Chemical inhibitors of ZNF613 operate through various molecular mechanisms to impede its function. Alsterpaullone serves as a cyclin-dependent kinase inhibitor, disrupting CDKs that are potentially essential for ZNF613's role in transcription regulation, thus obstructing its functional capacity in gene expression. Chelerythrine targets Protein Kinase C, which can phosphorylate substrates that modulate ZNF613's activity, and by inhibiting this kinase, the phosphorylation state and hence the activity of ZNF613 can be altered, leading to its inhibition. Furthermore, the compound Y-27632, recognized for its inhibition of ROCK, can disrupt cytoskeletal organization and dynamics, which may be crucial for ZNF613 localization or its transcriptional activity, culminating in a reduction of ZNF613's functional output.
Further detailing the chemical inhibition of ZNF613, Triptolide inhibits the NF-kB pathway, which might be integral to ZNF613's activity; by blocking this pathway, ZNF613's function can be inhibited. PD173074, an FGFR tyrosine kinase signaling inhibitor, and ICG-001, a Wnt/β-catenin/TCF transcription antagonist, both lead to the disruption of upstream signaling pathways that ZNF613 might rely on for its activity. SB431542 inhibits TGF-β receptor signaling, potentially intersecting with ZNF613-dependent pathways and thus indirectly inhibiting ZNF613 activity. Proteasome inhibitor Bortezomib leads to an accumulation of misfolded ZNF613 proteins, which can abrogate ZNF613's proper functioning. Inhibition of the mTOR pathway by Rapamycin can reduce the synthesis of proteins that interact with ZNF613, impacting its function. LY294002 disrupts PI3K activity and consequently can alter AKT signaling, which can be crucial for regulating ZNF613. SP600125 targets JNK, possibly affecting ZNF613-dependent signaling pathways, leading to inhibition. NUAK1 inhibitor WZ4003 can impair cellular functions regulated by ZNF613, leading to its functional inhibition.
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