Pin1 is a peptidyl-prolyl isomerase that induces the cis-trans conversion of specific Ser/Thr-Pro peptide bonds in phosphorylated proteins, leading to conformational changes through which Pin1 regulates protein stability and activity. Since down-regulation of Pin1 has been described in several neurodegenerative disorders, including Alzheimer's Disease (AD), Parkinson's Disease (PD) and Huntington's Disease (HD), we investigated its potential role in prion diseases. Animals generated on wild-type (Pin1^+/+), hemizygous (Pin1^+/−) or knock-out (Pin1^−/−) background for Pin1 were experimentally infected with RML prions. The study indicates that, neither the total depletion nor reduced levels of Pin1 significantly altered the clinical and neuropathological features of the disease.

Pin1是一种肽基-脯氨酰异构酶，可诱导磷酸化蛋白中特定Ser / Thr-Pro肽键的顺式转化，从而导致构象变化，Pin1通过其调节蛋白稳定性和活性。由于已经在多种神经退行性疾病（包括阿尔茨海默氏病（AD），帕金森氏病（PD）和亨廷顿氏病（HD））中描述了Pin1的下调，因此我们研究了其在病毒疾病中的潜在作用。以野生型（Pin1 ^{+ / +}），半合子（Pin1 ^+/-）或敲除（Pin1 ^-/-）产生的动物）Pin1的背景通过实验被RML pr病毒感染。该研究表明，Pin1的总耗竭或水平降低均不会显着改变该疾病的临床和神经病理特征。