear entry as induced by SB-203580 coincided with the efficacy by which this agent repressed the activity of the different TGFβ target genes.
Ese-1/Esx is a member of the Ets transcription factor family and is expressed mainly in epithelial tissue [ 30 ] . Its expression has been detected during mammary gland development and breast tumorigenesis [ 47 48 ] . It is noteworthy that Ese-1/Esx is a potential transcriptional regulator of the TGFβ type II receptor [ 31 ] and overexpression of Ese-1/Esx in non-invasive cells leads to a reduction in cell growth in the presence of TGFβ, presumably because of an increased TGFβ type II receptor level [ 49 ] . It is interesting that TGFβ-dependent downregulation of Ese-1/Esx is not affected by SB-203580.
The smad7 gene contains a perfect palindromic Smad binding element (GTCTAGAC) while the pai-1 and the pthrp promoters harbor AGAC tandem repeats [ 19 33 ] which binds Smad proteins less efficiently [ 34 ] . The upa gene contains only an AP1-binding site which resembles the Smad3/4-responsive AGAC motif [ 35 ] . A weaker binding site could require Smad3 to be present at higher concentrations for efficient binding and would make TGFβ-dependent transcription from a gene more vulnerable to reduced nuclear accumulation of the Smad3 protein.
One way by which Smad7 can inhibit TGFβ-dependent gene expression is by blocking phosphorylation, and, hence, nuclear import of Smad3 and Smad2 [ 23 ] . More recent data showing that Smad7 is able to interact with histone deacetylases suggest an additional role for Smad7 as a transcriptional co-repressor [ 50 ] . Thus, Smad7 might interfere directly with Ese-1/Esx gene transcription.
JNK has been described to drive TGFβ-dependent fibronectin synthesis independent of Smad4 and p38 [ 51 ] . In contrast to Smad3, JNK is activated by the TGFβ receptor I in a way that does not require the kinase domain [ 52 ] . This supports the notion that activation of Smad3 and JNK by TGFβ are independent events.
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