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WK Vogel GL Peterson DJ Broderick VA Mosser MI Schimerlik 《Canadian Metallurgical Quarterly》1999,361(2):283-294
Double mutant cycles provide a method for analyzing the effects of a mutation at a defined position in the protein structure on the properties of an amino acid at a second site. This approach was used to map potential interactions between aspartates 69, 97, and 103 in the m2 muscarinic acetylcholine receptor transmembrane helices 2 and 3. Receptors containing single and double aspartate to asparagine mutants were expressed in Chinese hamster ovary cells and their effects on ligand binding, signal transduction, and thermal stability determined. Analysis of the double mutant cycles showed that the mutations had approximately additive effects on ligand binding, signal transduction, and thermal stability. Ligand binding and thermal inactivation results support the conclusion that aspartate-103 is the ligand amine counterion. Effector coupling properties of the mutant receptors showed that aspartate-103 was also required for signal transduction activity. The mutation of aspartate-69 to asparagine completely eliminated signal transduction by the agonists acetylcholine, carbachol, and pilocarpine but not oxotremorine M, which caused reduced but significant inhibition of adenylyl cyclase and stimulation of phospholipase C. In contrast, adenylyl cyclase stimulation by the asparagine-69 mutant was elicited only by acetylcholine and carbachol but not by oxotremorine M. The variation in agonist-dependent effector coupling properties provides evidence that the asparagine-69 mutant can exist in activated receptor states that are different from the wild-type m2 muscarinic receptor. 相似文献
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H Lin ML Bondy LA Langford KR Hess GL Delclos X Wu W Chan MA Pershouse WK Yung PA Steck 《Canadian Metallurgical Quarterly》1998,4(10):2447-2454
The frequency of loss of heterozygosity (LOH) around MMAC/PTEN and DMBT1 loci and survival analyses based on the LOH status were assessed in 110 patients with different histological groups of gliomas. Twenty-six of the patients had anaplastic oligodendrogliomas, 31 had anaplastic astrocytomas, and 53 had glioblastomas multiforme (GM). At the DMBT1 locus, LOH was observed very frequently in all three histological groups, with no significant difference in the frequency of LOH among the three histological groups. At the MMAC/PTEN locus, patients with GM exhibited a significantly increased frequency of LOH (72%) compared with patients with anaplastic astrocytomas (29%) or anaplastic oligodendrogliomas (31%) (P < 0.0001). Kaplan-Meier survival plots showed that patients with LOH at the MMAC/PTEN locus had a significantly worse prognosis than did patients without LOH at the MMAC/PTEN locus [hazard ratio (LOH versus non-LOH), 2.65; 95% confidence interval (CI), 1.69-4.46; P < 0.0001]. Cox proportional hazards regression analysis, adjusted for age at surgery and histological grades (GM and non-GM), showed that LOH at the MMAC/PTEN locus was a significant predictor of shorter survival [hazard ratio (LOH versus non-LOH), 2.01; 95% CI, 1.1-3.5; P = 0.018). Our analysis failed to indicate a similar association between the frequency of LOH at the DMBT1 locus and patient survival [hazard ratio (LOH versus non-LOH), 2; 95% CI, 0.37-3.13; P = 0.2]. These results suggest that the DMBT1 gene may be involved early in the oncogenesis of gliomas, whereas alterations in the MMAC/PTEN gene may be a late event in the oncogenesis related to progression of gliomas and provide a significant prognostic marker for patient survival. 相似文献
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RK Maloney WK Chan R Steinert P Hersh M O'Connell 《Canadian Metallurgical Quarterly》1995,102(7):1042-52; discussion 1052-3
PURPOSE: The Summit Therapeutic Refractive Clinical Trial is a nine-center prospective, nonrandomized, self-controlled trial to assess the efficacy, stability, and safety of using a standardized technique of excimer laser photorefractive keratectomy (PRK) to correct residual myopia in eyes with previous refractive surgery or cataract surgery. PATIENTS AND METHODS: Eligible eyes with a mean residual myopia of -3.7 +/- 1.8 diopters (D) (range, -0.63 to -11.00 D) underwent PRK with a 193-nm excimer laser for myopic corrections between -1.50 and -7.50 D. Standardized settings were used for the ablation zone, ablation rate, repetition rate, and fluence. One hundred seven of the first 114 treated eyes were examined 1 year after PRK, with 98% of eyes having had refractive keratotomy and 2% having had cataract surgery. RESULTS: One year postoperatively, the mean manifest spherical equivalent refraction was -0.6 +/- 1.4 D (range, -6.50 to 2.50 D); 63% of eyes were within +/-1.00 D of the attempted correction; and uncorrected visual acuity was 20/40 or better in 74% of eyes. Twenty-nine percent of eyes lost two or more Snellen lines of best-corrected visual acuity, and central corneal haze was moderate or severe in 8% of eyes. CONCLUSIONS: Excimer laser PRK is effective in reducing residual myopia after previous refractive and cataract surgery. However, it is less accurate than PRK in eyes that did not undergo surgery and is more likely to cause a loss of best-corrected visual acuity 1 year after treatment. 相似文献
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The PTEN gene (also called MMAC1 and TEP1) at chromosome 10q23 is mutated in a variety of predominantly late-stage tumors and has been shown to suppress glioma cell growth in vitro and in vivo. Here we sought to determine the mechanism by which PTEN mediates growth inhibition. Using the mutant PTEN glioma cell line, U87MG, as a transfection recipient for a series of PTEN alleles, we provide direct evidence that this capacity requires phosphatase activity. Mutations mapping upstream, within, and downstream of the catalytic domain ablated activity toward a 3' phosphorylated phosphoinositide substrate of PTEN, whereas alleles with mutations flanking the catalytic domain retained activity toward the acidic protein polymer substrate, Glu4Tyr1. Thus, catalytic activity toward phosphoinositide substrates was required for growth suppression, whereas activity toward the protein substrate was dispensable for growth suppression. Finally, we used apoptotic and cell proliferation analyses to show that PTEN-mediated growth inhibition under reduced serum conditions was due to a G1 cell cycle block rather than to an induction of apoptosis. 相似文献