Date published: 2025-9-16

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EG434727 Activators

Fthl17c, a member of the ferritin heavy chain-like family, operates at the core of cellular iron homeostasis. Predicted to possess ferric and ferrous iron binding activities, Fthl17c is intricately involved in the intracellular sequestering of iron ions within the cytoplasm, particularly during early conceptus development. The orthologous expression to human FTHL17 underlines its biological significance and potential functional conservation. The activation of Fthl17c is governed by a spectrum of chemical modulators that exert their influence through various cellular pathways. Vorinostat, an HDAC inhibitor, enhances Fthl17c expression by facilitating chromatin accessibility and transcription factor binding in a dose-dependent manner. SB203580, a p38 MAPK inhibitor, indirectly activates Fthl17c by modulating downstream pathways associated with iron ion homeostasis. PMA, a PKC activator, up-regulates Fthl17c through PKC-mediated pathways, enhancing its transcriptional activity.

BAY 11-7082, an NF-κB inhibitor, indirectly promotes Fthl17c expression by modulating NF-κB signaling and its downstream targets. AICAR, an AMPK activator, influences AMPK/mTOR pathways, indirectly activating Fthl17c by modulating cellular energy sensing. Trifluoperazine, a calmodulin antagonist, indirectly stimulates Fthl17c through disruption of Ca2+/calmodulin signaling, influencing iron sequestration. NVP-BEZ235, a dual PI3K/mTOR inhibitor, modulates PI3K/mTOR pathways and indirectly promotes Fthl17c expression by affecting downstream effectors. C646, a CBP/p300 inhibitor, enhances Fthl17c expression through inhibition of acetyltransferase activity and alteration of histone acetylation. Wortmannin, a PI3K inhibitor, indirectly promotes Fthl17c by modulating PI3K/AKT signaling and influencing downstream targets. PD98059, a MEK1/2 inhibitor, influences the MAPK pathway, indirectly stimulating Fthl17c by modulating downstream effectors. Dipyridamole, an adenosine uptake inhibitor, indirectly activates Fthl17c by modulating adenosine signaling and influencing downstream pathways. CAY10585, an AMPK inhibitor, modulates AMPK/mTOR pathways, indirectly promoting Fthl17c expression by affecting cellular energy sensing. In summary, the intricate orchestration of these chemical regulators plays a pivotal role in finely tuning the activation of Fthl17c, ensuring its precise function in maintaining cellular iron homeostasis, particularly during early conceptus development. The multifaceted nature of these pathways highlights the complexity of Fthl17c regulation in cellular processes related to iron sequestration and storage.

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