[ 7 ] Hustert E, Zibat A, Presecan-Siedel E, et al. Natural protein variants of pregnane X receptor with altered transactivation activity toward CYP3A4[J]. Drug Metab Dispos, 2001, 29(11): 1454-1459.
[8]
[ 8 ] Gregg C. Drug interactions and anti-infective therapies[J]. Am J Med, 1999, 106(2): 227-237.
Nuclear Receptors Committee. A unified nomenclature system for the nuclear recept or super family[J]. Cell, 1999, 97: 161-163.
[12]
Ito K, Chung KF, Adcock IM. Update on glucocorticoid action and resistance[J]. J Allergy Clin Immunol, 2006, 117(3): 522-543.
[13]
Charmandari E, Kino T, Ichijo T, et al. Functional characterization of the natural human glucocorticoid receptor (hGR) mutants hGRalphaR477H and hGRalphaG679S associated with generalized glucocorticoid resistance[J]. J Clin Endocrinol Metab, 2006, 91(4): 1535-1543.
[14]
Charmandari E, Kino T, Chrousos GP. Familial/sporadic glucocorticoid resistance: clinical phenotype and molecular mechanisms[J]. Ann N Y Acad Sci, 2004, 1024: 168-181.
[15]
Hurley DM, Accili D, Stratakis CA, et al. Point mutation causing a single amino acid substitution in the hormone binding domain of the glucocorticoid receptor in familial glucocorticoid resistance[J]. J Clin Invest, 1991, 87(2): 680-686.
[16]
Karl M, Lamberts SW, Detera-Wadleigh SD, et al. Familial glucocorticoid resistance caused by a splice site deletion in the human glucocorticoid receptor gene[J]. J Clin Endocrinol Metab, 1993, 76(3): 683-689.
[17]
Malchoff DM, Brufsky A, Reardon G, et al. A mutation of the glucocorticoid receptor in primary cortisol resistance[J]. J Clin Invest, 1993, 91(5): 1918-1925.
[18]
Vottero A, Kino T, Combe H, et al. A novel, C-terminal dominant negative mutation of the GR causes familial glucocorticoid resistance through abnormal interactions with p160 steroid receptor coactivators[J]. Clin Endocrinol Metab, 2002, 87(6): 2658-2667.
[19]
Ruiz M, Lind U, G？fvels M, et al. Characterization of two novel mutations in the glucocorticoid receptor gene in patients with primary cortisol resistance[J]. Clin Endocrinol (Oxf), 2001, 55(3): 363-371.
[20]
Karl M, Lamberts SW, Koper JW, et al. Cushing’s disease preceded by generalized glucocorticoid resistance: clinical consequences of a novel, dominant-negative glucocorticoid receptor mutation[J]. Proc Assoc Am Physicians, 1996, 108(4): 296-307.
[21]
Kino T, Stauber RH, Resau JH, et al. Pathologic human GR mutant has a transdominant negative effect on the wild-type GR by inhibiting its translocation into the nucleus: importance of the ligand-binding domain for intracellular GR trafficking[J]. J Clin Endocrinol Metab, 2001, 86(11): 5600-5608.
Lee DK, Currie GP, Hall IP, et al. The arginine-16 beta2-adrenoceptor polymorphism predisposes to bronchoprotective subsensitivity in patients treated with formoterol and salmeterol[J]. Br J Clin Pharmacol, 2004, 57(1): 68-75.
[26]
Israel E, Chinchilli VM, Ford JG, et al. Use of regularly scheduled albuterol treatment in asthma: genotype-stratified, randomised, placebo-controlled cross-over trial[J]. Lancet, 2004, 364(9444): 1505-1512.
Sampson AP, Siddiqui S, Buchanan D, et al. Variant LTC(4) synthase allele modifies cysteinyl leukotriene synthesis in eosinophils and predicts clinical response to zafirlukast[J]. Thorax, 2000, 55 (Suppl 2): S28-S31.
[29]
Fenech AG, Ebejer MJ, Felice AE, et al. Mutation screening of the muscarinic M(2) and M(3) receptor genes in normal and asthmatic subjects[J]. Br J Pharmacol, 2001, 133(1): 43-48.
[30]
Kwatra D, Vadlapatla RK, Vadlapudi AD, et al. Interaction of gatifloxacin with efflux transporters: a possible mechanism for drug resistance[J]. Int J Pharm, 2010, 395(1-2): 114-121.
