Overview:

TPM3 or tropomyosin 3 is a member of the tropomyosin family of actin-binding proteins that are dimers of coiled-coil proteins that provide stability to actin filaments and regulate access of other actin-binding proteins. TPM3 involved in translocations with other loci, including anaplastic lymphoma receptor tyrosine kinase (ALK) and neurotrophic tyrosine kinase receptor type 1 (NTRK1), which result in the formation of fusion proteins that act as oncogenes. TPM3 protein is substituted for the external domain of a putative tyrosine-kinase cell surface receptor to create the TRK oncogene (1). TPM3 are a common cause of congenital fiber type disproportion (2).

Gene Aliases:

APM1; CFTD; hscp30; NEM1; OK/SW-cl.5; TM-5; TM3; TM30; TM30nm; TM5; TPMsk3

Genbank Number:

NM_152263

References:

1. Coulier, F.et.al: Mechanism of activation of the human TRK oncogene. Molec. Cell. Biol. 9: 15-23, 1989.

2. Clarke, N. F. et.al: Mutations in TPM3 are a common cause of congenital fiber type disproportion. Ann. Neurol. 63: 329-337, 2008.