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Altered microglia function has been implicated in the pathophysiological mechanisms of both migraine and chronic pain conditions [60, 61].
Indeed, Ate1 function has been implicated in the regulation of the cytoskeleton and a large subset of identified arginyltransferase substrates (including actin, tubulin, and dynein [6]) play key roles in cell division, meiotic chromosome segregation and sperm motility (see [13] [17] for overview).
Impaired barrier function has been implicated in the pathogenesis of inflammatory bowel disease (IBD).
Dysregulation of uNK cell function has been implicated in the aetiology of early implantation disorders and disorders of pregnancy.
Modulation of thalamocortical (TC) relay neuron function has been implicated in the sedative and hypnotic effects of general anaesthetics.
A low mitochondrial function has been implicated in the aetiology of insulin resistance and type 2 diabetes [ 1– 4].
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Recently, DDR2 function has been implicated in human skeletal growth.
Cholinergic neurons function has been implicated in learning and memory processes [ 14].
As a consequence, deficits in mitochondrial function have been implicated in various human degenerative diseases, aging, and cancer [5], [6].
Loss of function of DNA repair genes has been implicated in the development of many types of cancer.
More recently, transmembrane signaling has been implicated in the function of the DGC.
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