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In patients with FCMD, selective deficiency of -dystroglycan as well as a secondary deficiency in laminin-211/merosin, which is specifically expressed in skeletal muscle, Schwann cells and thymocytes 9 , results in the disruption of a series of connections between the basement membrane and the cytoskeleton maintained via -dystroglycan, leading to the development of muscular dystrophy

Tat also mobilizes Ca 2+ from IP3-sensitive stores and activates novel PKC isoforms, enhancing TNF- production across macrophages, neurons, and astrocytes [97, 98]

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