IMM-01 has been used as a formin activator to study its effects on motor neurons (MNs).[1]
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IMM-01 binds and activates formin thereby leading to autoinhinition.[1]
IMM-01 is an agonist of the mammalian Diaphanous (mDia)-related formins that triggers actin assembly and microtubule stabilization, serum response factor-mediated gene expression, cell-cycle arrest, and apoptosis. IMM-01 inhibits DID–DAD binding, which in turn activates mDia family of formins in cells. IMM-01 slows tumor growth in a mouse xenograft model of colon cancer.
IMM-01 is an agonist of the mammalian Diaphanous (mDia)-related formins that triggers actin assembly.
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease of unknown etiology. Although defects in nucleocytoplasmic transport (NCT) may be central to the pathogenesis of ALS and other neurodegenerative diseases, the molecular mechanisms modulating the nuclear pore function are still
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