neuroligin 2 Activators
The chemical class termed neuroligin 2 activators comprises a diverse array of compounds with distinct mechanisms of action converging on the modulation of NLGN2 expression. These compounds, ranging from lithium chloride to tranylcypromine, exert their effects through intricate cellular pathways. For instance, lithium chloride and its analog, lithium bromide, target the Wnt/β-catenin signaling pathway by inhibiting glycogen synthase kinase-3 beta (GSK-3β). This inhibition stabilizes β-catenin, allowing it to translocate into the nucleus and participate in the transcriptional activation of NLGN2. Forskolin, a potent adenylate cyclase activator, enhances NLGN2 expression through cAMP/PKA/CREB signaling. Similarly, valproic acid and trichostatin A, both histone deacetylase inhibitors, epigenetically regulate NLGN2 gene expression by promoting histone hyperacetylation, creating a permissive chromatin environment. Retinoic acid and its isomer 9-cis-retinoic acid function as ligands for retinoic acid receptors, forming complexes that bind to retinoic acid response elements in the NLGN2 promoter, driving transcription.
Compounds like bicuculline and A23187 indirectly activate NLGN2 by modulating GABAergic signaling and elevating intracellular calcium levels, respectively. Sodium butyrate, another HDAC inhibitor, supports NLGN2 expression by preventing histone deacetylation. SKF-96365 disrupts calcium signaling, potentially impacting pathways related to NLGN2 expression. Tranylcypromine, a monoamine oxidase inhibitor, influences NLGN2 through intricate interactions within the neuronal network, altering monoamine neurotransmitter levels. In summary, the neuroligin 2 activators class encompasses compounds with diverse molecular targets, including signaling pathways, epigenetic regulation, and neurotransmitter systems. Their collective influence on NLGN2 expression highlights the complexity of cellular regulation and provides a nuanced understanding of the mechanisms driving the modulation of this important synaptic adhesion molecule.
SEE ALSO...
Items 1 to 10 of 11 total
Display:
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Forskolin | 66575-29-9 | sc-3562 sc-3562A sc-3562B sc-3562C sc-3562D | 5 mg 50 mg 1 g 2 g 5 g | $76.00 $150.00 $725.00 $1385.00 $2050.00 | 73 | |
Forskolin activates adenylate cyclase, resulting in increased cAMP levels. Elevated cAMP stimulates PKA, which in turn activates CREB. The activated CREB binds to the promoter region of NLGN2, facilitating its transcription and subsequent expression. | ||||||
Valproic Acid | 99-66-1 | sc-213144 | 10 g | $85.00 | 9 | |
Valproic acid is a histone deacetylase (HDAC) inhibitor. By preventing histone deacetylation, it enhances chromatin accessibility. This epigenetic modification positively regulates NLGN2 gene expression, promoting its synthesis in neuronal cells. | ||||||
Retinoic Acid, all trans | 302-79-4 | sc-200898 sc-200898A sc-200898B sc-200898C | 500 mg 5 g 10 g 100 g | $65.00 $319.00 $575.00 $998.00 | 28 | |
Retinoic acid, a metabolite of vitamin A, acts as a ligand for retinoic acid receptors (RARs). RARs form complexes with coactivators, binding to retinoic acid response elements (RAREs) in the NLGN2 promoter and facilitating its transcriptional activation. | ||||||
(+)-Bicuculline | 485-49-4 | sc-202498 sc-202498A | 50 mg 250 mg | $80.00 $275.00 | ||
Bicuculline is a GABAA receptor antagonist. By inhibiting GABAergic signaling, it indirectly promotes excitatory neurotransmission. The increased neuronal activity can upregulate NLGN2 expression through mechanisms involving calcium influx and downstream pathways. | ||||||
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 is a potent HDAC inhibitor. Its action leads to histone hyperacetylation, creating an open chromatin conformation. This epigenetic modification enhances accessibility to NLGN2 gene regulatory regions, facilitating transcription and subsequent expression. | ||||||
Lithium | 7439-93-2 | sc-252954 | 50 g | $214.00 | ||
Lithium chloride influences the Wnt/β-catenin signaling pathway. By inhibiting GSK-3β, a component of the destruction complex, it stabilizes β-catenin, leading to the transcriptional activation of Neuroligin 2 (NLGN2) through the TCF/LEF binding sites. | ||||||
A23187 | 52665-69-7 | sc-3591 sc-3591B sc-3591A sc-3591C | 1 mg 5 mg 10 mg 25 mg | $54.00 $128.00 $199.00 $311.00 | 23 | |
A23187 is a calcium ionophore that induces a rapid increase in intracellular calcium levels. Elevated calcium can activate Ca2+/calmodulin-dependent protein kinase (CaMK), which, in turn, may influence signaling cascades leading to the upregulation of NLGN2 expression. | ||||||
Sodium Butyrate | 156-54-7 | sc-202341 sc-202341B sc-202341A sc-202341C | 250 mg 5 g 25 g 500 g | $30.00 $46.00 $82.00 $218.00 | 19 | |
Sodium butyrate, a short-chain fatty acid, functions as an HDAC inhibitor. By preventing histone deacetylation, it promotes an open chromatin structure, facilitating the binding of transcription factors to the NLGN2 promoter and supporting its transcriptional activation. | ||||||
9-cis-Retinoic acid | 5300-03-8 | sc-205589 sc-205589B sc-205589C sc-205589D sc-205589A | 1 mg 25 mg 250 mg 500 mg 5 mg | $70.00 $416.00 $3060.00 $5610.00 $145.00 | 10 | |
9-cis-Retinoic acid is an isomer of all-trans retinoic acid. It activates retinoic acid receptors (RARs), leading to the formation of RAR-coactivator complexes. These complexes bind to RAREs in the NLGN2 promoter, enhancing transcription and promoting NLGN2 expression. | ||||||
SK&F 96365 | 130495-35-1 | sc-201475 sc-201475B sc-201475A sc-201475C | 5 mg 10 mg 25 mg 50 mg | $101.00 $155.00 $389.00 $643.00 | 2 | |
SKF-96365 inhibits receptor-operated calcium channels (ROCs). By blocking calcium influx, it modulates intracellular calcium levels. This disruption in calcium signaling can impact pathways related to NLGN2 expression, influencing its transcription and subsequent synthesis. | ||||||