排序方式: 共有18条查询结果,搜索用时 0 毫秒
1.
2.
Abounouh Karima Kayesh Mohammad Enamul Hoque Altawalah Haya Kitab Bouchra Murakami Shuko Ogawa Shintaro Tanaka Yasuhito Dehbi Hind Pineau Pascal Kohara Michinori Benjelloun Soumaya Tsukiyama-Kohara Kyoko Ezzikouri Sayeh 《Molecular biology reports》2022,49(1):403-412
Molecular Biology Reports - Hepatitis B Virus (HBV) is the most common cause of chronic liver disease worldwide. The mechanisms that regulate HBV viral replication remain poorly defined. Here, we... 相似文献
3.
4.
5.
Arhin F Bélanger O Ciblat S Dehbi M Delorme D Dietrich E Dixit D Lafontaine Y Lehoux D Liu J McKay GA Moeck G Reddy R Rose Y Srikumar R Tanaka KS Williams DM Gros P Pelletier J Parr TR Far AR 《Bioorganic & medicinal chemistry》2006,14(17):5812-5832
The RNA polymerase holoenzyme is a proven target for antibacterial agents. A high-throughput screening program based on this enzyme from Staphylococcus aureus had previously identified a 2-ureidothiophene-3-carboxylate as a low micromolar inhibitor. An investigation of the relationships between the structures of this class of compounds and their inhibitory- and antibacterial activities is described here, leading to a set of potent RNA polymerase inhibitors with antibacterial activity. Characterization of this bioactivity, including studies of the mechanism of action, is provided, highlighting the power of the reverse chemical genetics approach in providing tools to inhibit the bacterial RNA polymerase. 相似文献
6.
Ethnic differences in associations between fat deposition and incident diabetes and underlying mechanisms: The SABRE study 下载免费PDF全文
7.
The molecular mechanisms that initiate the inflammatory response in heatstroke and their relation with tissue injury and lethality are not fully elucidated. We examined whether endogenous ligands released by damaged/stressed cells such as high-mobility group box 1 (HMGB1) signaling through Toll-like receptor 4 (TLR4) may play a pathogenic role in heatstroke. Mutant TLR4-defective (C3H/HeJ) and wild type (C3H/HeOuJ) mice were subjected to heat stress in an environmental chamber pre-warmed at 43.5°C until their core temperature reached 42.7°C, which was taken as the onset of heatstroke. The animals were then allowed to recover passively at ambient temperature. A sham-heated group served as a control. Mutant mice displayed more histological liver damage and higher mortality compared with wild type mice (73% vs. 27%, respectively, P<0.001). Compared to wild type mice, mutant mice exhibited earlier plasma release of markers of systemic inflammation such as HMGB1 (206±105 vs. 63±21 ng/ml; P = 0.0018 and 209±100 vs. 46±32 ng/ml; P<0.0001), IL-6 (144±40 vs. 46±20 pg/ml; P<0.001 and 184±21 vs. 84±54 pg/ml; P = 0.04), and IL-1β (27±4 vs. 1.7±2.3 pg/ml; P<0.0001 at 1 hour). Both strains of mice displayed early release of HMGB1 into the circulation upstream of IL-1β and IL-6 responses which remained elevated up to 24 h. Specific inhibition of HMGB1 activity with DNA-binding A Box (600 µg/mouse) protected the mutant mice against the lethal effect of heat stress (60% A Box vs. 18% GST protein, P = 0.04). These findings suggest a protective role for the TLR4 in the host response to severe heat stress. They also suggest that HMGB1 is an early mediator of inflammation, tissue injury and lethality in heatstroke in the presence of defective TLR4 signaling. 相似文献
8.
9.
Kassogue Yaya Diakite Brehima Kassogue Oumar Konate Issa Tamboura Kadidiatou Diarra Zoumana Dehbi Hind Nadifi Sellama Traore Cheick Bougadari Dao Sounkalo Doumbia Seydou Dolo Guimogo 《Molecular biology reports》2020,47(1):393-400
Molecular Biology Reports - Glutathione S-transferase genes, known to be highly polymorphic, are implicated in the process of phase II metabolism of many substrates, including xenobiotics,... 相似文献
10.
Jehad Abubaker Ali Tiss Mohamed Abu-Farha Fahad Al-Ghimlas Irina Al-Khairi Engin Baturcam Preethi Cherian Naser Elkum Maha Hammad Jeena John Sina Kavalakatt Abdelkrim Khadir Samia Warsame Said Dermime Kazem Behbehani Mohammed Dehbi 《PloS one》2013,8(7)
Obesity is a major risk factor for a myriad of disorders such as insulin resistance and diabetes. The mechanisms underlying these chronic conditions are complex but low grade inflammation and alteration of the endogenous stress defense system are well established. Previous studies indicated that impairment of HSP-25 and HSP-72 was linked to obesity, insulin resistance and diabetes in humans and animals while their induction was associated with improved clinical outcomes. In an attempt to identify additional components of the heat shock response that may be dysregulated by obesity, we used the RT2-Profiler PCR heat shock array, complemented with RT-PCR and validated by Western blot and immunohistochemistry. Using adipose tissue biopsies and PBMC of non-diabetic lean and obese subjects, we report the downregulation of DNAJB3 cochaperone mRNA and protein in obese that negatively correlated with percent body fat (P = 0.0001), triglycerides (P = 0.035) and the inflammatory chemokines IP-10 and RANTES (P = 0.036 and P = 0.02, respectively). DNAJB positively correlated with maximum oxygen consumption (P = 0.031). Based on the beneficial effect of physical exercise, we investigated its possible impact on DNAJB3 expression and indeed, we found that exercise restored the expression of DNAJB3 in obese subjects with a concomitant decrease of phosphorylated JNK. Using cell lines, DNAJB3 protein was reduced following treatment with palmitate and tunicamycin which is suggestive of the link between the expression of DNAJB3 and the activation of the endoplasmic reticulum stress. DNAJB3 was also shown to coimmunoprecipiate with JNK and IKKβ stress kinases along with HSP-72 and thus, suggesting its potential role in modulating their activities. Taken together, these data suggest that DNAJB3 can potentially play a protective role against obesity. 相似文献