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Although R-spondin-mediated endocytosis of ZNRF3 has partially explained the regulation of ZNRF3 (Hao et al., 2012), whether ZNRF3 undergoes auto-ubiquitination or is ubiquitinated by other E3 ligase(s) is not well defined.
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To evaluate how strongly these predicted motifs "explain" the regulation of transcription, we applied a machine-learning algorithm to simulate gene expression (Zou et al. 2011).
Therefore, the simple "F/Y switch" model may not be able to explain the regulation of the state specificity of the MLL1 complex.
In the current study, we examined FAs at steady-state, yet our results may also shed new light on two models previously constructed to explain the regulation of FA size [35], [36].
In a hypothetical model that explains the regulation of the photosynthetic apparatus in strain KT71T we propose that the expression of photosynthesis genes depends on the cellular redox state and is maximal under conditions that allow a balanced membrane redox state.
Further hypotheses explaining the regulation of circulating IL-7 levels in RA are therefore required.
Two mutually incompatible models have been proposed to explain the regulation of ssA7.
STAT6 is therefore unlikely to explain the regulation of MCP-1 by IFNβ downstream of TLR4 or 3 activation.
It was suggested an epigenetic regulation independent of the assortment of other genes could explain the regulation of these highly amplified gene copies [ 45, 49].
The up-regulation of an ADP-ribosylation factor described in this work (EF127) [GenBank: BU671885] would explain the regulation of the intracellular traffic through vesicles [ 88].
These results suggest a partial mechanism to explain the regulation of rVSMC behaviors, including migration, adhesion, and proliferation that may be responsible for the progression of restenosis.
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