Date published: 2025-11-25

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KBTBD8 Inhibitors

Chemical inhibitors of KBTBD8 operate through various mechanisms to interfere with the protein's function by targeting specific cellular processes and signaling pathways that are essential for its activity. Alsterpaullone and Roscovitine, for instance, are inhibitors of cyclin-dependent kinases (CDKs), a group of proteins that play a pivotal role in cell cycle regulation. By inhibiting CDKs, these chemicals impair the cell cycle control mechanisms, which are intrinsically linked to the role of KBTBD8 in protein degradation during neural crest formation. This disruption of cell cycle phases translates into a functional inhibition of KBTBD8, as it is unable to execute its role effectively in the absence of proper cell cycle progression.

Furthermore, a group of chemicals including Sotrastaurin, Go6983, Bisindolylmaleimide I, Chelerythrine, Ruboxistaurin, Midostaurin, Ro-31-8220, Enzastaurin, Staurosporine, and K252a, target the protein kinase C (PKC) family. KBTBD8 is involved in pathways that are regulated by PKC, which is crucial for modulating various cellular functions, including cytoskeletal organization and signal transduction. These inhibitors, by targeting PKC, alter the phosphorylation status of substrates within the cell, leading to a disruption of the normal signaling cascades. Since KBTBD8's activity is contingent upon these pathways, the inhibition of PKC effectively results in the functional inhibition of KBTBD8. The altered signaling dynamics consequent to PKC inhibition create a cellular environment where KBTBD8 cannot contribute to its usual processes, thereby reducing its functional impact within the cell.

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Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

K-252a

99533-80-9sc-200517
sc-200517B
sc-200517A
100 µg
500 µg
1 mg
$126.00
$210.00
$488.00
19
(2)

K252a is a potent kinase inhibitor, with activity against several kinases, including those involved in signaling pathways where KBTBD8 operates. Inhibition of these kinases would lead to functional inhibition of KBTBD8 due to disrupted signaling.