Date published: 2025-12-23

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calsyntenin-3 Inhibitors

Calsyntenin-3, a member of the calsyntenin family, is a neuronal cadherin-related protein that plays a pivotal role in the molecular dynamics of neural cells and synaptic function. Characterized by its involvement in the formation and maintenance of synaptic connections, calsyntenin-3 contributes to the intricate web of signaling that underpins neural communication and plasticity. As a transmembrane protein, it is integrated within the cellular architecture of neurons, facilitating interactions both within the cell and across the synaptic cleft. The expression of calsyntenin-3 is tightly regulated within the central nervous system, reflecting its significance in maintaining the delicate balance of neural activity. Given its foundational role in synaptic operations, the precise modulation of calsyntenin-3 levels is a subject of considerable interest, especially regarding the mechanisms that govern its expression.

The regulation of calsyntenin-3 expression can be influenced by various chemical compounds, which, while not directly targeting the protein itself, can modulate its production at the transcriptional or translational level. Certain compounds can downregulate calsyntenin-3 by altering chromatin structure, affecting gene accessibility and the binding of transcription factors. Other chemicals may modify the methylation status of the gene's promoter region, indirectly leading to a reduction in gene expression. Some compounds that interfere with DNA replication and repair can also impact the transcription levels of calsyntenin-3 by causing DNA damage, which must be repaired before normal gene expression can resume. Additionally, inhibitors of RNA synthesis can reduce the overall mRNA output for calsyntenin-3, while other agents may decrease the translation of proteins that regulate its expression. These varied mechanisms demonstrate the complexity of cellular regulation and the multiple ways in which chemical intervention can affect gene expression pathways.

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