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排序方式: 共有79条查询结果,搜索用时 15 毫秒
1.
S Grimaldi S Lio P Iacovacci F Carlini F Monaco J Roche 《Comptes rendus des séances de la Société de biologie et de ses filiales》1986,180(3):277-283
Two kinds of TBG polymorphism are described in human, one found in deglycosylated TBG from individual blood donors, the other is a genetically determined polymorphism. TBG from plasma samples from a patient with toxic goiter, not autoimmune, (p)TBG, from the patient's mother (m)TBG and from individual donors (n)TBG, were labeled with [125I]T4 or [125I]T3 and submitted to isoelectric focusing (IEF), followed by autoradiography. Three faint [125I]T4 radiolabeled bands were detectable in (p)TBG while four strong [125I]T4 radiolabeled bands were detectable in (m)TBG and (n)TBG), respectively. IEF of the [125I]T3 incubated serum samples resulted in no detectable isoelectric radiolabeled band for (p)TBG while a normal pattern was found in (m)TBG and in (n)TBG, respectively. These data suggest a new intraindividual not linked to sexual chromosome X polymorphism characterized by a loss in hormone binding. 相似文献
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3.
L. Vaccarino G. Triolo A. Accardo-Palombo L. Scola M. Palmeri M. Bova G. Candore D. Lio C. R. Balistreri 《Biochemical genetics》2013,51(11-12):967-975
Cytokines act as pleiotropic polypeptides able to regulate inflammatory/immune responses and to provide important signals in physiological and pathological processes. Several cytokines (Th1, Th2, and Th17) seem to be involved in the pathophysiology of Behçet’s disease, a chronic immune-mediated disease characterized by oral and genital lesions and ocular inflammation. Its individual susceptibility seems to be modulated by genetic variants in genes codifying these cytokines. Th1 and Th17 seem to be involved in the disease’s active phases, and Th2 seems to affect the development or severity of the disease; however, contrasting data are reported. In this study, some genetic variants of the Th1/Th2 cytokine genes were investigated in Sicilian patients and age- and gender-matched controls. Three very significant associations with Behçet’s disease were detected, and combined genotypes associated with increased disease risk were identified. Results obtained point to the key role of Th1/Th2 cytokine genetic variants in disease susceptibility. 相似文献
4.
Lio YC Mazin AV Kowalczykowski SC Chen DJ 《The Journal of biological chemistry》2003,278(4):2469-2478
The human Rad51 protein is essential for DNA repair by homologous recombination. In addition to Rad51 protein, five paralogs have been identified: Rad51B/Rad51L1, Rad51C/Rad51L2, Rad51D/Rad51L3, XRCC2, and XRCC3. To further characterize a subset of these proteins, recombinant Rad51, Rad51B-(His)(6), and Rad51C proteins were individually expressed employing the baculovirus system, and each was purified from Sf9 insect cells. Evidence from nickel-nitrilotriacetic acid pull-down experiments demonstrates a highly stable Rad51B.Rad51C heterodimer, which interacts weakly with Rad51. Rad51B and Rad51C proteins were found to bind single- and double-stranded DNA and to preferentially bind 3'-end-tailed double-stranded DNA. The ability to bind DNA was elevated with mixed Rad51 and Rad51C, as well as with mixed Rad51B and Rad51C, compared with that of the individual protein. In addition, both Rad51B and Rad51C exhibit DNA-stimulated ATPase activity. Rad51C displays an ATP-independent apparent DNA strand exchange activity, whereas Rad51B shows no such activity; this apparent strand exchange ability results actually from a duplex DNA destabilization capability of Rad51C. By analogy to the yeast Rad55 and Rad57, our results suggest that Rad51B and Rad51C function through interactions with the human Rad51 recombinase and play a crucial role in the homologous recombinational repair pathway. 相似文献
5.
