Vamp2, also known as vesicle-associated membrane protein 2, is a component of the SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) complex [2,4,5,6,7]. It plays a crucial role in vesicular trafficking and membrane fusion processes, which are vital for various biological functions such as neurotransmitter release, epidermal differentiation, and myelin formation [3,4,5,6]. It is also involved in pathways related to synaptic physiology and pathophysiology, as well as cellular autophagy [1,2,3]. Genetic models, especially KO/CKO mouse models, are valuable for studying Vamp2's function.

In murine studies, deletion of Vamp2 leads to aberrant skin stratification and enucleation, indicating its importance in epidermal differentiation and carcinogenesis [3]. Genetic inactivation of Vamp2/3 in myelinating oligodendrocytes causes severe hypomyelination and premature death, highlighting its role in CNS myelination [4]. Toxin-mediated cleavage of VAMP2/3 in the OL lineage of mice impairs the maturation of early oligodendrocytes into myelinating ones, further emphasizing its role in myelin formation [6].

In conclusion, Vamp2 is essential for processes like epidermal differentiation, CNS myelination, and oligodendrocyte maturation as revealed through mouse model-based research. These findings contribute to our understanding of diseases related to skin development, neurodegeneration, and demyelinating disorders.