Mice hemizygous for the human synuclein (alpha-syn) mutant transgene, (SNCA*A53T) are viable and fertile. Expression of SNCA*A53T is regulated by the tetracycline operator (tetO); also called tetracycline-responsive element (TRE, TetRE) or tet-operator). When mated to a mutant strain expressing tetracycline-controlled transactivator protein (tTA), expression of SNCA*A53T protein may be regulated with tetracycline or its analog doxycycline (dox) in the double mutant offspring. Mutations in alpha-syn greatly accelerate the formation of fibrillar aggregates causing various forms of cytotoxicity, including impairment of proteasomal and lysosomal activities, disruption of ER-Golgi traffic and microtubule-based transport, and dysfunction of mitochondria. SNCA*A53T mice develop age-dependent, progressive neurodegeneration. These mice may be useful for studying the Parkinson's disease pathogenesis and neurodegeneration elicited by the toxic effects of aggregation and somatic accumulation of SNCA.

These transgenic mice carry a humanized synuclein (alpha-syn) mutant (SNCA*A53T) gene regulated by a tetracycline operator (tetO). When mated to a mutant strain expressing tTA, expression of SNCA*A53T protein may be regulated with the tetracycline analog doxycycline in the double mutant offspring.

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STOCK Tg(tetO-SNCA*A53T)E2Cai/J Frozen Embryo