Wavelet change-point prediction of transmembrane proteins 总被引:3,自引:0,他引:3
MOTIVATION: A non-parametric method, based on a wavelet data-dependent threshold technique for change-point analysis, is applied to predict location and topology of helices in transmembrane proteins. A new propensity scale generated from a transmembrane helix database is proposed. RESULTS: We show that wavelet change-point performs well for smoothing hydropathy and transmembrane profiles generated using different scales. We investigate which wavelet bases and threshold functions are overall most appropriate to detect transmembrane segments. Prediction accuracy is based on the analysis of two data sets used as standard benchmarks for transmembrane prediction algorithms. The analysis of a test set of 83 proteins results in accuracy per segment equal to 98.2%; the analysis of a 48 proteins blind-test set, i.e. containing proteins not used to generate the propensity scales, results in accuracy per segment equal to 97.4%. We believe that this method can also be applied to the detection of boundaries of other patterns such as G + Cisochores and dot-plots. AVAILABILITY: The transmembrane database, TMALN and source code are available upon request from the authors. 相似文献
6.
Schild D Lio YC Collins DW Tsomondo T Chen DJ 《The Journal of biological chemistry》2000,275(22):16443-16449
In yeast, the Rad51-related proteins include Rad55 and Rad57, which form a heterodimer that interacts with Rad51. Five human Rad51 paralogs have been identified (XRCC2, XRCC3, Rad51B/Rad51L1, Rad51C/Rad51L2, and Rad51D/Rad51L3), and each interacts with one or more of the others. Previously we reported that HsRad51 interacts with XRCC3, and Rad51C interacts with XRCC3, Rad51B, and HsRad51. Here we report that in the yeast two-hybrid system, Rad51D interacts with XRCC2 and Rad51C. No other interactions, including self-interactions, were found, indicating that the observed interactions are specific. The yeast Rad51 interacts with human Rad51 and XRCC3, suggesting Rad51 conservation since the human yeast divergence. Data from yeast three-hybrid experiments indicate that a number of the pairs of interactions between human Rad51 paralogs can occur simultaneously. For example, Rad51B expression enhances the binding of Rad51C to XRCC3 and to HsRad51D, and Rad51C expression allows the indirect interaction of Rad51B with Rad51D. Experiments using 6xHis-tagged proteins in the baculovirus system confirm several of our yeast results, including Rad51B interaction with Rad51D only when Rad51C is simultaneously expressed and Rad51C interaction with XRCC2 only when Rad51D is present. These results suggest that these proteins may participate in one complex or multiple smaller ones. 相似文献
7.
Protein kinase C contributes to desensitization of ANG II signaling in adult rat cardiac fibroblasts 总被引:1,自引:0,他引:1
Meszaros JG Raphael R Lio FM Brunton LL 《American journal of physiology. Cell physiology》2000,279(6):C1978-C1985
We have studiedGq-linked ANG II signaling [inositol phosphate (IP)accumulation, Ca2+ mobilization] in primary cultures ofrat cardiac fibroblasts (CFs) and have found that ANG II initiates aprotein kinase C (PKC)-mediated negative feedback loop that rapidlyterminates the ANG II response. Pharmacological inhibition of PKC bystaurosporine and GF-109203X doubled IP production over that achievedin response to ANG II alone. Inhibition of PKC also led to largerCa2+ transients in response to ANG II, suggesting thatCa2+ mobilization was proportional toGq-phospholipase C-IP3 activity underthe conditions studied. Depletion of cellular PKC by overnight treatment with phorbol 12-myristate 13-acetate (PMA) similarly augmented ANG II-induced IP production. Acute activation of PKC by PMAhalved IP formation, with an EC501 nM; 4-PMA wasinactive. Time course data demonstrated that ANG II-mediated IPproduction fully desensitized within 30 s; PKC inhibition reducedthe rate and extent of this desensitization. In cells desensitized toANG II, a purinergic agonist still mobilized intracellularCa2+, indicating that desensitization was homologous. TheANG II-induced Ca2+ signal was fully resensitized within 30 min. The data demonstrate that a large portion of theIP-Ca2+ responses of rat CFs to ANG II are short-livedbecause of rapid, PKC-mediated desensitization. 相似文献
8.
