Promotes invasion of host epithelial cells by adhering to receptors on the host cell surface to facilitate endocytosis of the pathogen into host cells (PubMed:24355926, PubMed:32487760). Binds HSPA5/BiP protein on the cell surface of host nasal epithelial cells (PubMed:24355926). Interacts with HSPA5/BiP on the cell surface of host nasal epithelial cells. Expressed in spores (PubMed:24355926). Expressed in germlings (PubMed:24355926). Expressed during growth in host lung and brain, and during growth in presence of epithelial cells (PubMed:24355926). Induced in presence of high free iron (PubMed:27159390). Induced during growth in high glucose (PubMed:27159390). Induced in presence of 3-hydroxybutyric acid (BHB) (PubMed:27159390). RNAi-mediated knockdown decreases invasion of human nasal epithelial cells by R.delemar (PubMed:32487760). Simultaneous RNAi-mediated knockdown of CotH2 and CotH3 decreases invasion of human epithelial cells (PubMed:24355926). Simultaneous RNAi-mediated knockdown of CotH2 and CotH3 decreases virulence in a mouse model of ketoacidosis (PubMed:24355926, PubMed:27159390). Simultaneous RNAi-mediated knockdown of CotH2 and CotH3 does not lead to sensitivity to cell wall stress (induced by Congo Red, Calcofluor White, hydrogen peroxide, sodium dodecyl sulfate, or Triton X-100) or alter resistance to killing by phagocytes (PubMed:24355926). Antibodies against the protein protects a diabetic ketoacidotic (DKA) mouse model and a neutropenic mouse model from mucormycosis infection, and nasal epithelial cells from invasion by R.delemar, and thus could potentially be used to treat the disease.