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CDH1 — CDH3
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Troxell et al., J Cell Sci 2000
:
Mutant
E-cadherin overexpression
caused a dramatic reduction in endogenous
cadherin levels
Kintner et al., Cell 1992
:
Analysis of the mutant phenotype shows that at least two regions of the N-cadherin cytoplasmic domain can inhibit adhesion and that the mutant
cadherin can
inhibit catenin binding to
E-cadherin
Liu et al., J Cell Biol 2006
:
Experiments using microengineered substrates showed that
E-cadherin engagement stimulated the peak in proliferation at intermediate seeding densities, and that the proliferation arrest at high densities did not
involve E-cadherin , but rather resulted from a crowding dependent decrease in cell spreading against the underlying substrate
Macpherson et al., Oncogene 2007
(Carcinoma, Squamous Cell...) :
We show that the collective invasion of A431 cells depends on the presence of
cadherin mediated ( P- and
E-cadherin ) cell-cell contacts, which are lost in cells where p120 expression is knocked down
Sun et al., Am J Pathol 2011
(Colonic Neoplasms...) :
Inhibition of
P-cadherin expression also
induced the up-regulation of
E-cadherin and the down-regulation of ß-catenin and its downstream target molecules, including survivin and c-Myc
Fu et al., Neuro Oncol 2013
:
Finally, NPV-LDE-225 suppressed epithelial-mesenchymal transition by upregulating
E-cadherin and
inhibiting N-cadherin , Snail, Slug, and Zeb1 through modulating the miR-200 family
Nanta et al., Oncogenesis 2013
:
NVP-LDE-225 suppressed EMT by upregulating
E-cadherin and
inhibiting N-cadherin , Snail, Slug and Zeb1 by regulating the miR-200 family
Shimazui et al., Cancer Res 1996
(Urinary Bladder Neoplasms) :
In model systems, it has been shown that
cadherin function
requires not only proper
E-cadherin expression but also its linkage to the cytoskeleton through catenins