Clapham DE. TRP channels as cellular sensors. Nature. 2003;426(6966):517–24.
Oberwinkler J, Philipp SE. Trpm3. Handb Exp Pharmacol. 2014;222:427–59.
Nilius B, Szallasi A. Transient receptor potential channels as drug targets: from the science of basic research to the art of medicine. Pharmacol Rev. 2014;66(3):676–814.
Vennekens R, Menigoz A, Nilius B. TRPs in the brain. Rev Physiol Biochem Pharmacol. 2012;163:27–64.
Nilius B, Owsianik G. The transient receptor potential family of ion channels. Genome Biol. 2011;12(3):218.
Moran MM, et al. Transient receptor potential channels as therapeutic targets. Nat Rev Drug Discov. 2011;10(8):601–20.
Nieto-Posadas A, Jara-Oseguera A, Rosenbaum T. TRP channel gating physiology. Curr Top Med Chem. 2011;11(17):2131–50.
Feske S. Calcium signalling in lymphocyte activation and disease. Nat Rev Immunol. 2007;7(9):690–702.
Colsoul B, Vennekens R, Nilius B. Transient receptor potential cation channels in pancreatic beta cells. Rev Physiol Biochem Pharmacol. 2011;161:87–110.
Marshall-Gradisnik S, et al. Natural killer cells and single nucleotide polymorphisms of specific ion
channels and receptor genes in myalgic encephalomyelitis/chronic fatigue syndrome. Appl Clin Genet. 2016;9:39–47.
Marshall-Gradisnik S, et al. Single nucleotide polymorphisms and genotypes in transient receptor potential ion channel and acetylcholine receptor genes from isolated B lymphocytes in myalgic ecephalomyelitis/chronic fatigue syndrome patients. J Int Med Res. 2016 (in review).
Fukuda K, et al. The chronic fatigue syndrome: a comprehensive approach to its definition and study. International chronic fatigue syndrome study group. Ann Intern Med. 1994;121(12):953–9.
Brown MM, Jason LA. Functioning in individuals with chronic fatigue syndrome: increased impairment with co-occurring multiple chemical sensitivity and fibromyalgia. Dyn Med. 2007;6:6.
Carruthers BM, et al. Myalgic encephalomyelitis: international consensus criteria. J Intern Med. 2011;270(4):327–38.
Brenu EW, et al. Natural killer cells in patients with severe chronic fatigue syndrome. Auto Immun Highlights. 2013;4(3):69–80.
Brenu EW, et al. Role of adaptive and innate immune cells in chronic fatigue syndrome/myalgic encephalomyelitis. Int Immunol. 2014;26(4):233–42.
Caligiuri M, et al. Phenotypic and functional deficiency of natural killer cells in patients with chronic fatigue syndrome. J Immunol. 1987;139(10):3306–13.
Maher KJ, Klimas NG, Fletcher MA. Chronic fatigue syndrome is associated with diminished intracellular perforin. Clin Exp Immunol. 2005;142(3):505–11.
Ojo-Amaize EA, Conley EJ, Peter JB. Decreased natural killer cell activity is associated with severity of chronic fatigue immune dysfunction syndrome. Clin Infect Dis. 1994;18(Suppl 1):S157–9.
Aoki T, et al. Low NK syndrome and its relationship to chronic fatigue syndrome. Clin Immunol Immunopathol. 1993;69(3):253–65.
Brenu EW, et al. Longitudinal investigation of natural killer cells and cytokines in chronic fatigue syndrome/myalgic encephalomyelitis. J Transl Med. 2012;10:88.
Hardcastle SL, et al. Characterisation of cell functions and receptors in Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME). BMC Immunol. 2015;16:35.
Huth TK, et al. Pilot study of natural killer cells in chronic fatigue syndrome/myalgic encephalomyelitis and multiple sclerosis. Scand J Immunol. 2016;83(1):44–51.
Levine PH, et al. Dysfunction of natural killer activity in a family with chronic fatigue syndrome. Clin Immunol Immunopathol. 1998;88(1):96–104.
Barker E, et al. Immunologic abnormalities associated with chronic fatigue syndrome. Clin Infect Dis. 1994;18(Suppl 1):S136–41.
Klimas NG, et al. Immunologic abnormalities in chronic fatigue syndrome. J Clin Microbiol. 1990;28(6):1403–10.
Bradley AS, Ford B, Bansal AS. Altered functional B cell subset populations in patients with chronic fatigue syndrome compared to healthy controls. Clin Exp Immunol. 2013;172(1):73–80.
Klimas NG, Koneru AO. Chronic fatigue syndrome: inflammation, immune function, and neuroendocrine interactions. Curr Rheumatol Rep. 2007;9(6):482–7.
