Trk receptor

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Trk receptor is a type of protein that plays a crucial role in the nervous system. It is part of the receptor tyrosine kinase family, which is involved in many cellular processes, including cell growth, cell differentiation, and neuron survival.

History[edit | edit source]

The Trk receptor was first identified in the 1980s through studies of a oncogene in a colon carcinoma cell line. The name "Trk" stands for "tropomyosin receptor kinase," reflecting its initial identification as a fusion protein with tropomyosin.

Structure[edit | edit source]

Trk receptors are single-pass transmembrane proteins with an extracellular ligand-binding domain, a transmembrane domain, and an intracellular kinase domain. The extracellular domain is responsible for binding to neurotrophins, a family of growth factors that includes nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3).

Function[edit | edit source]

When a neurotrophin binds to the extracellular domain of a Trk receptor, it triggers a conformational change that activates the intracellular kinase domain. This leads to the phosphorylation of specific tyrosine residues in the receptor, initiating a cascade of intracellular signaling events. These signals can promote cell survival, differentiation, and growth, particularly in neurons.

There are three main types of Trk receptors: TrkA, TrkB, and TrkC. Each has a different affinity for the various neurotrophins. For example, TrkA binds most strongly to NGF, TrkB to BDNF and NT-4, and TrkC to NT-3.

Clinical significance[edit | edit source]

Abnormalities in Trk receptor function can lead to a variety of neurological disorders. For example, mutations in the TrkA gene can cause congenital insensitivity to pain with anhidrosis (CIPA), a rare disorder characterized by the inability to feel pain and temperature, and decreased or absent sweating.

Trk receptors are also implicated in certain types of cancer. Some tumors overexpress Trk receptors or produce mutant forms that are constitutively active, leading to uncontrolled cell growth and survival.

See also[edit | edit source]

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Contributors: Prab R. Tumpati, MD