EC Number   |
Application |
Reference |
|---|
   3.1.3.66 | medicine |
calpain-mediated inhibition of enzyme is involved in the phosphatidylinositol 3,4-bisphosphate accumulation in thrombin-stimulated platelets |
646456 |
| 3.1.3.66 | medicine |
colorectal carcinoma cell lines HCT-116, SW-620, DLD-1, and WiDr express significantly lower levels of INPP4B protein than the normal colonic epithelial cell lines CCD-841 CoTr and FHC. INPP4B mRNA expression in the colorectal carcinoma cell lines is significantly lower than in the normal colonic epithelial cells. Normal colonic mucosa displays uniform and strong-to-moderate INPP4B immunoreactivity, whereas 60.7% and 76.5% of the primary and metastatic colorectal carcinoma tissue samples exhibit reduced INPP4B expression, respectively |
749589 |
| 3.1.3.66 | medicine |
decreased expression of INPP4B correlates with poor outcome in both breast cancer and ovarian cancer patients, whereby the PI3K pathway is likely to play a major role in driving this subset of cancers. Loss of INPP4B expression may provide a marker for selecting patients who will respond to PI3K drugs |
707954 |
| 3.1.3.66 | medicine |
in acute myeloid leukemia, isoform IPNPP4B is significantly overexpressed, in association with reduced responses to chemotherapy, early relapse, and poor overall survival, independent of other risk factors. Ectopic overexpression of INPP4B confers leukemic resistance to cytosine arabinoside, daunorubicin, and etoposide. Expression of phosphatase inert variant C842A fails to abrogate resistance of acute myeloid leukemiacells to chemotherapy in vitro or in vivo. Targeted suppression of endogenously overexpressed INPP4B by RNAi sensitizes acute myeloid leukemia cell lines and primary acute myeloid leukemia to chemotherapy |
750175 |
| 3.1.3.66 | medicine |
in prostate cancer cell lines INPP4B regulates androgen recetor transcriptional activity and the oncogenic signaling pathways Akt and PKC. In prostate cancer patient cohorts, a positive correlation between INPP4B expression and both androgen receptor mRNA levels and transcriptional output exists |
751762 |
| 3.1.3.66 | medicine |
in Triple-negative breast cancer cells, which lack expression of estrogen receptor, progesterone receptor, and amplification of HER2/Neu, silencing isoform INPP4B decreases basal phospho-Akt (pAkt) and cellular proliferation, and in most cases sensitizes cells to phosphatidylinositol-3-kinase PI3K-alpha and PI3K-beta isoform-specific inhibitors. Overexpression of INPP4B desensitizes cells to PI3K inhibitors in a phosphatase activity-dependent manner |
751546 |
| 3.1.3.66 | medicine |
inositol polyphosphate 4-phosphatase type II is a direct target of microRNA-590-3p. Enforced expression of microRNA-590-3p leads to repression of inositol polyphosphate 4-phosphatase type II messenger RNA and protein expression, as well as upregulation of p-Akt, p-FoxO3a, and cyclin D1 and downregulation of p21 expression in prostate cancer cell lines. Overexpression of inositol polyphosphate 4-phosphatase type II can reduce microRNA-590-3p-induced cell proliferation and invasion as well as tumor growth, and decrease microRNA-590-3p-mediated upregulation of cyclin D1 and downregulation of p21 expression in prostate cancer cells |
752313 |
| 3.1.3.66 | medicine |
INPP4A is identified as a novel asthma candidate gene |
677505 |
| 3.1.3.66 | medicine |
INPP4B is low expressed in osteosarcoma tissues and in osteosarcoma cell lines. INPP4B overexpression significantly decreases cell viability and induces apoptosis in SaOS2 and U2OS cells. Combination of INPP4B overexpression and poly-ADP ribose polymerase inhibitor rucaparib declines Myc, cyclin E1 and cyclin D1 expressions, enhances Bad, Bax, and cleaves caspase3 expressions, and blocks PI3K/AKT signal pathway in SaOS2 and U2OS cells. Combination of INPP4B overexpression and rucaparib inhibits tumor formation in vivo |
751184 |
| 3.1.3.66 | 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 |
750257 |
