AnxA11

AnxA11 is a Ca²⁺-regulated annexin that supports cell division by localizing to the midbody and enabling terminal cytokinesis^[1]. Its cell-cycle function connects with calcium-dependent nuclear-envelope association, indicating that ANXA11 signaling links Ca²⁺ dynamics to mitotic membrane remodeling^[2]. Mechanistically, AnxA11 also coordinates with ALG-2 to stabilize Sec31A at endoplasmic-reticulum exit sites, supporting early secretory pathway organization^[3]. In disease genetics, ANXA11 was identified as a sarcoidosis susceptibility locus, placing this calcium-dependent phospholipid-binding protein in inflammatory disease research^[4]. In neurodegenerative disease models, ALS-associated ANXA11 mutations altered calcyclin binding, promoted cytoplasmic aggregation, and implicated defective intracellular protein trafficking in pathogenesis^[5]. Additional ALS studies linked ANXA11 variants to disrupted intracellular Ca²⁺ homeostasis and impaired stress-granule disassembly, extending its relevance to RNA-protein granule biology^[6]. Compared with related annexins, AnxA11 combines a conserved calcium-binding C-terminal annexin core with an intrinsically disordered N-terminal region that is emphasized as ANXA11-specific and mutation-sensitive^[7]. Therefore, ANXA11 research mainly uses genetic variants, knockdown models, aggregation assays, calcium imaging, trafficking assays, and stress-granule readouts rather than validated small-molecule agonists or inhibitors^[3][5][6].

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