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CDH2 — FUT1

Text-mined interactions from Literome

Choi et al., Am J Physiol Gastrointest Liver Physiol 2009 (Liver Cirrhosis, Experimental) : Q-HSC activation in vitro ( culture ) and in vivo ( CCl ( 4 ) -induced cirrhosis ) resulted in decreased expression of Hh-interacting protein ( Hhip, an Hh antagonist ), the EMT inhibitors bone morphogenic protein ( BMP-7 ) and inhibitor of differentiation ( Id2 ), the adherens junction component E-cadherin , and epithelial keratins 7 and 19 and increased expression of Gli2 ( an Hh target gene ) and mesenchymal markers, including the mesenchyme associated transcription factors Lhx2 and Msx2, the myofibroblast marker alpha-smooth muscle actin, and matrix molecules such as collagen
Bromberg et al., Blood 2012 : To determine whether osteoblastic N-cadherin is required for HSC regulation, we used a genetic murine model in which deletion of Cdh2, the gene encoding N-cadherin, has been targeted to cells of the osteoblastic lineage
Arai et al., Ann N Y Acad Sci 2012 : Furthermore, overexpression of N-cadherin in HSCs promoted quiescence and preserved HSC activity during serial bone marrow ( BM ) transplantation ( BMT )