COL1A2 and osteogenesis imperfecta: Some but not all mutations in COL1A1 and COL1A2 caused ER accumulation of collagen, increased expression of binding immunoglobulin protein (BiP), a chaperone that directly binds to collagen to support its folding and assembly, as well as UPR activation, autophagy and apoptosis in OI fibroblasts [211].