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In recent years, directly targeting cell-signaling pathways to inhibit cancer growth has gained momentum, with the development of rationally designed peptide inhibitors, monoclonal antibodies and small molecules.
Thus, GNA might act through the PTEN/PI3K/AKT pathways to inhibit resistant cell proliferation.
However, in CSCLCs, the overexpression of OCT4, NANOG, and SOX2 modulates signaling pathways to inhibit apoptosis.
These results indicate that senescence and apoptosis may be important pathways to inhibit proliferation of murine mammary tumor cells treated with T-oligo and IR.
Therefore, there is an unmet need to develop novel chemotherapeutic agents that target multiple molecular pathways to inhibit prosurvival signals and induce apoptosis in the GBM cells.
Thus, subjects with only one copy of PPYR1 may produce less protein, which will regulate energy homeostasis through agonists or other pathways to inhibit obesity.
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Potential targets of AMPK to alter insulin signaling of GLUT4 translocation through a direct inhibition of AS160 or via the mTOR pathway to inhibit Akt.
This led to the observation that both DHEA and resveratrol utilize the glycolytic pathway to inhibit TXNIP, however, they acted through two separate pathways mediated respectively by the inhibition of G6PDH and the activation of AMPK.
Last but most importantly, anti-CD146 therapy could present a promising approach to combine with existing strategies targeting VEGF pathway to inhibit tumor angiogenesis.
Furthermore, TAM-derived exosomes can target the miR-146b-5p/TRAF6/NF-κB/MMP2 pathway to inhibit endothelial cell migration, a process that is subject to reversal by long non-coding RNAs (lncRNAs) delivered by SKOV3-released exosomes (Wu et al., 2017b).
These findings suggest that affibody molecules specific for H-Ras and Raf-1 can affect intracellular signal transduction through the MAP kinase pathway to inhibit cell proliferation and production of inflammatory mediators by synovial cells.
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