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Abstract Myasthenia gravis (MG) is an autoimmune disease caused by antibodies against the acetylcholine receptor (AChR), muscle-specific kinase (MuSK) or other AChR-related proteins in the postsynaptic muscle membrane

Collagen VI encodes antimicrobial activity: novel innate host defense properties of the extracellular matrix

pSTAT3 translocates to the nucleus, where it increase the expression of POMC and inhibits that of NPY (St-Pierre and Tremblay, 2012) (Figure 1)