[1] Caterina MJ, Schumacher MA, Tominaga M, et al. The capsaicin receptor: a heat-activated ion channel in the pain pathway[J]. Nature, 1997, 389: 816.
[2] Caterina MJ, Leffler A, Malmberg AB, et al. Impaired nociception and pain sensation in mice lacking the capsaicin receptor[J]. Science, 2000, 288: 306.
[3] Miyamoto R, Tokuda M, Sakuta T, et al. Expression and characterization of vanilloid receptor subtype 1 in human dental pulp cell cultures[J]. J Endod, 2005, 31: 652.
[4] Gunthorpe MJ, Chizh BA. Clinical development of TRPV1 antagonists: targeting a pivotal point in the pain pathway[J]. Drug Discov Today, 2009, 14: 56.
[5] Southall MD, Li T, Gharibova LS, et al. Activation of epidermal vanilloid receptor-1 induces release of proinflammatory mediators in human keratinocytes[J]. J Pharmacol Exp Ther, 2003, 304: 217.
[6] Szolcsanyi J. Hot target on nociceptors: perspectives, caveats and unique features[J]. Br J Pharmacol, 2008, 155: 1142.
[7] De Benedetto A, Agnihothri R, McGirt LY, et al.Atopic dermatitis: a disease caused by innate immune defects[J]. J Invest Dermatol, 2009, 129(1):14.
[8] Vennekens R, Owsianik G, Nilius B.Vanilloid transient receptor potential cation channels:an overview[J].Curr Pharm Des, 2008, 14(1):18.
[9] Huang J, Qiu L, Ding L, et al. Ginsenoside Rb1 and paeoniflorin inhibit transient receptor potential vanilloid-1-activated IL-8 and PGE2 production in a human keratinocyte cell line HaCaT[J]. Int Immunopharmacol,2010, 10: 1279.
[10] Huang J, Ding L, Shi D, et al. Transient receptor potential vanilloid-1 participates in the inhibitory effect of ginsenoside Rg1 on capsaicin-induced interleukin-8 and prostaglandin E2 production in HaCaT cells[J]. J Pharm Pharmacol, 2012, 64: 252.
[11] Eber SW, Pekrun A, Bardosi A, et al. Triosephosphate isomerase deficiency: haemolytic anaemia, myopathy with altered mitochondria and mental retardation due to a new variant with accelerated enzyme catabolism and diminished specific activity[J]. Eur J Pediatr, 1991, 150: 761.
[12] Olah J, Orosz F, Keseru GM, et al. Triosephosphate isomerase deficiency: a neurodegenerative misfolding disease[J]. Biochem Soc Trans, 2002, 30: 30.
[13] Iori E, Millioni R, Puricelli L, et al. Glycolytic enzyme expression and pyruvate kinase activity in cultured fibroblasts from type 1 diabetic patients with and without nephropathy[J]. Biochim Biophys Acta, 2008, 1782: 627.
[14] Wygrecka M, Marsh LM, Morty RE, et al. Enolase-1 promotes plasminogen-mediated recruitment of monocytes to the acutely inflamed lung[J]. Blood, 2009, 113(22):5588.
[15] Kobayashi H, Takahashi M, Takahashi H, et al.CD4+ T-cells from peripheral blood of a patient wiIh psoriasis recognize keratin 14 Deptide but not 'homologous'streptococcal M-protein epitope[J].J Dermatol Sci., 2002, 30(3): 240.
[16] Freedberg M, Tomic-Canic M, Komine M, et al.Keratins and thekeratinocyte activation cycle[J].J lnvest Dermatol, 2001,116(5): 633.
[17] Martinez, Azorin F,Remacha M,et al.Functional characterization of ribosomal P1/P2 proteins in human cells[J].Biochem J, 2008, 413(3):527.
[18] Gardner-Thorpe J, Ito H, Ashley SW, et al.Ribosomal protein P2:a potential molecular target for antisense therapy of human malignancies[J].Anticaneer Res, 2003, 23 (6C): 4549.