Date published: 2025-9-13

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CCDC164 Activators

Chemical activators of CCDC164 can influence the protein's activity through various cellular signaling pathways and molecular mechanisms. Forskolin, for example, can directly stimulate adenylate cyclase, which increases intracellular cAMP levels. The rise in cAMP can activate protein kinase A (PKA), which in turn can phosphorylate CCDC164, leading to its activation. Ionomycin, by raising intracellular calcium levels, can activate calcium-dependent protein kinases such as calmodulin-dependent kinase (CaMK), which can also phosphorylate CCDC164, resulting in its activation. Phorbol 12-myristate 13-acetate (PMA) activates protein kinase C (PKC), which is known for phosphorylating a variety of protein substrates, possibly including CCDC164. This direct phosphorylation by PKC can function as an activation mechanism for CCDC164.

Inhibitors of protein phosphatases, such as Calyculin A and Okadaic Acid, can indirectly maintain CCDC164 in an activated state by preventing its dephosphorylation, ensuring that it remains phosphorylated and active. Anisomycin, which activates stress-activated protein kinases including JNK and p38 MAP kinase, can phosphorylate CCDC164 as part of the cellular stress response, thereby activating it. Epidermal Growth Factor (EGF) stimulates the MAPK/ERK pathway, leading to the activation and phosphorylation of various proteins, which may include CCDC164. S-Nitroso-N-acetylpenicillamine (SNAP) can release nitric oxide that activates guanylate cyclase, which raises cGMP levels, potentially activating kinases that phosphorylate CCDC164. BAY 11-7082's inhibition of the NF-κB pathway could alter phosphorylation patterns within the cell, inadvertently leading to CCDC164's activation. Dibutyryl-cAMP (db-cAMP) is a permeable analog of cAMP that can activate PKA and may phosphorylate CCDC164. Ouabain inhibits the Na+/K+ ATPase, which can increase intracellular calcium and potentially activate CaMK, leading to the phosphorylation and activation of CCDC164. Lastly, insulin initiates the PI3K/AKT signaling pathway, which is involved in a series of phosphorylation events that can lead to the activation of CCDC164.

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