Tìm thấy 10+ kết quả cho từ khóa "NF-κB pathway"
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Consistently, we find TGEV infection upregulates RIG-I and TLR3 and induces the activation of NF-κB pathway in IPEC-J2 cells, indicating TGEV. a Venn diagram shows the number of overlap genes in target genes of differentially expressed miRNAs. study, TGEV infection activates the Jak-STAT signaling pathway in IPEC-J2 cells, consistent with previous studies..
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These data suggest that NF-κB is a potential upstream regulator of TRIM27 in RCC. Iκbα has been identified as the major regulator of the NF-κB pathway [19], and dissociation of NF-κB from Iκbα is a critical step in translocation to the nucleus. 3 oeTRIM27 rescues the function of TRIM27 in siTRIM27-transfected cells. The proliferations of Caki-2 and 786 – 0 cells transfected with siTRIM27, oeTRIM27, or siTRIM27 + oeTRIM27 at and 48 h respectively.
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Hence, upregula- tion of the NF-κB pathway is frequently observed in cancer cells, which may contribute to their resistance to anticancer treatments [14]. In resting cells, the NF-κB transcription factors are sequestered in the cytoplasm by association with members of the I κ B inhibitory protein family.
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Ivermectin induces apoptosis of ESCC cells through NF‑κB pathway. The NF-κB signaling pathway is involved in ESCC car- cinogenesis and progression and is hyperactivated in ESCC cells and promotes cell survival. Subsequently, we also found that the phosphorylation of IκBα, an upstream regulatory molecule of NF-κB pathway, was inhibited in ESCC cells after ivermectin treatment (Fig. Taken together, these results indicated that ivermec- tin induces apoptosis of ESCC cells through NF-κB pathway..
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In particular, anti-IL-17A might decrease NF-κB pathway levels in sevoflurane-treated aged rats to a level sufficient to restore normal function, but did not change the expressions of sevoflurane-treated young adult rats which had originally normal levels of NF-κB pathway..
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Interestingly, there are a number of reports sug- gesting the formation of DR-induced complexes including procaspase-8, IKK and the components of the NF-κB path- way that drive NF-κB induction [19]. that c-FLIP might serve as a key link between recruitment of these complexes into DED filaments and induction of the NF-κB pathway.. These observations might be resulting from a low stability of the peptides in the cell.
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The similar results were also found in NF-κB pathway, indicating that Notch/NF-κB pathway was involved in the protection of DMED on OGD- induced nerve injury. Further studies performed with Notch or NF-κB inhibitor proved the involvements of the Notch/NF-κB pathway in the neuroprotection of DMED in OGD-induced neuronal injury.. In our study, the protective effects of DMED were also proved in the primary neuronal cells..
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Burkitt lymphoma (BL) is an aggressive type of pediatric and adult B cell lymphoma originating from GCB cells (Deffenbacher et al., 2012). apoptosis Willis et al., 2000. apoptosis Schuetz et al., 2012. reaction Willis et al., 2000. expression Pascualucci et al., 2003. coiled-coil domain 9.6 NF-κB pathway Lenz et al., 2008. NF-κB pathway Davis et al., 2010;. Schmitz et al., 2018 CD79A ITAM deletion, splice site. of histone H3 (H3K27) Morin et al., 2010.
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Indeed, studies on corals have shown that LPS can trigger an im- mune response in several species and more specifically genes of the TLR-to-NF-κB pathway [34, 50].. Overall, these results suggest that in cnidarians lacking TLR homologs, LPS can still trigger the produc- tion of cytokines and antimicrobial peptides independ- ently of the TLR-to-NF-κB pathway..
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PA infection caused significant upregulation of the genes re- lated to NF-κB pathway and members of the PKC family.. Also, PA infection up-regulated Furin gene, which plays a critical role in the activation of exotoxin A, a major virulence factor of PA.
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In the present study, we postulated that miR-214, ROCK1, and NF-κB may be involved in DEX-mediated protective ef- fects against CIRI in rats.
