Showing 1,081 - 1,100 results of 26,949 for search '(( 50 ((we decrease) OR (nn decrease)) ) OR ( 100 ((ng decrease) OR (a decrease)) ))', query time: 0.86s Refine Results
  1. 1081

    MicroRNA-138 Regulates Hypoxia-Induced Endothelial Cell Dysfunction By Targeting S100A1 by Anagha Sen (482673)

    Published 2013
    “…Bioinformatic analysis suggested that microRNA -138 (MiR-138) could target the 3′UTR of S100A1. Patients with critical limb ischemia (CLI) or mice subjected to femoral artery resection (FAR) displayed increased MiR-138 levels and decreased S100A1 protein expression. …”
  2. 1082

    Purified recombinant WT-C100Flag dimer and trimer showed reduced Aβ production. by Joo In Jung (650746)

    Published 2014
    “…<p>(A) The purified recombinant WT-C100Flag monomer, dimer, and trimer eluates were loaded on a SDS-PAGE gel. …”
  3. 1083

    GluN2A(D731N) reduces the agonist potency. by Kai Gao (120150)

    Published 2017
    “…(<b>C,E</b>) The composite glutamate (in the presence of 100 μM glycine) concentration-response curves reveal a significant decrease in glutamate potency in both di-heteromeric (<b>C</b>) and tri-heteromeric (<b>E</b>) GluN2A(D731N)-containing NMDARs compared to wild type receptors. …”
  4. 1084
  5. 1085

    Table_2_PE_PGRS31-S100A9 Interaction Promotes Mycobacterial Survival in Macrophages Through the Regulation of NF-κB-TNF-α Signaling and Arachidonic Acid Metabolism.docx by Sheng Liu (279488)

    Published 2020
    “…Our results revealed that M. tb Rv1768 promotes mycobacterial survival in macrophages by regulating NF-κB-TNF-α signaling and arachidonic acid metabolism via S100A9. Disturbing the interaction between Rv1768 and S100A9 may be a potential therapeutic target for tuberculosis.…”
  6. 1086

    Image_4_PE_PGRS31-S100A9 Interaction Promotes Mycobacterial Survival in Macrophages Through the Regulation of NF-κB-TNF-α Signaling and Arachidonic Acid Metabolism.TIF by Sheng Liu (279488)

    Published 2020
    “…Our results revealed that M. tb Rv1768 promotes mycobacterial survival in macrophages by regulating NF-κB-TNF-α signaling and arachidonic acid metabolism via S100A9. Disturbing the interaction between Rv1768 and S100A9 may be a potential therapeutic target for tuberculosis.…”
  7. 1087

    Table_1_PE_PGRS31-S100A9 Interaction Promotes Mycobacterial Survival in Macrophages Through the Regulation of NF-κB-TNF-α Signaling and Arachidonic Acid Metabolism.docx by Sheng Liu (279488)

    Published 2020
    “…Our results revealed that M. tb Rv1768 promotes mycobacterial survival in macrophages by regulating NF-κB-TNF-α signaling and arachidonic acid metabolism via S100A9. Disturbing the interaction between Rv1768 and S100A9 may be a potential therapeutic target for tuberculosis.…”
  8. 1088

    Image_2_PE_PGRS31-S100A9 Interaction Promotes Mycobacterial Survival in Macrophages Through the Regulation of NF-κB-TNF-α Signaling and Arachidonic Acid Metabolism.TIF by Sheng Liu (279488)

    Published 2020
    “…Our results revealed that M. tb Rv1768 promotes mycobacterial survival in macrophages by regulating NF-κB-TNF-α signaling and arachidonic acid metabolism via S100A9. Disturbing the interaction between Rv1768 and S100A9 may be a potential therapeutic target for tuberculosis.…”
  9. 1089

    Image_3_PE_PGRS31-S100A9 Interaction Promotes Mycobacterial Survival in Macrophages Through the Regulation of NF-κB-TNF-α Signaling and Arachidonic Acid Metabolism.TIF by Sheng Liu (279488)

    Published 2020
    “…Our results revealed that M. tb Rv1768 promotes mycobacterial survival in macrophages by regulating NF-κB-TNF-α signaling and arachidonic acid metabolism via S100A9. Disturbing the interaction between Rv1768 and S100A9 may be a potential therapeutic target for tuberculosis.…”
  10. 1090

    Image_1_PE_PGRS31-S100A9 Interaction Promotes Mycobacterial Survival in Macrophages Through the Regulation of NF-κB-TNF-α Signaling and Arachidonic Acid Metabolism.TIF by Sheng Liu (279488)

    Published 2020
    “…Our results revealed that M. tb Rv1768 promotes mycobacterial survival in macrophages by regulating NF-κB-TNF-α signaling and arachidonic acid metabolism via S100A9. Disturbing the interaction between Rv1768 and S100A9 may be a potential therapeutic target for tuberculosis.…”
  11. 1091

    Data_Sheet_1_Molecular Mechanisms by Which S100A4 Regulates the Migration and Invasion of PGCCs With Their Daughter Cells in Human Colorectal Cancer.zip by Fei Fei (794241)

    Published 2020
    “…The tumorigenic and metastatic ability of PGCCs with their daughter cells in vivo was significantly stronger compared to the untreated cells, which was significantly decreased after S100A4 knockdown. Moreover, the expression of S100A4-related proteins was positively correlated with the malignancy degree of human CRC, and maintained a high level in lymph node metastasis. …”
  12. 1092
  13. 1093

    GluN2A(D731N) enhances sensitivity to endogenous proton and zinc ions. by Kai Gao (120150)

    Published 2017
    “…Di-heteromeric (h2A-D731N), one-copy and two-copy mutant tri-heteromeric (D731N/2A and D731N/D731N) receptors show a decreased current ratio, indicating enhanced proton sensitivity. …”
  14. 1094
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  16. 1096

    Effect of partial Glo-I inhibition by EP on LPS-induced production of TNF-α, collagen-I and α-SMA in HSC. by Marcus Hollenbach (376231)

    Published 2017
    “…Co-treatment of LPS and EP indicated significant dose-dependent reduction of LPS-induced markers of inflammation <b>(A1)</b> and fibrosis <b>(B1, C1)</b>. Presence of LPS and treatment with low-level concentrations of MGO (indicating partial inhibition of Glo-I activity without complete enzyme inhibition) showed significant decrease of LPS-induced release of TNF-α (absence vs. presence of 10mM MGO: 371.8±22.7 vs. 60.9±11.2 pg/ml; p<0.001), collagen-I (10.0±0.3 vs. 1.8±0.5 ng/ml; p<0.001) and α-SMA (68.6±3.6 vs. 43.8±2.2 ng/ml; p<0.001) <b>(A2, B2, C2)</b>. …”
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