Huntingtin: Difference between revisions
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== Pathology == | == Pathology == | ||
The general consensus is that the toxicity originates from the gain of function of mHTT, as the polyQ solely could still stretch and let to the development of neurological symptoms in | The general consensus is that the toxicity originates from the gain of function of mHTT, as the polyQ solely could still stretch and let to the development of neurological symptoms in mouse models <ref>DOI 10.1038/ng0696-196</ref><ref>DOI 10.1016/s0092-8674(00)81369-0</ref><ref>10.1016/s0092-8674(00)80464-x</ref>. However, the contribution of loss of function of the wild-type HTT cannot be abandoned, as wild-type HTT inactivation or deletion leads to neurodegeneration as well <ref>DOI 10.1016/s0006-8993(98)01312-2</ref><ref>DOI 10.1038/81593</ref>. | ||
== References == | == References == | ||
<references/> | <references/> | ||