Jianchang Zhou Paul C. Dimayuga Xiaoning Zhao Juliana YanoWai Man Lio Portia TrinidadTomoyuki Honjo Bojan CercekPrediman K. Shah Kuang-Yuh Chyu 《Biochemical and biophysical research communications》2014
Background
It is increasingly evident that CD8+ T cells are involved in atherosclerosis but the specific subtypes have yet to be defined. CD8+CD25+ T cells exert suppressive effects on immune signaling and modulate experimental autoimmune disorders but their role in atherosclerosis remains to be determined. The phenotype and functional role of CD8+CD25+ T cells in experimental atherosclerosis were investigated in this study.Methods and results
CD8+CD25+ T cells were observed in atherosclerotic plaques of apoE(−/−) mice fed hypercholesterolemic diet. Characterization by flow cytometric analysis and functional evaluation using a CFSE-based proliferation assays revealed a suppressive phenotype and function of splenic CD8+CD25+ T cells from apoE(−/−) mice. Depletion of CD8+CD25+ from total CD8+ T cells rendered higher cytolytic activity of the remaining CD8+CD25− T cells. Adoptive transfer of CD8+CD25+ T cells into apoE(−/−) mice suppressed the proliferation of splenic CD4+ T cells and significantly reduced atherosclerosis in recipient mice.Conclusions
Our study has identified an athero-protective role for CD8+CD25+ T cells in experimental atherosclerosis. 相似文献9.
Role of homologous recombination in the alpha-particle-induced bystander effect for sister chromatid exchanges and chromosomal aberrations 总被引:4,自引:0,他引:4
Nagasawa H Peng Y Wilson PF Lio YC Chen DJ Bedford JS Little JB 《Radiation research》2005,164(2):141-147
The bystander effect for sister chromatid exchanges (SCEs) and chromosomal aberrations was examined in hamster cell lines deficient in either DNA-PKcs (V3 cells, deficient in nonhomologous end joining, NHEJ) or RAD51C (irs3 cells, deficient in homologous recombination, HR). Cells synchronized in G0/G1 phase were irradiated with very low fluences of alpha particles such that < 1% of the nuclei were traversed by an alpha particle. Wild-type cells showed a prominent bystander response for SCE induction; an even greater effect was observed in V3 cells. On the other hand, no significant induction of SCE was observed in the irs3 RAD51C-deficient bystander cells irradiated at various stages in the cell cycle. Whereas a marked bystander effect for chromosomal aberrations occurred in V3 cells, the induction of chromosomal aberrations in irs3 bystander cells was minimal and similar to that of wild-type cells. Based on these findings, we hypothesize that HR is essential for the induction of SCE in bystander cells; however, HR is unable to repair the DNA damage induced in NHEJ-deficient bystander cells that leads to either SCE or chromosomal aberrations. 相似文献
10.
Federico?LicastroEmail author Giuseppina?Candore Domenico?Lio Elisa?Porcellini Giuseppina?Colonna-Romano Claudio?Franceschi Calogero?Caruso 《Immunity & ageing : I & A》2005,2(1):8
The process of maintaining life for the individual is a constant struggle to preserve his/her integrity. This can come at
a price when immunity is involved, namely systemic inflammation. Inflammation is not per se a negative phenomenon: it is the
response of the immune system to the invasion of viruses or bacteria and other pathogens. During evolution the human organism
was set to live 40 or 50 years; today, however, the immune system must remain active for much a longer time. This very long
activity leads to a chronic inflammation that slowly but inexorably damages one or several organs: this is a typical phenomenon
linked to ageing and it is considered the major risk factor for age-related chronic diseases. Alzheimer's disease, atherosclerosis,
diabetes and even sarcopenia and cancer, just to mention a few – have an important inflammatory component, though disease
progression seems also dependent on the genetic background of individuals. Emerging evidence suggests that pro-inflammatory
genotypes are related to unsuccessful ageing, and, reciprocally, controlling inflammatory status may allow a better chance
of successful ageing. In other words, age-related diseases are "the price we pay" for a life-long active immune system: this
system has also the potential to harm us later, as its fine tuning becomes compromised. Our immune system has evolved to control
pathogens, so pro-inflammatory responses are likely to be evolutionarily programmed to resist fatal infections with pathogens
aggressively. Thus, inflammatory genotypes are an important and necessary part of the normal host responses to pathogens in
early life, but the overproduction of inflammatory molecules might also cause immune-related inflammatory diseases and eventually
death later. Therefore, low responder genotypes involved in regulation of innate defence mechanisms, might better control
inflammatory responses and age-related disease development, resulting in an increased chance of long life survival in a "permissive"
environment with reduced pathogen load, medical care and increased quality of life. 相似文献