Huntingtin: Difference between revisions
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Ivan Šonský (talk | contribs) No edit summary |
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Wild-type HTT is well known for its scaffolding function. It interacts with β-tubulin and binds to microtubules. Besides, it interacts with the dynein/dynactin complex, thereby regulating vesicular transport <ref>DOI 10.1073/pnas.0610628104</ref>. <ref>DOI 10.1016/j.neuron.2010.06.027</ref> | Wild-type HTT is well known for its scaffolding function. It interacts with β-tubulin and binds to microtubules. Besides, it interacts with the dynein/dynactin complex, thereby regulating vesicular transport <ref>DOI 10.1073/pnas.0610628104</ref>. Furthermore, HTT has been shown to localize to spindle poles during mitosis, regulating spindle orientation in mouse neuronal cells<ref>DOI 10.1016/j.neuron.2010.06.027</ref>. On the other hand, the abnormal scaffolding function for molecular motors operated via mHTT results in abrupted axonal transport. That leads to inefficient distribution of mitochondria within nerve cells, causing low | ||
== Disease == | == Disease == | ||
