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DIP2B Interacts With α-Tubulin to Regulate Axon Outgrowth.

Frontiers in cellular neuroscience (2020-03-11)
Zhen-Kai Xing, Lu-Qing Zhang, Yu Zhang, Xue Sun, Xiao-Lin Sun, Hua-Li Yu, Yao-Wu Zheng, Zi-Xuan He, Xiao-Juan Zhu
RESUMO

Axonal development is essential to the establishment of neuronal morphology and circuitry, although the mechanisms underlying axonal outgrowth during the early developmental stages remain unclear. Here, we showed that the conserved disco-interacting protein B (DIP2B) which consists of a DMAP1 domain and a crotonobetaine/carnitine CoA ligase (Caic) domain, is highly expressed in the excitatory neurons of the hippocampus. DIP2B knockout led to excessive axonal outgrowth but not polarity at an early developmental stage. Furthermore, the loss of DIP2B inhibited synaptic transmission for both spontaneous and rapid release in cultured hippocampal neurons. Interestingly, DIP2B function during axonal outgrowth requires tubulin acetylation. These findings reveal a new conserved regulator of neuronal morphology and provide a novel intervention mechanism for neurocognitive disorders.

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Sigma-Aldrich
Anticorpo anti-NeuN, clone A60, clone A60, Chemicon®, from mouse
Sigma-Aldrich
Anti-Acetylated Tubulin antibody, Mouse monoclonal, clone 6-11B-1, purified from hybridoma cell culture
Sigma-Aldrich
Monoclonal Anti-GABA antibody produced in mouse, clone GB-69, ascites fluid
Sigma-Aldrich
Anti-DIP2B antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution