Dysadherin Activators
Dysadherin, also known as FXYD5, is a transmembrane protein that belongs to the FXYD family, which regulates the activity of Na,K-ATPase, a key ion transporter essential for maintaining cellular ion gradients and membrane potential. Dysadherin is predominantly expressed in epithelial tissues, where it plays critical roles in cell-cell adhesion, migration, and invasion. Through its interaction with Na,K-ATPase, dysadherin modulates ion transport activity, thereby influencing various cellular processes involved in tissue homeostasis and development. Dysadherin has been implicated in cancer progression and metastasis, as its dysregulation is associated with increased tumor invasiveness and metastatic potential in various cancer types. Additionally, dysadherin may function as a signaling molecule, transducing extracellular signals into intracellular responses to regulate cell behavior and tissue architecture.
Activation of dysadherin involves multiple molecular mechanisms that converge to modulate its expression, localization, and functional activity. Transcriptional regulation plays a crucial role in controlling dysadherin expression, with various transcription factors and signaling pathways implicated in its transcriptional activation or repression. Post-translational modifications, such as phosphorylation, glycosylation, and ubiquitination, also regulate dysadherin function and stability, affecting its interaction with binding partners and subcellular localization. Moreover, dysadherin activity can be modulated by protein-protein interactions with other cellular components, including cell adhesion molecules, cytoskeletal proteins, and signaling effectors. The precise mechanisms governing dysadherin activation likely vary depending on cellular context and environmental cues, highlighting the complexity of dysadherin regulation in physiological and pathological conditions. Understanding the molecular basis of dysadherin activation is essential for elucidating its roles in normal physiology and disease progression, offering targets for intervention in dysadherin-associated pathologies.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Lithium | 7439-93-2 | sc-252954 | 50 g | $214.00 | ||
Lithium chloride activates Dysadherin by modulating the Wnt/β-catenin signaling pathway. Activation of Wnt signaling leads to the stabilization and nuclear translocation of β-catenin, which interacts with TCF/LEF transcription factors to upregulate Dysadherin expression, promoting cell adhesion and migration. | ||||||
Resveratrol | 501-36-0 | sc-200808 sc-200808A sc-200808B | 100 mg 500 mg 5 g | $60.00 $185.00 $365.00 | 64 | |
Resveratrol, a polyphenolic compound found in various plants, is known to inhibit Dysadherin indirectly by modulating the PI3K/Akt pathway. It exerts its effects by suppressing the phosphorylation of Akt, thereby downregulating Dysadherin expression through a negative regulatory loop within the PI3K/Akt signaling cascade. | ||||||
GW-441756 | 504433-23-2 | sc-200683 sc-200683A | 10 mg 50 mg | $141.00 $565.00 | 3 | |
GW441756, a specific c-Met inhibitor, acts as an indirect Dysadherin inhibitor by disrupting the HGF/c-Met signaling pathway. Dysadherin expression is regulated by c-Met activation, and GW441756 inhibits this pathway, leading to decreased Dysadherin levels and impaired cellular adhesion. | ||||||
Dexamethasone | 50-02-2 | sc-29059 sc-29059B sc-29059A | 100 mg 1 g 5 g | $76.00 $82.00 $367.00 | 36 | |
Dexamethasone activates Dysadherin by inhibiting NF-κB signaling. NF-κB activation suppresses Dysadherin expression by binding to its promoter region. Dexamethasone inhibits NF-κB translocation to the nucleus, thereby preventing its binding to the Dysadherin promoter and allowing for increased Dysadherin expression, promoting cell-cell adhesion and migration. | ||||||
Sorafenib | 284461-73-0 | sc-220125 sc-220125A sc-220125B | 5 mg 50 mg 500 mg | $56.00 $260.00 $416.00 | 129 | |
Sorafenib, a multi-kinase inhibitor, indirectly inhibits Dysadherin by targeting the Raf/MEK/ERK signaling pathway. By interfering with this pathway, Sorafenib downregulates Dysadherin expression, impacting cell adhesion and migration. | ||||||
LY 294002 | 154447-36-6 | sc-201426 sc-201426A | 5 mg 25 mg | $121.00 $392.00 | 148 | |
LY294002, a PI3K inhibitor, directly inhibits Dysadherin expression by blocking the PI3K/Akt signaling pathway. This inhibition results in decreased phosphorylation of Akt, leading to reduced Dysadherin levels and impaired cell adhesion. | ||||||
Tyrphostin AG 1478 | 175178-82-2 | sc-200613 sc-200613A | 5 mg 25 mg | $94.00 $413.00 | 16 | |
AG1478, an EGFR tyrosine kinase inhibitor, acts as an indirect Dysadherin inhibitor by disrupting the EGFR signaling pathway. By inhibiting EGFR activation, AG1478 downregulates Dysadherin expression, influencing cell adhesion and migration. | ||||||
SB 203580 | 152121-47-6 | sc-3533 sc-3533A | 1 mg 5 mg | $88.00 $342.00 | 284 | |
SB203580, a p38 MAPK inhibitor, indirectly inhibits Dysadherin by modulating the p38 MAPK signaling pathway. It suppresses the phosphorylation of p38 MAPK, leading to reduced Dysadherin expression and affecting cellular adhesion and invasion. | ||||||
Bortezomib | 179324-69-7 | sc-217785 sc-217785A | 2.5 mg 25 mg | $132.00 $1064.00 | 115 | |
Bortezomib, a proteasome inhibitor, indirectly inhibits Dysadherin by preventing its proteasomal degradation. This leads to the accumulation of Dysadherin, impacting cell adhesion and invasion. | ||||||
Wortmannin | 19545-26-7 | sc-3505 sc-3505A sc-3505B | 1 mg 5 mg 20 mg | $66.00 $219.00 $417.00 | 97 | |
Wortmannin, a PI3K inhibitor, directly inhibits Dysadherin expression by blocking the PI3K/Akt signaling pathway. It hinders Akt phosphorylation, resulting in reduced Dysadherin levels and impaired cell adhesion. | ||||||