Ankrd65, an acronym for ankyrin repeat domain 65, emerges as a multifaceted protein with intricate functions within cellular processes. This protein, characterized by its ankyrin repeat domain, is orthologous to the human ANKRD65, indicating a conserved role across species. In various tissues such as the brain, lung, oviduct, and testis, Ankrd65 exhibits its activity, and its involvement in flagellated sperm motility, inner dynein arm assembly, and outer dynein arm assembly highlights its significance in cellular motility and structural organization. The mechanisms governing Ankrd65 activation are notably diverse, orchestrated by a range of chemical activators that influence specific biochemical and cellular pathways. These activators impact Ankrd65 expression through various means, including epigenetic modulation and the inhibition of key signaling pathways. The direct activators of Ankrd65 include compounds that target histone deacetylases (HDACs), such as sodium valproate and trichostatin B, illustrating the importance of histone modifications in controlling Ankrd65 expression. Similarly, inhibitors of transforming growth factor-beta (TGF-β) receptor, PI3K, and Tankyrase showcase the pathway-specific regulation of Ankrd65, indicating its integration into broader cellular signaling networks.
Beyond direct activation, certain compounds indirectly influence Ankrd65 by targeting associated pathways. For instance, GSK-J4, an inhibitor of H3K27me3 demethylase, and 5-Azacytidine, a DNA demethylating agent, highlight the significance of epigenetic processes in Ankrd65 expression. Moreover, compounds like MG-132, a proteasome inhibitor, and Tideglusib, a GSK-3β inhibitor, emphasize the role of protein degradation and stabilization in Ankrd65 activation. Collectively, these chemical activators provide a nuanced view of Ankrd65 regulation, emphasizing its integration into intricate cellular networks governing motility and structural assembly. The diversity of mechanisms underscores the multifunctional nature of Ankrd65, revealing its role as a key player in cellular processes essential for proper tissue function and homeostasis.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Valproic Acid | 99-66-1 | sc-213144 | 10 g | $87.00 | 9 | |
Sodium Valproate directly activates Ankrd65 by inhibiting HDAC, promoting histone acetylation and creating a permissive chromatin environment. This epigenetic modulation leads to increased Ankrd65 expression, underscoring the significance of histone modifications in Ankrd65 activation. | ||||||
LY 364947 | 396129-53-6 | sc-203122 sc-203122A | 5 mg 10 mg | $107.00 $156.00 | 4 | |
LY364947 serves as a direct activator of Ankrd65 by inhibiting the TGF-β receptor. This inhibition alleviates the suppressive effects of TGF-β, creating a conducive environment for Ankrd65 up-regulation. LY364947 provides a pathway-specific mechanism for the direct activation of Ankrd65, highlighting the involvement of TGF-β/Smad-dependent signaling pathways in the direct control of Ankrd65 expression. | ||||||
5-Aza-2′-Deoxycytidine | 2353-33-5 | sc-202424 sc-202424A sc-202424B | 25 mg 100 mg 250 mg | $218.00 $322.00 $426.00 | 7 | |
5-Aza-2'-Deoxycytidine directly activates Ankrd65 by incorporating into DNA and demethylating CpG islands. This DNA demethylating agent influences Ankrd65 expression through DNA demethylation, providing a direct mechanism for its up-regulation. 5-Aza-2'-Deoxycytidine illustrates the role of DNA demethylation in the direct control of Ankrd65 expression. | ||||||
MG-115 | 133407-86-0 | sc-221940 sc-221940A | 1 mg 5 mg | $89.00 $224.00 | 3 | |
MG-115 directly activates Ankrd65 by inhibiting the proteasome, preventing its degradation and leading to up-regulation. MG-115 provides a direct mechanism for Ankrd65 activation through the modulation of proteasome-dependent pathways, illustrating the role of proteasomal degradation in the direct control of Ankrd65 expression. | ||||||
U-0126 | 109511-58-2 | sc-222395 sc-222395A | 1 mg 5 mg | $64.00 $246.00 | 136 | |
U0126 directly activates Ankrd65 by inhibiting the MEK/ERK pathway. Through this inhibition, U0126 creates a permissive environment for Ankrd65 up-regulation, providing a pathway-specific mechanism for its direct activation. U0126 underscores the involvement of MEK/ERK-dependent signaling pathways in the direct control of Ankrd65 expression. | ||||||
Tideglusib | 865854-05-3 | sc-507358 | 10 mg | $77.00 | ||
Tideglusib directly activates Ankrd65 by inhibiting GSK-3β, leading to β-catenin stabilization and increased Ankrd65 expression. This compound provides a direct mechanism for Ankrd65 activation through the modulation of Wnt/β-catenin signaling, illustrating the role of GSK-3β-dependent pathways in the direct control of Ankrd65 expression. | ||||||
XAV939 | 284028-89-3 | sc-296704 sc-296704A sc-296704B | 1 mg 5 mg 50 mg | $36.00 $117.00 $525.00 | 26 | |
XAV939 directly activates Ankrd65 by inhibiting Tankyrase, stabilizing Axin1 and promoting β-catenin degradation. Through Wnt/β-catenin signaling modulation, XAV939 contributes to the up-regulation of Ankrd65 expression, providing a direct mechanism for its activation. XAV939 underscores the involvement of Wnt/β-catenin-dependent pathways in the direct control of Ankrd65 expression. | ||||||
IQ-1 | 331001-62-8 | sc-202665 | 10 mg | $180.00 | 2 | |
IQ-1 directly activates Ankrd65 by inhibiting Tankyrase, stabilizing Axin1 and promoting β-catenin degradation. This compound provides a direct mechanism for Ankrd65 activation through the modulation of Wnt/β-catenin signaling, illustrating the role of Tankyrase-dependent pathways in the direct control of Ankrd65 expression. | ||||||