Natelson BH, Haghighi MH, Ponzio NM. Evidence for the presence of immune dysfunction in chronic fatigue syndrome. Clin Diagn Lab Immunol. 2002;9(4):747–52.
Robertson MJ, et al. Lymphocyte subset differences in patients with chronic fatigue syndrome, multiple sclerosis and major depression. Clin Exp Immunol. 2005;141(2):326–32.
Ramos S, et al. Characterisation of B cell subsets and receptors in chronic fatigue syndrome patients. J Clin Cell Immunol. 2015;16:35.
Marshall-Gradisnik S, et al. Examination of single nucleotide polymorphisms (SNPs) in transient receptor potential (TRP) ion channels in chronic fatigue syndrome patients. Immunol Immunogenet Insights. 2015;7:1–6.
Ramos S, et al. Characterisation of B cell subsets and receptors in chronic fatigue syndrome patients. J Clin Cell Immunol. 2015;16(1):35.
Ding WX, et al. Differential effects of endoplasmic reticulum stress-induced autophagy on cell survival. J Biol Chem. 2007;282(7):4702–10.
Bootman MD, et al. 2-aminoethoxydiphenyl borate (2-APB) is a reliable blocker of store-operated Ca2+ entry but an inconsistent inhibitor of InsP3-induced Ca2 + release. FASEB J. 2002;16(10):1145–50.
Bryceson YT, et al. Synergy among receptors on resting NK cells for the activation of natural cytotoxicity and cytokine secretion. Blood. 2006;107(1):159–66.
Rossbacher J, Shlomchik MJ. The B cell receptor itself can activate complement to provide the complement receptor 1/2 ligand required to enhance B cell immune responses in vivo. J Exp Med. 2003;198(4):591–602.
Desai BN, Clapham DE. TRP channels and mice deficient in TRP channels. Pflugers Arch. 2005;451(1):11–8.
Wu LJ, Sweet TB, Clapham DE. International union of basic and clinical pharmacology. LXXVI. current progress in the mammalian TRP ion channel family. Pharmacol Rev. 2010;62(3):381–404.
Badheka D, Borbiro I, Rohacs T. Transient receptor potential melastatin 3 is a phosphoinositide-dependent ion channel. J Gen Physiol. 2015;146(1):65–77.
Parekh AB. Mitochondrial regulation of store-operated CRAC channels. Cell Calcium. 2008;44(1):6–13.
Delon J, et al. Imaging antigen recognition by naive CD4+ T cells: compulsory cytoskeletal alterations for the triggering of an intracellular calcium response. Eur J Immunol. 1998;28(2):716–29.
Bhakta NR, Oh DY, Lewis RS. Calcium oscillations regulate thymocyte motility during positive selection in the three-dimensional thymic environment. Nat Immunol. 2005;6(2):143–51.
Lyubchenko TA, Wurth GA, Zweifach A. Role of calcium influx in cytotoxic T lymphocyte lytic granule exocytosis during target cell killing. Immunity. 2001;15(5):847–59.
Xu SZ, et al. Block of TRPC5 channels by 2-aminoethoxydiphenyl borate: a differential, extracellular and voltage-dependent effect. Br J Pharmacol. 2005;145(4):405–14.
Ouyang Q, et al. Telomere length in human natural killer cell subsets. Hematopoietic Stem Cells Vi. 2007;1106:240–52.
Chan A, et al. CD56(bright) human NK cells differentiate into CD56(dim) cells: role of contact with peripheral fibroblasts. J Immunol. 2007;179(1):89–94.
Nagler A, et al. Comparative studies of human FcRIII-positive and negative natural killer cells. J Immunol. 1989;143(10):3183–91.
Jacobs R, et al. CD56brightNK cells differ in their KIR repertoire and cytotoxic features from CD56dim NK cells. Eur J Immunol. 2001;31(10):3121–6.
Ellis TM, Fisher RI. Functional heterogeneity of Leu 19″bright” + and Leu 19″dim” + lymphokine-activated killer cells. J Immunol. 1989;142(8):2949–54.
Fletcher MA, et al. Biomarkers in chronic fatigue syndrome: evaluation of natural killer cell function and dipeptidyl peptidase IV/CD26. PLoS ONE. 2010;5(5):e10817.
Woyach JA, Johnson AJ, Byrd JC. The B-cell receptor signaling pathway as a therapeutic target in CLL. Blood. 2012;120(6):1175–84.
Lewis RS. The molecular choreography of a store-operated calcium channel. Nature. 2007;446(7133):284–7.
Marshall-Gradisnik S, et al. Examination of single nucleotide polymorphisms in acetylcholine receptors in chronic fatigue syndrome patients. Immunol Immunogenet Insights. 2015;7:7–20.