CCA1 and LHY repress transcript expression of TOC1 by binding directly to its promoter, and as shown recently TOC1 negatively regulates the transcription of CCA1 and LHY [ 13, 14], establishing negative feedback loop [ 11, 15].
IκBs bind NF-κB in the nucleus, leading to an export of the IκB/NF-κB-complexes to the cytoplasm, hence inhibiting the NF-κB signal establishing negative feedback loops [ 2, 13– 15].
This establishes negative feedback loops to attenuate HIF expression.
As such, it was of obvious interest to determine whether ectopic expression of DUSP16 could re-establish negative feedback of JNK signalling in cells lacking endogenous expression.
miR-1 and miR-133 modulate skeletal-muscle-cell proliferation and differentiation by repressing the activity of HDAC4 (histone deacetylase 4; a signal-dependent inhibitor of muscle differentiation) and SRF, respectively, thereby establishing negative-feedback loops for muscle-cell differentiation [ 23].
Kumbrink, J., Gerlinger, M. & Johnson, J.P. Egr-1 induces the expression of its corepressor Nab2 by activation of the Nab2 promoter thereby establishing a negative feedback loop.
Kumbrink, J., Kirsch, K.H. & Johnson, J.P. EGR1, EGR2, and EGR3 activate the expression of their coregulator NAB2 establishing a negative feedback loop in cells of neuroectodermal and epithelial origin.
Once the complexes reach their destination, CRY inhibits the CLOCK/BMAL1 driven transcription, thereby establishing a negative feedback loop [5] [7].
Conversely, Hsp90 represses gene expression from Hsf1-dependent promoters [ 44], establishing a negative feedback loop for its own expression.
Intriguingly, mutations in components of the NRD pathway also increase expression of Nrd1 itself, CF IB (aka HRP1), Pcf11 and the U1 snRNA binding protein A1 (MUD1), thereby establishing a negative feedback control on termination [138,198,201 203].
