Apmap, also known as adipocyte plasma membrane-associated protein, is a glycosyl type II transmembrane protein mainly distributed in the plasma membrane and endoplasmic reticulum of adipocytes. It is an arylesterase that plays a crucial role in adipogenesis. Apmap is involved in multiple biological processes such as lipid transport, epithelial-mesenchymal transition, and may be associated with pathways like Wnt/β-catenin. It also has implications in maintaining endoplasmic reticulum-associated lipid and lipoprotein homeostasis [2,3,6].

In cancer cells, loss-of-function studies using CRISPR knockout screens identified Apmap as a regulator of susceptibility to antibody-dependent cellular phagocytosis (ADCP). Loss of Apmap synergizes with tumour antigen-targeting monoclonal antibodies and/or CD47-blocking monoclonal antibodies to drive increased phagocytosis across various cancer cell types and inhibit tumour growth in mice [1]. In cervical cancer, knockdown of Apmap significantly inhibited the migration ability of cancer cells, indicating its role in promoting epithelial-mesenchymal transition and metastasis through activating the Wnt/β-catenin pathway [3]. In a mouse model of Alzheimer's disease, constitutive deletion of Apmap worsened spatial memory phenotype and led to increased Aβ production and deposition into senile plaques [4]. In Rex rabbits, knockdown of FTO, which can increase Apmap expression, affected intramuscular fat deposition as Apmap promotes adipocyte differentiation [5]. Knockout of full-length Apmap in mice led to an improved metabolic phenotype upon diet-induced obesity, with enhanced insulin sensitivity, preserved glucose tolerance, etc., and Apmap was found to interact with extracellular collagen cross-linking matrix proteins [7].

In conclusion, Apmap has diverse functions in adipogenesis, lipid and lipoprotein homeostasis, and is involved in various disease conditions such as cancer, Alzheimer's disease, and metabolic disorders. Gene knockout mouse models have been instrumental in revealing these functions, providing valuable insights into the underlying mechanisms and potential therapeutic targets for these diseases.