IMPAD1 catalyzes the hydrolysis of phosphoadenosine phosphate (PAP) to AMP in the Golgi lumen, preventing PAP-induced cytotoxicity . This activity is essential for glycosaminoglycan sulfation during skeletal development .
Studies highlight IMPAD1's dual role in lung cancer metastasis:
AMPK-Notch1-HEY1 Pathway Activation: Accumulated AMP upregulates pAMPK, driving Notch1/HEY1 signaling to promote metastasis .
Mitochondrial ROS Suppression: Inhibits Complex I of the electron transport chain, reducing ROS levels and enhancing cancer cell survival .
EMT Regulation: Repressed by miR-200/miR-96 during epithelial-to-mesenchymal transition (EMT), IMPAD1 upregulation alters Golgi dynamics and secretome composition to facilitate invasion .
IMPAD1 Mouse Bioactive is utilized in:
Western Blotting: Detected at ~42 kDa in neuroblastoma (Neuro-2A) and pheochromocytoma (PC-12) cell lines .
Immunocytochemistry: Localizes to the cytoplasm in chondrocyte-differentiated mesenchymal stem cells .
Functional Assays: Validates enzymatic activity via PAP-to-AMP conversion kinetics .
In Vivo Metastasis: IMPAD1 knockdown reduces lung cancer metastasis in mouse models by 60–70% .
Golgi Dynamics: Interaction with Synaptotagmin XI (Syt11) enhances vesicular trafficking, modifying extracellular matrix components like collagen and fibronectin .
Therapeutic Targeting: ADORA1 inhibition reverses AMPK-HEY1 signaling in IMPAD1-overexpressing cells, suggesting potential therapeutic avenues .
IMPAD1 catalyzes the hydrolysis of phosphoadenosine phosphate (PAP) to adenosine monophosphate (AMP) . This reaction is essential for maintaining the balance of inositol phosphates within the cell, which are critical for various cellular functions, including signal transduction and membrane biogenesis.
IMPAD1 is studied for its role in neurodevelopmental disorders and neurodegenerative diseases. Its involvement in inositol phosphate metabolism makes it a potential target for therapeutic interventions aimed at modulating cellular signaling pathways.