Date published: 2026-2-22

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Dkk-4 Activators

The chemical class known as Dkk-4 Activators comprises a diverse spectrum of compounds carefully selected for their potential to modulate the activity of Dkk-4, a protein encoded by the DKK-4 gene. While specific direct activators may not be conclusively identified, these compounds operate through intricate interactions with the Wnt/β-catenin signaling pathway and associated cellular processes, suggesting a nuanced regulatory influence on Dkk-4 function. Actvators of this class inhibit GSK-3β and potentially activate Dkk-4 through the stabilization of β-catenin. Inhibition of GSK-3β distrupts the phosphorylation and subsequent degradation of β-catenin, allowing its accumulation. The stabilized β-catenin may then interact with Dkk-4, influencing Dkk-4 activation through modulation of the Wnt/β-catenin pathway. Similarly, activators promote Dkk-4 by stabilizing axin, a negative regulator of the Wnt pathway. Inhibition disrupts the degradation of axin, facilitating increased destruction complex formation. This mechanism may lead to the activation of the Wnt/β-catenin pathway, indirectly influencing Dkk-4 activation.

Furthermore, activators act on Dkk-4 by disrupting β-catenin-mediated transcriptional repression, indirectly influencing Dkk-4 activity. Activators can promote Dkk-4 by blocking GSK-3β-mediated phosphorylation and degradation of β-catenin. Lastly, activators operate through the modulation of intracellular calcium signaling, impacting cellular processes related to Dkk-4 activation. Collectively, the Dkk-4 activators constitute a chemically diverse group that intricately navigates the complexities of the Wnt/β-catenin pathway, shedding light on potential avenues for the regulation of Dkk-4 function within cellular processes.

SEE ALSO...

Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

Lithium

7439-93-2sc-252954
50 g
$214.00
(0)

Lithium, a GSK-3β inhibitor, can potentially activate Dkk-4 by preventing GSK-3β-mediated degradation. Inhibition of GSK-3β leads to the stabilization of β-catenin, which may interact with Dkk-4. This interaction could potentially activate Dkk-4 through modulation of the Wnt/β-catenin pathway.

GSK-3 Inhibitor IX

667463-62-9sc-202634
sc-202634A
sc-202634B
1 mg
10 mg
50 mg
$58.00
$188.00
$884.00
10
(1)

BIO is a GSK-3β inhibitor that can activate Dkk-4 by preventing GSK-3β-mediated phosphorylation and degradation of β-catenin. Inhibition of GSK-3β allows for the stabilization of β-catenin, potentially facilitating its interaction with Dkk-4 and leading to the activation of Dkk-4 through modulation of the Wnt/β-catenin pathway.

Norcantharidin

29745-04-8sc-280719
5 g
$113.00
2
(0)

Norcantharidin activates the Wnt/β-catenin pathway, potentially influencing Dkk-4 activation. By inhibiting protein phosphatase 2A (PP2A), norcantharidin prevents the dephosphorylation of β-catenin, leading to its stabilization. The stabilized β-catenin may interact with Dkk-4, indirectly activating Dkk-4 through modulation of the Wnt pathway.

XAV939

284028-89-3sc-296704
sc-296704A
sc-296704B
1 mg
5 mg
50 mg
$36.00
$117.00
$525.00
26
(1)

XAV-939, a tankyrase inhibitor, can activate Dkk-4 by stabilizing axin, a negative regulator of the Wnt/β-catenin pathway. Inhibition of tankyrase prevents the degradation of axin, leading to increased destruction complex formation. This may result in the activation of the Wnt/β-catenin pathway, influencing Dkk-4 activation.

NSC 23766

733767-34-5sc-204823
sc-204823A
10 mg
50 mg
$151.00
$609.00
75
(4)

NSC23766, an inhibitor of Rac1, may activate Dkk-4 by inhibiting the Rac1 signaling pathway. Inhibition of Rac1 can potentially influence cellular processes related to Dkk-4 activation, as Rac1 is involved in cytoskeletal remodeling and signaling cascades that may impact Dkk-4 function.

Thiazovivin

1226056-71-8sc-361380
sc-361380A
10 mg
25 mg
$284.00
$634.00
15
(1)

IWP-2 is a Wnt pathway inhibitor that can activate Dkk-4 by blocking Wnt secretion. Inhibition of Wnt secretion by IWP-2 may result in the stabilization of the destruction complex, preventing the degradation of β-catenin. This could potentially activate Dkk-4 through modulation of the Wnt/β-catenin pathway.