Tmem169, also known as transmembrane protein 169, is located on human chromosome 2q35. Its function and associated pathways were previously uncharacterized, but its study via genetic models like knockout (KO) mouse models can potentially reveal much about its role in biological processes [1].

In a study using male mouse dorsal forebrain conditional knockout (CKO) of Tmem169, it was found that Tmem169 is highly expressed in the nervous system. Its deletion led to neuronal morphological abnormalities and synaptic dysfunction. Tmem169 -deficient mice of both sexes showed autism-like behavioral traits. Further, Tmem169 was shown to interact with several key neuronal proteins, many involved in neurodevelopmental diseases, and it promotes neuronal process and synapse development through interaction with Shank3 [1].

In conclusion, Tmem169 plays a crucial role in the development of cortical neurons and synapses in the nervous system. The Tmem169 CKO mouse model has revealed its significance in the context of autism-like behaviors, suggesting its potential importance in understanding the pathological mechanisms of neurodevelopmental disorders [1].