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101.
Histone deposition protein Asf1 maintains DNA replisome integrity and interacts with replication factor C 总被引:9,自引:0,他引:9
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Chromatin assembly and DNA replication are temporally coupled, and DNA replication in the absence of histone synthesis causes inviability. Here we demonstrate that chromatin assembly factor Asf1 also affects DNA replication. In budding yeast cells lacking Asf1, the amounts of several DNA replication proteins, including replication factor C (RFC), proliferating cell nuclear antigen (PCNA), and DNA polymerase epsilon (Pol epsilon), are reduced at stalled replication forks. In contrast, DNA polymerase alpha (Pol alpha) accumulates to higher than normal levels at stalled forks in asf1Delta cells. Using purified, recombinant proteins, we demonstrate that RFC directly binds Asf1 and can recruit Asf1 to DNA molecules in vitro. We conclude that histone chaperone protein Asf1 maintains a subset of replication elongation factors at stalled replication forks and directly interacts with the replication machinery. 相似文献
102.
Genetic instability in superficial bladder cancer and adjacent mucosa: an interphase cytogenetic study 总被引:5,自引:0,他引:5
Cianciulli AM Leonardo C Guadagni F Marzano R Iori F De Nunzio C Franco G Merola R Laurenti C 《Human pathology》2003,34(3):214-221
A systematic analysis of both tumors and the surrounding urothelium to help identify what lies behind the mechanism of multifocal tumor development has not yet been performed. In this study we investigated chromosome 1, 7, 9, and 17 aneusomy in 25 superficial papillary carcinomas and in 51 tissue samples taken from sites of macroscopically uninvolved urothelium surrounding the tumors, using the fluorescence in situ hybridization method. Our data demonstrated a close genetic relationship between all examined tumors and normal-appearing mucosa. Numeric aberrations of chromosomes 1, 7, 9, and 17 were found to exhibit similar patterns in all analyzed specimens, although with different frequencies. 相似文献
103.
104.
Paola Origone Carlo Bellini Debora Sambarino Barbara Banelli Guido Morcaldi Carmen La Rosa Franco Stanzial Claudio Castellan Domenico A. Coviello Cecilia Garrè Eugenio Bonioli 《Human mutation》2003,22(4):341-341
In the original version of this article, the title was incorrect. Please find the correct title given here. The publisher deeply regrets this error. The original article to which this Erratum refers was published in Human Mutation 22:179–180 Human Mutation(2003) 22(2) 179–180 相似文献
105.
Franco R Rodríguez R Pasantes-Morales H 《Pflügers Archiv : European journal of physiology》2004,449(2):159-169
Reducing osmolarity by 35% increased 3H-taurine efflux from Swiss 3T3 fibroblasts from 0.5% to a peak of 5.7%. The presence of ATP (10–100 µM; EC50 1.5 µM) increased taurine efflux up to 10%, and decreased the set point for hyposmotically stimulated taurine release (HTR). ATP potentiation was mimicked by UTP, reduced by addition of suramin and pyridoxal phosphate-6-azophenyl-2,4-disulphonic acid (PPADS) and unaffected by ADP, ,-methylene-ATP (,-ATP) or 2-methylthio-ATP (Me-ATP), suggesting its mediation by purinergic P2Y2 and P2Y4 metabotropic receptors. Under isosmotic conditions ATP increased the cytosolic [Ca2+] ([Ca2+]i) markedly, but did not increase taurine release. HTR was independent of external Ca2+ but was reduced (by 56–59%) by BAPTA-AM, thapsigargin-induced depletion of intracellular Ca2+ stores, or phospholipase C (PLC) inhibition. Blockade of calmodulin (CaM) or calmodulin kinase II (CaMKII) reduced HTR by 54% and 76%, respectively. The ATP-mediated potentiation was prevented fully by all these treatments. HTR was reduced by 30–50% by blockers of protein tyrosine kinases (AG18), phosphoinositide 3-kinase (PI3K) (wortmannin), p21rho (toxin B), p21rho-kinase (Y27632) and the stress-activated kinase p38 (PD169316). ATP-mediated potentiation was reduced similarly by these blockers. Simultaneous inhibition of PI3K and CaMKII abolished HTR. Altogether, these results suggest a modulatory effect of ATP, probably exerted by a potentiation of the Ca2+-dependent fraction of HTR. This fraction has as signalling elements a PLC-dependent [Ca2+]i increase, resulting from Ca2+ released from thapsigargin-sensitive internal stores, followed by activation of CaM/CaMKII reactions. The Ca2+/ATP effect operates only when the Ca2+-independent, tyrosine kinase-mediated pathway is already activated. Suggested elements of cross-talk between the two pathways are PLC, PI3K and CaMKII. 相似文献
106.
