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INPP4B encodes the inositol polyphosphate 4-phosphatase type II, one of the enzymes involved in phosphatidylinositol signaling pathways. Additionally we are shipping INPP4B Antibodies (26) and INPP4B Kits (1) and many more products for this protein.
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Data provides evidence that INPP4B may play a role in regulating callosal axon formation by the formation of Satb2 (show SATB2 Proteins)-positive pyramidal neurons and controlling axon polarization.
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 (show AKT1 Proteins) signaling at the endosomes.
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.
ERalpha (show ESR1 Proteins) plays a protective role in bladder cancer initiation and growth at least partly via modulating the INPP4B/Akt (show AKT1 Proteins) pathway.
mice carrying the longer-latency Inpp4b allele(474R/548P)) exhibited significantly longer cortical motor evoked potential latencies indicating that INPP4B regulates nerve conduction velocity
Hyperactivation of the PI3K/AKT (show AKT1 Proteins) pathway caused by the decrease in INPP4B in granulosa cells promotes an ovarian environment defective in folliculogenesis and conducive to teratoma (show DND1 Proteins) formation.
In vivo mice deficient in Inpp4b displayed increased osteoclast differentiation rate and potential resulting in decreased bone mass and osteoporosis
This study provides first insight for a physiological role of PI-4-phosphatase II in the proerythroblast by controlling Epo (show EPO Proteins) responsiveness through a negative regulation of the PI3K/Akt (show AKT1 Proteins) pathway
INPP4B is down-regulated in colorectal adenocarcinomas.
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.
Study shows that IRF2 (show IRF2 Proteins) knockdown inhibits growth, colony formation of OCI/AML-2 (show RUNX3 Proteins), OCI/AML-3 (show RUNX2 Proteins), and THP-1 cells. In addition, IRF2 (show IRF2 Proteins) knockdown induces apoptosis of acute myeloid leukemia (show BCL11A Proteins) (AML (show RUNX1 Proteins)) cells by regulating apoptotic effectors. Further mechanism analysis shows that INPP4B contributes to the effects of IRF2 (show IRF2 Proteins) on apoptosis and growth of AML (show RUNX1 Proteins) cells. Thus, IRF2 (show IRF2 Proteins) serves as an important regulator in AML (show RUNX1 Proteins) by targeting INPP4B.
Immunohistochemical assessment of nestin (show NES Proteins) 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
This study sthe (show GLRA1 Proteins) 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.
presented data indicate that INPP4B is crucial for docetaxel-resistant PCa (show FLVCR1 Proteins) cell survival, potentially by regulating EMT (show ITK Proteins) through the PI3K (show PIK3CA Proteins)/Akt (show AKT1 Proteins) signaling pathway
Mechanism analyses found polyphosphate 4-phosphatase type II (INPP4B) was the target of miR (show MLXIP Proteins)-937, miR (show MLXIP Proteins)-937 directly bound to the 3'UTR of INPP4B, knockdown of INPP4B in A549 with miR (show MLXIP Proteins)-937 inhibitor promoted anchorage -dependent and -independent growth, suggesting miR (show MLXIP Proteins)-937 contributed to cell proliferation of lung cancer
INPP4B expression is associated with enhanced ATM (show ATM Proteins)-dependent DNA double strand break repair, which could be mediated by p65 (show GORASP1 Proteins) nuclear translocation.
Studies indicate that phosphatidylinositol 4-phosphate phosphatase (INPP4B) that acting as tumor suppressors by antagonizing AKT (show AKT1 Proteins) signaling at endosomes.
The incidence of INPP4B loss of heterozygosity was significantly higher in the triple-negative breast tumor subtype and positively correlated with PTEN loss of heterozygosity.
INPP4B encodes the inositol polyphosphate 4-phosphatase type II, one of the enzymes involved in phosphatidylinositol signaling pathways. This enzyme removes the phosphate group at position 4 of the inositol ring from inositol 3,4-bisphosphate. There is limited data to suggest that the human type II enzyme is subject to alternative splicing, as has been established for the type I enzyme.
inositol polyphosphate 4-phosphatase type II beta isoform
, type II inositol 3,4-bisphosphate 4-phosphatase
, type II inositol-3,4-bisphosphate 4-phosphatase
, inositol polyphosphate 4-phosphatase type II
, inositol polyphosphate-4-phosphatase type II 105kD
, inositol polyphosphate-4-phosphatase, type II, 105kD
, inositol polyphosphate 4-phosphatase II; 4-phosphatase II