anti-Inositol Polyphosphate-4-Phosphatase, Type II, 105kDa (INPP4B) Antibodies

Mouse (Murine) Inositol Polyphosphate-4-Phosphatase, Type II, 105kDa (INPP4B) interaction partners

1. data show that INPP4B modulates AR activity in normal prostate and its loss contributes to the AR-dependent transcriptional profile in prostate cancer.

2. Data provides evidence that INPP4B may play a role in regulating callosal axon formation by the formation of Satb2-positive pyramidal neurons and controlling axon polarization.

3. Study provides evidence that INPP4B loss can promote follicular-like thyroid cancer progression and metastasis in the context of PTEN haploinsufficiency through the isoform-specific regulation of AKT signaling at the endosomes.

4. Results provide evidence that INPP4B is a bona fide tumor suppressor whose function is particularly important in situations of PTEN deficiency. Biochemical data demonstrates that INPP4B directly dephosphorylates PtdIns(3,4,5)P3.

5. ERalpha plays a protective role in bladder cancer initiation and growth at least partly via modulating the INPP4B/Akt pathway.

6. mice carrying the longer-latency Inpp4b allele(474R/548P)) exhibited significantly longer cortical motor evoked potential latencies indicating that INPP4B regulates nerve conduction velocity

7. Hyperactivation of the PI3K/AKT pathway caused by the decrease in INPP4B in granulosa cells promotes an ovarian environment defective in folliculogenesis and conducive to teratoma formation.

8. In vivo mice deficient in Inpp4b displayed increased osteoclast differentiation rate and potential resulting in decreased bone mass and osteoporosis

9. This study provides first insight for a physiological role of PI-4-phosphatase II in the proerythroblast by controlling Epo responsiveness through a negative regulation of the PI3K/Akt pathway

10. Inpp4bbeta localized to the Golgi apparatus whereas Inpp4balpha was mainly cytosolic, suggesting a different cellular function for this isoform.

Human Inositol Polyphosphate-4-Phosphatase, Type II, 105kDa (INPP4B) interaction partners

1. The identification of altered gene expression, including INPP4B and c-kit, highlights novel signaling pathways involved in the neuronal and interstitial cells of Cajal changes underlying primary achalasia.

2. INPP4B acts as a tumour suppressor in cervical cancer cells.

3. data show that gastric cancer and colorectal cancer with microsatellite instability-high could harbor INPP4B truncation mutation that might alter PI3K pathway

4. Women with IHC basal breast cancers defined as "nestin+ or INPP4B-" have superior overall survival.

5. overexpression of INPP4B promotes NPM1-mutated leukemia cell proliferation through SGK3 activation. High levels of INPP4B are at least partially induced by the NPM1 mutant via ERK/Ets-1 signaling.

6. data show that INPP4B modulates AR activity in normal prostate and its loss contributes to the AR-dependent transcriptional profile in prostate cancer.

7. Luciferase reporter assay revealed that miR-1290 directly bound to the 3'-UTR of INPP4B; the mutated seed sites in miR-1290 abrogated this effect. Double knockdown of INPP4B and miR-1290 promoted CRC cell proliferation, suggesting miR-1290 promoted CRC cell proliferation by targeting INPP4B.

8. High INPP4B expression is associated with melanoma.

9. INPP4B role in regulating phosphatidylinositol-3-kinase signaling in the triple-negative breast cancer cells.

10. Fisher's exact SubID was used to reveal EVI1 as a transcriptional regulator of INPP4B in AML; a finding which was validated in vitro. Next, we used CoxPH SubID to conduct a pan-cancer analysis of INPP4B's prognostic significance

11. INPP4B acted as a tumour suppressor in human prostate cancer

12. INPP4B is down-regulated in colorectal adenocarcinomas.

13. Collectively, these results suggest that INPP4B may function as an oncogenic driver in colon cancer, with potential implications for targeting INPP4B as a novel approach to treat this disease.

14. Study shows that IRF2 knockdown inhibits growth, colony formation of OCI/AML-2, OCI/AML-3, and THP-1 cells. In addition, IRF2 knockdown induces apoptosis of acute myeloid leukemia (AML) cells by regulating apoptotic effectors. Further mechanism analysis shows that INPP4B contributes to the effects of IRF2 on apoptosis and growth of AML cells. Thus, IRF2 serves as an important regulator in AML by targeting INPP4B.

15. Immunohistochemical assessment of nestin and INPP4b provides an accurate, accessible and inexpensive tool to identify basal-like breast cancer subtype in the clinically problematic setting of weak oestrogen receptor positivity

16. This study sthe identification of a novel small transcript variant of INPP4B (INPP4B-S) that has a role in promoting proliferation of colon and breast cancer cells. INPP4B-S differed from full length INPP4B (INPP4B-FL) by the insertion of a small exon between exons 15 and 16 and the deletion of exons 20-24.

17. presented data indicate that INPP4B is crucial for docetaxel-resistant PCa cell survival, potentially by regulating EMT through the PI3K/Akt signaling pathway

18. Low PINPP4B expression is associated with luminal breast cancer.

19. Mechanism analyses found polyphosphate 4-phosphatase type II (INPP4B) was the target of miR-937, miR-937 directly bound to the 3'UTR of INPP4B, knockdown of INPP4B in A549 with miR-937 inhibitor promoted anchorage -dependent and -independent growth, suggesting miR-937 contributed to cell proliferation of lung cancer

20. INPP4B expression is associated with enhanced ATM-dependent DNA double strand break repair, which could be mediated by p65 nuclear translocation.