AMN1 encodes a protein that functions as an antagonist of the mitotic exit network (MEN), playing a crucial role in cell cycle regulation and cytokinesis. The protein operates through a dual mechanism to downregulate the Tem1 GTPase: it evicts Tem1 from spindle pole bodies and escorts it into the nucleus, while simultaneously promoting Tem1 degradation as part of a SCF ubiquitin ligase complex 1. This dual action helps extinguish MEN activity after cytokinesis is complete, contributing to proper cell cycle reset 1. AMN1 shows asymmetric expression, appearing preferentially in daughter cells versus mother cells during budding yeast division 1. In pathogenic fungi like Candida albicans, AMN1 participates in morphological transitions, forming a feedback loop with the transcription factor Ace2 and influencing lateral yeast formation from hyphae 2. The protein has also been identified as a potential E3 ubiquitin ligase involved in dystrophin protein turnover, suggesting broader roles in protein quality control 3. Additionally, AMN1 appears in various disease contexts, with altered expression observed in Alzheimer's disease brain cortices 4 and potential interactions affecting early embryonic development 5.