The latent transforming growth factor β binding protein (LTBP) family

Rahmi Oklu, R. Hesketh

Research output: Contribution to journalReview article

136 Citations (Scopus)

Abstract

The transforming growth factor β (TGFβ) cytokines are a multi-functional family that exert a wide variety of effects on both normal and transformed mammalian cells. The secretion and activation of TGFβs is regulated by their association with latency-associated proteins and latent TGFβ binding proteins (LTBPs). Over the past few years, three members of the LTBP family have been identified, in addition to the protoype LTBP1 first sequenced in 1990. Three of the LTBP family are expressed in a variety of isoforms as a consequence of alternative splicing. This review summarizes the differences between the isoforms in terms of the effects on domain structure and hence possible function. The close identity between LTBPs and members of the fibrillin family, mutations in which have been linked directly to Marfan's syndrome, suggests that anomalous expression of LTBPs may be associated with disease. Recent data indicating that differential expression of LTBP1 isoforms occurs during the development of coronary heart disease is considered, together with evidence that modulation of LTBP function, and hence of TGFβ activity, is associated with a variety of cancers.

Original languageEnglish (US)
Pages (from-to)601-610
Number of pages10
JournalBiochemical Journal
Volume352
Issue number3
DOIs
StatePublished - Dec 15 2000
Externally publishedYes

Fingerprint

Transforming Growth Factors
Carrier Proteins
Protein Isoforms
Marfan Syndrome
Alternative Splicing
Coronary Disease
Chemical activation
Cells
Modulation
Association reactions
Cytokines
Mutation
Neoplasms
Proteins

Keywords

  • Atherosclerosis
  • Cancer
  • Fibrillin
  • Marfan's syndrome
  • TGFβ

ASJC Scopus subject areas

  • Biochemistry

Cite this

The latent transforming growth factor β binding protein (LTBP) family. / Oklu, Rahmi; Hesketh, R.

In: Biochemical Journal, Vol. 352, No. 3, 15.12.2000, p. 601-610.

Research output: Contribution to journalReview article

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