Because HIF is the major mediator in cellular adaption to hypoxia, increased HIF1α and HIF2α might be involved in mediating the endocytosis of Na+-K+ ATPase.
Hypoxia-inducible factor-1 (HIF-1) is the key mediator in cellular oxygen homeostasis that facilitates the adaptation to oxygen deprivation by regulating expression of gene products that are involved in cellular energy metabolism and glucose transport, angiogenesis, and erythropoiesis, among others (7).
These receptors trigger a cascade of signaling mechanisms with subsequent expression of vascular cell adhesion molecule-1 (VCAM-1), induction of vascular leakage, and increased chemotaxis of mononuclear phagocytes and release of pro-inflammatory mediators resulting in cellular dysfunction [ 12- 15].
This co-ordinated and potent mechanism, with opposite effects on the main Cl− influx and Cl− efflux mediators involved in cellular Cl− homoeostasis, is of obvious interest for drug development.
The analyses of A. thaliana transgenic plants that express the auxin-inducible marker DR5:uidA, and the response of the auxin-resistant mutants axr2 and aux1 7 to dichromate suggest that auxins do not participate as mediators in the cellular and physiological responses to this metal.
Also, protein localization processes, e.g., based on phosphorylation state, are important mediators in (localized) cellular processes.
PKD has been implicated as a mediator in diverse cellular functions, including proliferation, survival, cellular trafficking and regulation of transcription.
The latter has emerged as a significant lipid mediator in many cellular processes.
Ceramide has been identified as a bioactive mediator in various cellular functions, including apoptosis and the cell cycle (10, 11).
