Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 1999 Jun;44(6):890-5.
doi: 10.1136/gut.44.6.890.

Trefoil peptides

W M Wong  1 , R Poulsom, N A Wright
Affiliations
Review

Trefoil peptides

W M Wong et al. Gut. 1999 Jun.
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1
A diagrammatic representation of the three leafed trefoil domain in a dimer of TFF3, both components of which are shown with their N- and C-terminal ends labelled. The position of the cysteine residues are indicated by the unshaded residues and the associated disulphide bonds are also shown.
Figure 2
Figure 2
In situ hybridisation using 35S riboprobes for TFF1, TFF2 and TFF3 mRNAs showing their expression in rat gastric glands regenerating in a healing gastric ulcer after cryoprobe injury. Note the heavy overexpression of both TFF1 and TFF2 almost throughout the length of the gastric glands, and the focal ectopic expression of TFF3, not normally seen in the gastric mucosa. These observations demonstrate the strong upregulation of trefoil peptide gene expression during gastric mucosal regeneration after damage.
Figure 3
Figure 3
A diagram showing a mature ulcer associated cell lineage (UACL) gland in the small intestine and the regenerating monolayer growing over the surface of an intestinal (or gastric) ulcer. The sites of expression of the trefoil factors are indicated.
Figure 4
Figure 4
A diagram, modelled after Marcel et al,84 representing the possible association between a putative TFF receptor, the E-cadherin-β-catenin system and growth factor receptors. TFF3 is known to cause β-catenin phosphorylation; growth factors such as hepatocyte growth factor (HGF), which bind the c-met receptor, and EGF, which binds the epidermal growth factor receptor, also phosphorylate β-catenin. β-catenin phosphorylation is associated with reduced expression of E-cadherin, decreased cell-cell and cell-substratum adhesion, downregulation of the expression of APC and α- and β-catenin, translocation of APC from the cytoplasm to the nucleus, and the induction of apoptotic changes. TFF3 also affects ERK, a member of the mitogen activated protein kinases family, indicating a role in signal transduction.
See this image and copyright information in PMC

References

    1. Br J Cancer. 1989 Aug;60(2):168-75 - PubMed
    1. Int J Cancer. 1989 Nov 15;44(5):806-12 - PubMed
    1. Nature. 1990 Jan 4;343(6253):82-5 - PubMed
    1. Br J Cancer. 1990 Jan;61(1):32-8 - PubMed
    1. FEBS Lett. 1990 Jan 15;260(1):145-8 - PubMed

Publication types