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排序方式: 共有289条查询结果,搜索用时 15 毫秒
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Vilà JM Calvo J Places L Padilla O Arman M Gimferrer I Aussel C Vives J Lozano F 《Journal of immunology (Baltimore, Md. : 1950)》2001,166(1):396-402
CD5 is a transmembrane coreceptor that modulates activation and differentiation signals mediated by the Ag-specific receptor present on both T and B1a lymphocytes. CD5 lacks intrinsic catalytic activity, and its immunomodulatory properties result from intracellular interactions mediated by the CD5 cytoplasmic tail. The nature of these interactions is currently a matter of investigation. Here, we present a selective mutagenesis analysis of two conserved threonine residues (T410 and T412) located at the membrane-proximal cytoplasmic region of CD5. These residues are contained within consensus phosphorylation motifs for protein kinase C and are shown here to be critical for in vivo protein kinase C-mediated phosphorylation of CD5. Functional studies revealed that the integrity of T410 and T412 is also critical for CD5-mediated phosphatidylcholine-specific phospholipase C (PC-PLC) activation and phorbol ester-mediated inhibition of Ab-induced internalization of CD5. These results strongly argue in favor of a role for T410 and T412 in the signaling mediated by CD5. 相似文献
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A DNA fragment containing the SRM12/ADA1 gene sequence inserted into a recombinant circular plasmid improves its maintenance in budding yeast (Saccharomyces cerevisiae) cells. Plasmid stabilization caused by the integrated SRM12 sequence does not require the SRM12 function complementing the srm12 mutation and depends on the orientation of the inserted fragment in the vector. This stabilization is mainly due to a decrease in spontaneous plasmid underreplication/copy loss rather than an increase in the fidelity of mitotic plasmid segregation. 相似文献
25.
This study was designed to measure the effect of iron supplementation on antioxidant status in iron-deficient anemia, including
the time for hemoglobin normalization and at the time of filling of iron body stores. The extent of plasma lipid peroxidation
was evaluated by measuring the levels of malondialdehyde and glutathione peroxidase (GSH-Px), and the activities of superoxide
dismutase (SOD) and catalase in 63 patients with iron-deficiency anemia before and after 6 wk of iron supplementation and
at the time when body iron stores are saturated. After 6 wk of iron supplementation, a significant decrease of oxidative stress
was observed in the treated subjects relative to controls (p<0.05). No significant differences existed between treated patients at 6 wk and at the end of the study. The erythrocyte levels
of catalase, SOD, and GSH-Px were significantly lower in treated patients relative to controls (p<0.05). These levels increased after 6 wk of supplementation (p<0.05) and showed no significant differences with those at the end of the study. 相似文献
26.
Omer Ateş Levent Dalyan Gulen Hatemi Vedat Hamuryudan Aysegul Topal-Sarıkaya 《Molecular biology reports》2010,37(7):3637-3641
We aim to ascertain the possible involvement of functional IL10 and TNF-α promoter polymorphisms on the susceptibility to Behçet’s syndrome (BS), to examine whether IL10 and TNF-α genotypes might work synergistically influencing susceptibility to BS. IL10 ?1082G/A, ?819C/T and ?592C/A and TNF ?308G/A polymorphisms were analyzed in 102 Turkish patients with BS and 102 healthy subjects by using amplification refractory mutation system-polymerase chain reaction (ARMS-PCR). We have found no significant associations between IL10 ?1082G/A, ?819C/T, ?592C/A, TNF-α ?308G/A polymorphisms and BS. Also, no significant correlation was found between IL10 GCC, ACC, ATA haplotypes, GCC+/GCC+, GCC+/GCC?, GCC?/GCC? genotypes. There was no significant association between combined TNF-α/IL10 genotypes and BS. Our study indicates that functional TNF-α, IL10 genotypes or combined TNF-α, IL10 genotypes do not play a role in BS susceptibility in Turkish BS patients. 相似文献
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IKK beta suppression of TSC1 links inflammation and tumor angiogenesis via the mTOR pathway 总被引:3,自引:0,他引:3
Lee DF Kuo HP Chen CT Hsu JM Chou CK Wei Y Sun HL Li LY Ping B Huang WC He X Hung JY Lai CC Ding Q Su JL Yang JY Sahin AA Hortobagyi GN Tsai FJ Tsai CH Hung MC 《Cell》2007,130(3):440-455
TNFalpha has recently emerged as a regulator linking inflammation to cancer pathogenesis, but the detailed cellular and molecular mechanisms underlying this link remain to be elucidated. The tuberous sclerosis 1 (TSC1)/TSC2 tumor suppressor complex serves as a repressor of the mTOR pathway, and disruption of TSC1/TSC2 complex function may contribute to tumorigenesis. Here we show that IKKbeta, a major downstream kinase in the TNFalpha signaling pathway, physically interacts with and phosphorylates TSC1 at Ser487 and Ser511, resulting in suppression of TSC1. The IKKbeta-mediated TSC1 suppression activates the mTOR pathway, enhances angiogenesis, and results in tumor development. We further find that expression of activated IKKbeta is associated with TSC1 Ser511 phosphorylation and VEGF production in multiple tumor types and correlates with poor clinical outcome of breast cancer patients. Our findings identify a pathway that is critical for inflammation-mediated tumor angiogenesis and may provide a target for clinical intervention in human cancer. 相似文献
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Effects of coenzyme Q10 on the heart ultrastructure and nitric oxide synthase during hyperthyroidism
Oztay F Ergin B Ustunova S Balci H Kapucu A Caner M Demirci C 《The Chinese journal of physiology》2007,50(5):217-224
Coenzyme Q10 is an important component of mitochondrial electron transport chain and antioxidant. Hyperthyroidism manifests hyperdynamic circulation with increased cardiac output, increased heart rate and decreased peripheral resistance. The heart is also under the oxidative stress in the hyperthyroidism. The aim of this study was to examine both how the coenzyme Q10 can affect heart ultrastructure in the hyperthyroidism and how the relationship between nitric oxide synthase (NOS) and heart damage and coenzyme Q10. Swiss Black C57 mice received 5 mg/kg L-thyroxine. Coenzyme Q10 (1.5 mg/kg) and L-thyroxine together was given to second group mice. Coenzyme Q10 and serum physiologic were applied to another two groups, respectively. All treatments were performed daily for 15 days by gavage. Free triiodothyronine and thyroxine were increased in two groups given L-thyroxine; thyroid-stimulating hormone level did not change. Hyperthyroid heart showed an increased endothelial NOS (eNOS) and inducible NOS (iNOS) immunoreactivity in the tissue. Coenzyme Q10 administration decreased these NOS immunoreactivities in the hyperthyroid animals. Cardiomyocytes of the hyperthyroid animals was characterized by abnormal shape and invaginated nuclei, and degenerative giant mitochondria. Desmosome plaques reduced in density. In hyperthyroid mice given coenzyme Q10, the structural disorganization and mitochondrial damage regressed. However, hearts of healthy mice given coenzyme Q10 displayed normal ultrastructure, except for increased mitochondria and some of them were partially damaged. Coenzyme Q10 increased the glycogen in the cardiomyocytes. In conclusion, coenzyme Q10 administration can prevent the ultrastructural disorganization and decrease the iNOS and eNOS increment in the hyperthyroid heart. 相似文献