Disease relevance of Cdh17

• In the present study we investigated LI-cadherin expression immunohistochemically using our newly established monoclonal antibody in a large set (n = 102) of tumor specimens from patients with ductal adenocarcinoma of the pancreas, and correlated the findings with the patients' survival [1].

High impact information on Cdh17

• Consistent with these findings, LI-cadherin was not resistant to detergent extraction and did not induce a reorganization of the actin cytoskeleton [2].
• In contrast to classical cadherins, LI-cadherin, when expressed in mouse L cells, was neither associated with catenins nor did it induce an upregulation of beta-catenin [2].
• The possible functions of BILL-cadherin in B cell development are discussed [3].
• Treatment of Swiss 3T3 cells with bombesin rapidly induced tyrosine phosphorylation of the p130 Crk-associated substrate (p130(cas)) [4].
• Ksp- and LI-cadherin are structurally homologous proteins coexpressed with E-cadherin in renal and intestinal epithelia, respectively [5].

Biological context of Cdh17

• During mouse embryogenesis, LI-cadherin expression begins at embryonic day 12 [6].
• LI-cadherin gene expression during mouse intestinal development [6].
• These findings strengthen our assumption that LI-cadherin originated from an ancestral cadherin with five domains by a partial gene duplication event [7].
• Intestinal cell adhesion molecules. Liver-intestine cadherin [8].

Anatomical context of Cdh17

• Whereas LI-cadherin has been shown to mediate Ca2+-dependent homotypic cell-cell adhesion independent of stable interactions with the cytoskeleton, little is known about the physiological role of Ksp-cadherin [5].
• 5. With the exception of transient expression in the urogenital sinus and the common bile duct on day 13.5, LI-cadherin was found exclusively in the intestinal epithelium [6].
• LI-cadherin occupies all cell surfaces of the deeper layers of the epithelium, distributing to basolateral surfaces only in the cells of the outer epithelial layer [6].
• BILL-cadherin deficiency caused a threefold proB cell accumulation, as well as a reduction to half of the numbers of immature B cells in bone marrow [9].
• In the peritoneal cavity of mutant mice IgM(+)Mac-1(+)CD5(+) B1a cell, that express high BILL-cadherin in wild-type mice, was also reduced in number [9].

Associations of Cdh17 with chemical compounds

• Furthermore, galectin-3 was identified as being coimmunoprecipitated with LI-cadherin and this interaction was inhibited by lactose in a dose-dependent manner, but not by sucrose [1].

Other interactions of Cdh17

• LI-cadherin (Liver-Intestine cadherin) is a member of a subclass (7-D cadherins) within the cadherin superfamily [6].

References