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These studies suggest that C2H2-ZFPs may not be specific to one particular stress but may regulate responses to several stresses.
Thus BMP6 may modulate Hamp1 in response to changes tissue iron whereas Atoh8 may regulate responses to serum iron and/or changes in erythropoietic activity that dominate under certain circumstances.
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These findings suggest that CIC may regulate immune responses and immune disorders.
Epithelial cells constitute the interface between gut microbiota and host tissue, and may regulate host responses to commensal enteric bacteria.
Park et al extend these observations by studying how the p85 XBP1 interaction may regulate insulin responses.
Therefore mosquito fat-spondin may regulate immune responses during nectar feeding.
PPARγ also may regulate neuronal responses to ischemia since conditional deletion of PPARγ in neurons increases their susceptibility to ischemia in vitro (Zhao et al., 2009).
This leads to the intriguing possibility that IL-18 may regulate Th17 responses by directly supporting MIP-3α/CCL20 and IL-17 expression in STs.
Zinc cluster proteins are distantly related to metazoan nuclear hormone receptors (Naar & Thakur, 2009), suggesting that MDT-15 and its metazoan counterparts may regulate similar responses by involving such proteins.
In addition, there is still a possibility that similar to other EDCs, NP and 4-OP may regulate hormonal responses by directly modulating cell-signaling pathways rather than interacting with hormone receptors (Tabb and Blumberg 2006).
Whelan et al. have also recently suggested a possible role for autophagy in post-MI tissues, and thus the argument that autophagy occurs in and may regulate cellular responses in post-MI heart in addition to necrosis is established in the literature.
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