Microtubule-associated protein 2C (MAP-2C) is an integral component of the neuronal cytoskeletal network, playing a pivotal role in stabilizing microtubules as well as in facilitating the processes of neuronal outgrowth, differentiation, and structural plasticity. A member of the MAP-2 family, MAP-2C's expression and function are particularly prominent during early stages of neuronal development, where it contributes to the intricate architecture of the developing nervous system. The modulation of MAP-2C expression is a finely tuned process, influenced by a variety of intracellular signaling pathways and external molecular cues that can increase or stimulate its production. Understanding the regulation of MAP-2C is essential for deciphering the complexities of neurodevelopment and the maintenance of the neuronal structure in the adult brain.
Within the cellular milieu, the expression of MAP-2C can be upregulated by an array of chemical activators that trigger specific signaling cascades. Compounds such as forskolin, for instance, are known to raise intracellular cyclic AMP (cAMP) levels, thereby activating protein kinase A (PKA) and potentially leading to the enhanced transcription of MAP-2C. Similarly, histone deacetylase inhibitors like trichostatin A (TSA) and sodium butyrate induce hyperacetylation of histone proteins, resulting in a more transcriptionally active chromatin state and possibly stimulating MAP-2C expression. Additionally, lithium chloride's inhibitory action on glycogen synthase kinase 3 beta (GSK-3β) can lead to downstream increases in gene transcription, potentially affecting MAP-2C levels. Other compounds, such as retinoic acid, engage with their specific nuclear receptors to initiate transcriptional activation that can include genes like MAP-2C. These chemical activators, each through their unique mechanisms, underscore the complex regulatory network governing MAP-2C expression, which is essential for the dynamic processes of neuronal development and function.
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