DNM1L-Polyclonal Antibodies

l as normal cell growth and development is controlled, in part, by the phosphorylation of DNM1L at Ser616 by Cdk1/cyclin B and at Ser637 by protein kinase A (PKA) (reviewed in 6). When phosphorylated at Ser616, DNM1L stimulates mitochondrial fission during mitosis. Conversely, fission is inhibited when DNM1L is phosphorylated at Ser637 (reviewed in 6). Dephosphorylation at Ser637 by calcineurin reverses this inhibition (7). In addition to phosphorylation, sumoylation of DNM1L is also an enhancer of mitochondrial fission (8). Balancing fission and fusion events is essential for proper mitochondrial function. Research studies have demonstrated mitochondrial defects in a variety of neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease (reviewed in 6).

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