Fthl17b, a member of the ferritin heavy chain-like family, plays a crucial role in cellular iron homeostasis. Predicted to possess ferric and ferrous iron binding activities, Fthl17b is implicated in the intracellular sequestering of iron ions, particularly in the cytoplasm during early conceptus development. The orthologous relationship to human FTHL17 highlights its evolutionary conservation and functional significance. Activation of Fthl17b involves a sophisticated network of chemical regulators. Trichostatin A, a histone deacetylase inhibitor, facilitates Fthl17b activation by enhancing chromatin accessibility. SB431542 indirectly influences Fthl17b through TGF-β receptor inhibition, altering downstream signaling and gene expression. Forskolin, a cAMP activator, up-regulates Fthl17b via PKA-mediated pathways, enhancing its transcriptional activity. LY294002, a PI3K inhibitor, indirectly promotes Fthl17b by modulating AKT/mTOR signaling.
JQ1, a BET bromodomain inhibitor, enhances Fthl17b expression through epigenetic regulation. ATRA, a retinoic acid agonist, activates Fthl17b by modulating RAR/RXR pathway dynamics. U0126, a MEK1/2 inhibitor, indirectly stimulates Fthl17b via MAPK pathway modulation. Resveratrol, a SIRT1 activator, promotes Fthl17b by influencing histone acetylation dynamics. Bortezomib, a proteasome inhibitor, indirectly promotes Fthl17b by stabilizing relevant regulators. Dasatinib, a Src kinase inhibitor, modulates downstream signaling cascades to indirectly activate Fthl17b expression. Rapamycin, an mTOR inhibitor, influences protein translation, indirectly promoting Fthl17b expression. Ionomycin, a calcium ionophore, activates Fthl17b through the Ca2+/NFAT pathway, facilitating transcriptional activation. In summary, Fthl17b activation is a finely tuned process influenced by a diverse array of chemical regulators, each impacting specific cellular pathways and processes. This orchestrated network ensures the proper functioning of Fthl17b in iron homeostasis during early conceptus development.
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