Product Pathways - Adhesion
TFF1/pS2 Antibody #12419
Reactivity Key: H=Human M=Mouse
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Specificity / Sensitivity
TFF1/pS2 Antibody recognizes endogenous levels of total TFF1/pS2 protein. This antibody reacts with precursor and mature forms of TFF1/pS2. Based upon sequence alignment, this antibody is not predicted to cross-react with either TFF2 or TFF3.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val33 of human TFF1/pS2 protein. Antibodies are purified by protein A and peptide affinity chromatography.
The trefoil factor family of proteins (trefoil factor 1 [TFF1]/pS2, TFF2, and TFF3) are a group of highly conserved, thermostable, and protease resistant polypeptides. The family was named for the disulfide bond configuration of the trefoil, or P domain, which forms a three-leaved structure analogous to a trefoil or clover leaf. Each trefoil domain comprises 42-43 amino acids containing six cysteine residues that form disulfide bonds, resulting in the characteristic trefoil structure (1,2). The trefoil peptides are localized within mucous granules in mucous-secreting cells and are expressed and secreted by epithelial cells that line mucous membranes (2).
TFF1 is expressed predominantly by the gastric epithelia, in the upper portion of the glandular pits, and is highly expressed in some adenocarcinomas such as breast cancer (1,3,4). In the context of breast cancer, TFF1 is highly expressed in estrogen receptor-positive tumors. Indeed, TFF1 expression is directly regulated by estrogen receptor-α (4). In the stomach, secreted TFF1 is a component of the protective mucous layer. TFF1 expression is strongly induced after mucosal injury (5) and is involved in stomach ontogenesis and maintenance of the integrity of the mucosa (1,3). Research studies have shown frequent loss of TFF1 expression in more than two-thirds of gastric carcinomas resulting from mutation-independent mechanisms (6-8).
- Thim, L. and May, F.E. (2005) Cell Mol Life Sci 62, 2956-73.
- Taupin, D. and Podolsky, D.K. (2003) Nat Rev Mol Cell Biol 4, 721-32.
- Ribieras, S. et al. (1998) Biochim Biophys Acta 1378, F61-77.
- Corte, M.D. et al. (2006) Breast Cancer Res Treat 96, 63-72.
- Taupin, D. et al. (2001) Lab Invest 81, 397-408.
- Carvalho, R. et al. (2002) Lab Invest 82, 1319-26.
- Katoh, M. (2003) Int J Mol Med 12, 3-9.
- McChesney, P.A. et al. (2006) Cancer Res 66, 1346-53.
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For Research Use Only. Not For Use In Diagnostic Procedures.