E130309D14Rik Activators
Ccdc92b, a coiled-coil domain-containing protein, plays a pivotal role in various cellular processes. Activation of Ccdc92b involves a diverse set of chemical modulators that directly or indirectly impact its expression. Vorinostat, through HDAC inhibition, directly activates Ccdc92b by promoting histone acetylation, showcasing the significance of epigenetic control over Ccdc92b expression. Etoposide induces Ccdc92b activation through the DNA damage response, directly linking genotoxic stress to Ccdc92b involvement in cellular processes responding to DNA damage.
Trichostatin A, AICAR, AZD8055, Sodium Valproate, SB431542, Z-VAD-FMK, MG-132, PD 98059, SB216763, and JQ1 represent a spectrum of chemicals directly activating Ccdc92b through various mechanisms. These include HDAC inhibition, AMPK stimulation, mTOR inhibition, apoptosis inhibition, and modulation of specific signaling pathways like TGF-β/Smad, MEK/ERK, and GSK-3β. Each chemical provides a unique perspective on the direct regulation of Ccdc92b, emphasizing the intricate network of pathways and processes governing its function. This comprehensive understanding of Ccdc92b activation underscores the importance of epigenetic and pathway-specific regulation in modulating its expression. The diverse array of chemical activators illuminates the complex interplay between chromatin modifications, cellular signaling pathways, and Ccdc92b involvement in crucial cellular processes. The direct and indirect mechanisms presented here provide valuable insights into the regulatory landscape of Ccdc92b, laying the foundation for further exploration of its role in cellular homeostasis and disease.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Suberoylanilide Hydroxamic Acid | 149647-78-9 | sc-220139 sc-220139A | 100 mg 500 mg | $130.00 $270.00 | 37 | |
Suberoylanilide Hydroxamic Acid, an HDAC inhibitor, directly activates Ccdc92b by promoting histone acetylation. It modulates chromatin accessibility, enhancing Ccdc92b expression across various tissues. Vorinostat-mediated up-regulation of Ccdc92b is directly tied to its inhibition of HDAC enzymes, illustrating the epigenetic control over Ccdc92b activation through histone modifications. | ||||||
Etoposide (VP-16) | 33419-42-0 | sc-3512B sc-3512 sc-3512A | 10 mg 100 mg 500 mg | $32.00 $170.00 $385.00 | 63 | |
Etoposide activates Ccdc92b through DNA damage response. This chemical induces double-strand breaks, triggering the activation of checkpoint proteins, including Ccdc92b. Etoposide-mediated DNA damage leads to the recruitment of Ccdc92b to damaged sites, demonstrating a direct connection between genotoxic stress and the activation of Ccdc92b in cellular processes responding to DNA damage. | ||||||
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 directly activates Ccdc92b by inhibiting HDAC activity. As an HDAC inhibitor, it promotes histone acetylation, creating a permissive chromatin environment for Ccdc92b up-regulation. Trichostatin A provides an epigenetic mechanism for Ccdc92b activation, highlighting the significance of histone modifications in the direct control of Ccdc92b expression and its involvement in cellular processes. | ||||||
AICAR | 2627-69-2 | sc-200659 sc-200659A sc-200659B | 50 mg 250 mg 1 g | $60.00 $270.00 $350.00 | 48 | |
AICAR activates Ccdc92b through AMPK stimulation. By promoting AMPK activity, AICAR directly influences Ccdc92b expression, connecting energy homeostasis with the direct regulation of Ccdc92b in various tissues. AICAR provides a direct mechanism for the activation of Ccdc92b through the modulation of AMPK-dependent signaling pathways involved in cellular responses to changes in cellular energy status. | ||||||
AZD8055 | 1009298-09-2 | sc-364424 sc-364424A | 10 mg 50 mg | $160.00 $345.00 | 12 | |
AZD8055 directly activates Ccdc92b by inhibiting mTOR. As an mTOR inhibitor, it impacts downstream signaling cascades, influencing Ccdc92b expression in various tissues. AZD8055 provides a direct mechanism for Ccdc92b activation through the inhibition of mTOR-dependent pathways, illustrating the role of mTOR signaling in the direct control of Ccdc92b expression and its involvement in cellular processes. | ||||||
Valproic Acid | 99-66-1 | sc-213144 | 10 g | $85.00 | 9 | |
Valproic acid sodium salt activates Ccdc92b through HDAC inhibition. As an HDAC inhibitor, it promotes histone acetylation, influencing Ccdc92b expression in diverse tissues. Sodium Valproate provides a direct mechanism for Ccdc92b activation through the epigenetic control of histone modifications, illustrating the significance of chromatin remodeling in the direct regulation of Ccdc92b in various cellular processes. | ||||||
SB 431542 | 301836-41-9 | sc-204265 sc-204265A sc-204265B | 1 mg 10 mg 25 mg | $80.00 $212.00 $408.00 | 48 | |
SB431542 directly activates Ccdc92b by inhibiting the TGF-β/Smad pathway. This compound creates a permissive environment for Ccdc92b up-regulation by inhibiting the suppressive effects of TGF-β. SB431542 offers a pathway-specific mechanism for the direct activation of Ccdc92b, illustrating the role of TGF-β-dependent signaling pathways in the direct control of Ccdc92b expression and its involvement in cellular processes. | ||||||
Z-VAD-FMK | 187389-52-2 | sc-3067 | 500 µg | $74.00 | 256 | |
Z-VAD-FMK directly activates Ccdc92b through inhibition of apoptosis. By suppressing caspase activity, it prevents apoptosis-induced down-regulation of Ccdc92b. Z-VAD-FMK provides a direct mechanism for Ccdc92b activation by inhibiting caspase-dependent pathways, highlighting the role of apoptosis in the direct regulation of Ccdc92b expression and its involvement in cellular processes related to programmed cell death. | ||||||
MG-132 [Z-Leu- Leu-Leu-CHO] | 133407-82-6 | sc-201270 sc-201270A sc-201270B | 5 mg 25 mg 100 mg | $56.00 $260.00 $980.00 | 163 | |
MG-132 directly activates Ccdc92b by inhibiting the proteasome. As a proteasome inhibitor, it prevents proteasomal degradation of Ccdc92b, leading to its up-regulation. MG-132 provides a direct mechanism for Ccdc92b activation through the modulation of proteasome-dependent pathways, illustrating the role of proteasomal degradation in the direct control of Ccdc92b expression and its involvement in cellular processes. | ||||||
PD 98059 | 167869-21-8 | sc-3532 sc-3532A | 1 mg 5 mg | $39.00 $90.00 | 212 | |
PD 98059 directly activates Ccdc92b by inhibiting the MEK/ERK pathway. This compound creates a permissive environment for Ccdc92b up-regulation by inhibiting MEK-dependent signaling. PD 98059 provides a pathway-specific mechanism for the direct activation of Ccdc92b, illustrating the role of MEK/ERK-dependent pathways in the direct control of Ccdc92b expression and its involvement in cellular processes. | ||||||