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DCC netrin 1 receptor

The DCC gene provides instructions for making a protein called the netrin-1 receptor, which is involved in the development of the nervous system. This protein attaches (binds) to a protein called netrin-1, and these two proteins fit together like a lock and key. The binding of netrin-1 to its receptor helps direct the growth of specialized nerve cell extensions called axons. Axons transmit nerve impulses that can signal muscle movement.

Normal function

The DCC gene provides instructions for making a protein called the netrin-1 receptor, which is involved in the development of the nervous system. This protein attaches (binds) to a protein called netrin-1, and these two proteins fit together like a lock and key. The binding of netrin-1 to its receptor helps direct the growth of specialized nerve cell extensions called axons. Axons transmit nerve impulses that can signal muscle movement.

When the brain sends a signal to trigger muscle movement, the signal usually travels from one half of the brain to the opposite side of the body. The binding of netrin-1 to its receptor allows axons to develop this signaling pathway.

The netrin-1 receptor is also thought to act as a dependence receptor, which means it functions differently depending on whether or not it is bound to its protein. When the netrin-1 receptor is bound to netrin-1, it plays a role in nervous system development. When it is not bound to netrin-1, the netrin-1 receptor acts as a tumour suppressor, which means that it keeps cells from growing and dividing too fast or in an uncontrolled way. When the netrin-1 receptor is acting as a tumour suppressor, studies suggest that the netrin-1 receptor triggers the self-destruction of cells when they are no longer needed (apoptosis).

Conditions referring to this gene or chromosome

Otros nombres

CRC18

CRCR1

DCC_HUMAN

IGDCC1

MRMV1

netrin receptor DCC

NTN1R1

tumour suppressor protein DCC

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La información en esta página está escrita y revisada por pares por clínicos calificados.
  • 19 May 2025 | Última versión
  • 1 May 2025 | Publicado originalmente

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