ADAM22
- ADAM22
ADAM22 is a gene that encodes a member of the ADAM (a disintegrin and metalloproteinase) family of proteins. These proteins are involved in a variety of biological processes, including cell signaling, adhesion, and migration. ADAM22, in particular, plays a crucial role in the nervous system.
Structure[edit | edit source]
The ADAM22 protein is characterized by several distinct domains:
- **Prodomain**: This region is involved in the regulation of the protein's activity.
- **Metalloproteinase domain**: Although ADAM22 is classified as a metalloproteinase, it lacks proteolytic activity due to the absence of a critical zinc-binding motif.
- **Disintegrin domain**: This domain is involved in cell-cell and cell-matrix interactions.
- **Cysteine-rich domain**: This region may play a role in protein-protein interactions.
- **EGF-like domain**: This domain is similar to epidermal growth factor and may be involved in signaling.
- **Transmembrane domain**: This region anchors the protein to the cell membrane.
- **Cytoplasmic tail**: This part of the protein is involved in intracellular signaling pathways.
Function[edit | edit source]
ADAM22 is primarily expressed in the brain and is involved in synaptic transmission and plasticity. It interacts with several proteins, including LGI1 (leucine-rich glioma-inactivated 1), which is important for synaptic function. ADAM22 is crucial for the proper functioning of the nervous system and has been implicated in neurological disorders.
Clinical Significance[edit | edit source]
Mutations in the ADAM22 gene have been associated with neurological conditions such as epilepsy and intellectual disability. The interaction between ADAM22 and LGI1 is particularly important in the context of epilepsy, as disruptions in this interaction can lead to seizures.
Research[edit | edit source]
Ongoing research is focused on understanding the precise mechanisms by which ADAM22 and its interacting partners contribute to neurological function and disease. Studies are also exploring potential therapeutic targets for conditions associated with ADAM22 dysfunction.
Also see[edit | edit source]
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Contributors: Prab R. Tumpati, MD
