Endoplasmic reticulum stress in vasopressin neurons of familial diabetes insipidus model mice: aggregate formation and mRNA poly(A) tail shortening

•  What is the topic of this review? Familial neurohypophysial diabetes insipidus (FNDI) is caused by a mutation in the vasopressin (AVP) gene locus. While mutant AVP precursors are reported to accumulate in the endoplasmic reticulum of AVP neurons, it is not clear how AVP neurons cope with the accumulation of misfolded proteins. •  What advances does it highlight? We show that AVP mRNA poly(A) tail length is shortened and the mRNA expression is decreased in the FNDI mouse model. The shortening of the mRNA poly(A) tail could be a novel unfolded protein response by which aggregate accumulation is reduced.

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