Franco Laccone Ivonne Jünemann Sharon Whatley Rhian Morgan Rachel Butler Peter Huppke David Ravine 《Human mutation》2004,23(4):395-395
The original article to which this Erratum refers was published in Human Mutation 23:234–244 Human Mutation(2004) 23(3) 234–244 相似文献
107.
Trisomy 8 in myelodysplasia and acute leukemia is constitutional in 15-20% of cases. 总被引:2,自引:0,他引:2
Emanuela Maserati Fiorenza Aprili Fabrizio Vinante Franco Locatelli Giovanni Amendola Adriana Zatterale Giuseppe Milone Antonella Minelli Franca Bernardi Francesco Lo Curto Francesco Pasquali 《Genes, chromosomes & cancer》2002,33(1):93-97
The trisomy 8 found in malignancies may derive from a constitutional trisomy 8 mosaicism (CT8M), and in these cases the trisomy itself may be regarded as the first mutation in a multistep carcinogenetic process. To assess the frequency of CT8M in hematological dysplastic and neoplastic disorders with trisomy 8, an informative sample of 14 patients was collected. The data ascertained included chromosome analyses of fibroblast cultures and of PHA-stimulated blood cultures in patients with normal blood differential count, as well as possible CT8M clinical signs. One patient showed trisomy 8 in all cell types analyzed and undoubtedly has a CT8M; a second patient consistently showed trisomy 8 in PHA-stimulated blood cultures when no immature myeloid cells were present in blood and should be considered as having CT8M; a third patient, with Philadelphia-positive chronic myelocytic leukemia, was more difficult to interpret, but the possibility that she had CT8M is likely. A few clinical signs of CT8M were also present in these three patients. Our data indicate that the frequency of CT8M in hematological dysplastic and neoplastic disorders with trisomy 8 is approximately 15-20%. 相似文献
108.
109.
Gonadotrophin-releasing hormone agonist dose-dependency of pituitary desensitization during controlled ovarian hyperstimulation in IVF 总被引:2,自引:2,他引:2
Janssens RM; Vermeiden JP; Lambalk CB; Schats R; Schoemaker J 《Human reproduction (Oxford, England)》1998,13(9):2386-2391
The aim of this study was to find the minimal effective daily s.c. dose of
the gonadotrophin-releasing hormone (GnRH) agonist, triptorelin acetate,
that suppresses the GnRH-induced release of luteinizing hormone (LH) at
time of human chorionic gonadotrophin (HCG) injection and thereby prevents
spontaneous LH surges during in-vitro fertilization (IVF) stimulation
cycles. Therefore, a double-blind, prospective and randomized titration
study was performed. A total of 48 IVF patients were divided into four
groups of 12 patients. Each group received a different dose of triptorelin
acetate, namely 5, 15, 50 or 100 microg s.c. daily. Standard ovarian
stimulation was carried out using urinary follicle stimulating hormone
(FSH) preparations. A 500 microg GnRH test was performed 90 min before the
HCG injection in order to measure the degree of pituitary desensitization.
Spontaneous LH surges were not detected in any of the groups, although
three patients in the 5 microg group had ovulated at the time of ovum
retrieval. The pituitary LH response to the GnRH test at time of HCG,
expressed as area under the curve (AUC), appeared to be dose-dependent.
Thus, a daily s.c. dose of 100 microg triptorelin acetate appears to be too
high, since adequate desensitization of the pituitary (i.e. no spontaneous
LH surge) can be achieved with doses as low as 15 and 50 microg.
相似文献
110.
Domenico Lapenna Andrea Mezzetti Sergio de Gioia Agostino Consoli Davide Festi Carmine Di Ilio Franco Cuccurullo 《Pflügers Archiv : European journal of physiology》1994,427(5-6):432-436
The left ventricular subendocardial and subepicardial layers of six perfused rabbit hearts were tested for enzymatic and non-enzymatic antioxidant defences and for lipid peroxidation. The subendocardium showed significantly lower catalase activity and contents of non-protein thiol compounds and vitamin E associated with a higher degree of lipid peroxidation. The activities of Cu,Zn- and Mn-superoxide dismutases, glutathione reductase, -glutamylcysteine synthetase and -glutamyl transpeptidase showed no significant transmural differences, and Se-independent glutathione peroxidase activity was not detectable in either layer. Comparable results were observed in another group of six unperfused rabbit hearts. In five H2O2-perfused rabbit hearts, lipid peroxidation was higher, and myocardial creatine phosphokinase activity lower, in the subendocarium than in the subepicardium. In this group, only the subendocardium had significantly higher lipid peroxidation levels than the control hearts. Thus, a lower antioxidant capacity and a greater oxidative stress are present in the rabbit subendocardium. These findings could provide insight into the problem of subendocardial vulnerability to free radical-mediated processes, such as occurs in ischaemia-reperfusion injury. 相似文献