Nexmif, identified as the neurite extension and migration factor, emerges as a pivotal player in the orchestration of fundamental processes within cellular development, particularly in the context of the nervous system. Its predicted functions include negative regulation of cell adhesion and neuron migration, positioning it upstream in the intricate landscape of nervous system development. This gene, expressed in critical structures such as the brain, neural tube mantle layer, sensory organ, skeleton, and tarsus, has garnered attention due to its implications in autism spectrum disorder and non-syndromic X-linked intellectual disability 98. While the precise role of Nexmif remains underexplored, its association with neurodevelopmental disorders underscores its importance in unraveling the molecular underpinnings of such conditions.
Activation mechanisms of Nexmif are a complex interplay of various signaling pathways and cellular processes. Although direct activators are yet to be unequivocally identified, a range of chemicals indirectly influences Nexmif through modulation of key pathways. These pathways include GSK-3β inhibition, CDK4/6 inhibition affecting cell cycle regulation, p38 MAPK pathway modulation, disruption of PI3K/Akt signaling, JNK pathway inhibition, histone deacetylase inhibition altering chromatin structure, MEK1/2 inhibition dampening the MAPK pathway, PI3K inhibition, DNA methyltransferase inhibition influencing epigenetic modifications, protein phosphatase inhibition, and signaling molecule impact. Each of these pathways potentially impacts Nexmif by altering gene expression or post-translational modifications, contributing to its predicted functions related to negative regulation of cell adhesion and neuron migration. The intricate network of these signaling events emphasizes the multifaceted regulation governing Nexmif activity, shedding light on the complexity of its role in neurodevelopmental processes. Understanding Nexmif's activation involves unraveling the intricacies of these pathways, providing a foundation for further exploration into the molecular mechanisms that govern its involvement in fundamental cellular processes critical for nervous system development.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Lithium | 7439-93-2 | sc-252954 | 50 g | $214.00 | ||
Lithium chloride, a GSK-3β inhibitor, indirectly influences Nexmif. By inhibiting GSK-3β, it may modulate Wnt signaling, potentially impacting Nexmif through downstream effects on negative regulation of cell adhesion and neuron migration. Lithium chloride offers an indirect activation route by altering the GSK-3β-mediated regulatory network associated with Nexmif's predicted functions. | ||||||
Trichostatin A | 58880-19-6 | sc-3511 sc-3511A sc-3511B sc-3511C sc-3511D | 1 mg 5 mg 10 mg 25 mg 50 mg | $149.00 $470.00 $620.00 $1199.00 $2090.00 | 33 | |
Trichostatin A, a histone deacetylase inhibitor, indirectly influences Nexmif through epigenetic modifications. By inhibiting HDACs, it may alter chromatin structure, affecting gene expression associated with Nexmif's role in nervous system development. This proposed indirect activation pathway underscores the potential impact of epigenetic regulation on Nexmif function in processes related to negative regulation of cell adhesion and neuron migration. | ||||||
PGE2 | 363-24-6 | sc-201225 sc-201225C sc-201225A sc-201225B | 1 mg 5 mg 10 mg 50 mg | $56.00 $156.00 $270.00 $665.00 | 37 | |
Prostaglandin E2 (PGE2), a signaling molecule, indirectly modulates Nexmif. By influencing intracellular signaling pathways, PGE2 may impact gene expression or post-translational modifications associated with Nexmif's functions in negative regulation of cell adhesion and neuron migration. This proposed indirect activation pathway suggests a link between PGE2-mediated signaling and the intricate regulation of Nexmif. | ||||||
Bisindolylmaleimide I (GF 109203X) | 133052-90-1 | sc-24003A sc-24003 | 1 mg 5 mg | $103.00 $237.00 | 36 | |
Bisindolylmaleimide I (GF 109203X), a protein kinase C inhibitor, indirectly influences Nexmif. By inhibiting PKC, it may modulate downstream signaling cascades, impacting gene expression or post-translational modifications associated with Nexmif's predicted functions in negative regulation of cell adhesion and neuron migration. The proposed indirect activation pathway highlights the intricate network of signaling events modulating Nexmif through PKC-mediated regulation. | ||||||