Date published: 2025-9-21

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ECAT1 Inhibitors

Chemical inhibitors of ECAT1 can influence the protein's function through various biochemical and cellular pathways. Palbociclib, as a CDK4/6 inhibitor, can inhibit the cell cycle, which can decrease the proliferation of cells expressing ECAT1, potentially reducing ECAT1's regulatory effects on cell division and pluripotency. Trichostatin A, a histone deacetylase inhibitor, can alter chromatin structure and transcription factor accessibility, thereby reducing ECAT1's interaction with transcriptional machinery. This disengagement from the transcriptional complex can hinder ECAT1's functional role in gene expression regulation. The DNA methyltransferase inhibitor 5-Azacytidine can lead to DNA hypomethylation, which can disrupt the epigenetic control of ECAT1, affecting its function in embryonic development and cell differentiation.

Furthermore, Y-27632, a ROCK inhibitor, can interfere with the cytoskeleton organization and cellular morphology, which can influence ECAT1's role in maintaining cellular structure. LY294002 acts as a PI3K inhibitor and can block the PI3K/AKT pathway, impacting ECAT1's involvement in cell survival and metabolism. Thapsigargin, by inhibiting the SERCA pump, can cause an increase in cytosolic calcium levels, affecting ECAT1's function in calcium signaling pathways. Brefeldin A disrupts Golgi apparatus function and vesicular trafficking, which can influence ECAT1's role in cellular processing and transport. U0126 and PD98059, both MEK inhibitors, can block the MAPK/ERK pathway, affecting ECAT1's involvement in cell proliferation and differentiation. SB431542, as a TGF-beta receptor inhibitor, can reduce signaling pathways integral to ECAT1's function in cell fate determination. Rapamycin, an mTOR inhibitor, can suppress cell growth and proliferation, which has implications for ECAT1's role in the regulation of these processes. Lastly, DAPT, a gamma-secretase inhibitor, can block Notch signaling, influencing ECAT1's involvement in cell differentiation and tissue homeostasis. Through these various pathways, each chemical can inhibit specific aspects of ECAT1's regulatory functions within cells.

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