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On one hand, the NF-κB protein was required for the association of MKL1 protein with the promoter regions of target genes, thus initiating the following COMPASS complex-induced histone modification and transcription activation [21, 31]. On the other hand, the introduction of MKL1 protein could also enhance the nuclear enrichment of the NF-kB protein and strength the binding of NF-kB protein with target gene promoter, therefore promoting further elevated expression of NF- kB target genes [21].
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Described effects of FX-9 like in- duction of cell cycle inhibitor CDKN1A, activation of NF-κB signaling pathway and senescence can be caused by DNA damage . org/10.1186/s y.. https://doi.. org/10.1002/adsc.201600169.. https://doi.org/10.1016/j.bmcl . https://doi.org/10.1016/S . https://doi.org/1 0.1016/j.ejmech . https://doi.org/10.1093/carcin/bgt133.. https://doi.org/10.1016/j.ejmech . https://doi.org/10.4062/biomolther.2018.199.. org/10.3390/ijms20225567.. https://doi.org/10.1038/nm0103-140..
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Đoạn gen sau đó được nhân bội bằng phương pháp PCR sử dụng cặp mồi NF-κB p65-F, NF-κB p65-R có chứa vị trí cắt của enzyme giới hạn BamHI và EcoRI. Kích thước này tương ứng với kích thước của đoạn gen mã hóa NF-κB p65 cần nhân dòng. Kết quả này chỉ ra rằng, gen mã hóa cho NF-κB p65 đã được nhân dòng thành công bằng kỹ thuật PCR sử dụng cặp mồi đặc hiệu NF-κB p65-F, NF-κB p65-R.. Kết quả PCR đoạn gen mã hóa nhân tố phiên mã NF-κB p65.
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These data suggest that inhibition of the nuclear factor-κB pathway (NF-κB) may be a mechanism under- lying the neuroprotective action of DEX [14]. Addition- ally, DEX has been shown to improve post-operative cognitive dysfunction in aging mice by inhibition of the hippocampal inflammatory response and reduction of neuronal apoptosis [16]. Taken together, these data sug- gest that DEX has anti-inflammatory properties in the central nervous system (CNS)..
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Tác nhân kích hoạt NF- kappa B và gene gây ung thư điều. hòa bởi NF-kappa B.. Kích hoạt NF-kappa B bởi các tác nhân viêm nhiễm, hóa chất gây hay thúc đẩy ung thư, protein virút, hóa chất dùng trong hóa trị liệu, và phóng xạ gamma.. quá trình tồn tại, sinh trưởng, tăng sinh mạch máu, phản ứng viêm,. xâm lấn và di căn của tế bào được điều hòa bởi NF-kappa B được kích hoạt..
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More- over, both CM of BEAS-2B cells and HBECs could pro- mote lung fibroblasts activation. 3 Regulation of IL-8 production by HB-EGF via NF-κB–mediated signaling pathway. The effect of NF-κB inhibitor on HB-EGF–mediated IL-8 mRNA expression (a) and IL-8 release (b) from BEAS-2B and HBECs. BEAS-2B and HBECs were transfected with the NF-κB-reporter plasmid and then treated with various concentrations of rhHB-EGF for 6 h. 0.05 versus control of BEAS-2B cells.
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Second, the details of drought-responsive cis-elements in the PpNF-Y pro- moters were shown, which is useful for exploring the upstream elements of the PpNF-Y genes involved in the drought resistance pathway.
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Thirteen genes depicted in the CellDesigner Nf-κB map, where genes whose ratio of similarity scores to consensus sequence is higher than 0.6, are visualized in Fig. Many Nf-κB target genes are part of the immune system such as the ICAM1 gene. Nf-κB is found to be essential for the basal activity of the mouse TAPBP (tapasin) promoter [48]. Also, several transcription factor candidates were found to po- tentially co-regulate these genes together with Nf-κB..
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Comparative transcriptomic analysis reveals an association of gibel carp fatty liver with ferroptosis pathway. Transcriptomic analysis between fatty liver and normal liver showed a totally different transcriptional trajectory. LPIA identified an activated ferroptosis pathway in the fatty liver. Therefore, the current study provides a clue for future studies on fish fatty liver problems.. https://doi.org/10.1186/s .