Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 3.1.3.66 extracted from

  • Zhang, B.; Wang, W.; Li, C.; Liu, R.
    Inositol polyphosphate-4-phosphatase type II plays critical roles in the modulation of cadherin-mediated adhesion dynamics of pancreatic ductal adenocarcinomas (2018), Cell Adh. Migr., 12, 548-563 .
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
medicine INPP4B manipulates cadherin switch in certain pancreatic ductal adenocarcinoma cell lines through a phosphorylated AKT-inactivation. The knockdown of INPP4B in AsPC-1 cells results in a more invasive phenotype, and overexpression of INPP4B in PANC-1 leads to partial reversion of mesenchymal status and impediment of in vitro invasion but not migration. E-cadherin is enriched in the early and sorting endosomes containing INPP4B which enables its recycling rather than degradation. INPP4B acts as an tumor suppressor in pancreatic ductal adenocarcinomas which attenuates AKT activation and participates in preservation of E-cadherin in endocytic pool and cellular membrane Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens O15327
-
-

Source Tissue

Source Tissue Comment Organism Textmining
adenocarcinoma cell pancreatic ductal adenocarcinoma Homo sapiens
-
AsPC-1 cell
-
Homo sapiens
-
BxPC-3 cell
-
Homo sapiens
-
PANC-1 cell
-
Homo sapiens
-
SW-1990 cell
-
Homo sapiens
-