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The MD acts to repress ClpB disaggregase activity, and DnaK binding relieves this repression (Oguchi et al., 2012; Seyffer et al., 2012).
Removal of CFTR relieves this repression and so raises basal activity of the NF-κB pathway.
Rapid transcriptional down-regulation of c-Myc by TGFβ relieves this repression, allowing binding of the heteromeric Smad complex [5].
WNT signaling relieves this repression by causing β-catenin/ARM to accumulate in the nucleus and convert dTCF to a transcriptional activator, possibly by displacing or overriding the default co-repressor(s) [37].
It is thus plausible that BMP signalling assembles a SMAD-dependent transcriptional repression complex on the Olig2 promoter and that FGF2 signalling via MAPK activity relieves this repression by sequestering SMAD1 in the cytoplasm.
Knockdown of Cdk1 relieves this repression, resulting in the activation of Cdx2 and differentiation of mouse ESCs into trophoectodermal lineages.
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We show that removal of the pgk-neo cassette is able to relieve this repression.
In a similar way, FOXO may also bind to another TF acting as a transcriptional repressor and relieve this repression, as seems to happen with p53 repression of SIRT1 transcription [29] or Cs1 repression of Hes1 [106].
Fusion of HD2 to 12S relieved this repression.
However, neuronal depolarization that triggers Ca2+ dependent phosphorylation of MeCP2 has been reported to relieve this repression.
One hypothesis put forward was that phosphorylated PhoP represses transcription of afsS and inhibits actinorhodin synthesis until a time when, perhaps, a more severe form of phosphate starvation or another independent mechanism sets in to relieve this repression [ 21].
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