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INPP4B encodes the inositol polyphosphate 4-phosphatase type II, one of the enzymes involved in phosphatidylinositol signaling pathways. De plus, nous expédions INPP4B Anticorps (25) et INPP4B Protéines (5) et beaucoup plus de produits pour cette protéine.
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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.
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 (Montrer AKT1 Kits ELISA) 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 (Montrer ESR1 Kits ELISA) plays a protective role in bladder cancer initiation and growth at least partly via modulating the INPP4B/Akt (Montrer AKT1 Kits ELISA) 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 pathway caused by the decrease in INPP4B in granulosa cells promotes an ovarian environment defective in folliculogenesis and conducive to teratoma 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 (Montrer EPO Kits ELISA) responsiveness through a negative regulation of the PI3K/Akt (Montrer AKT1 Kits ELISA) pathway
INPP4B acted as a tumour suppressor in human prostate cancer
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 (Montrer IRF2 Kits ELISA) knockdown inhibits growth, colony formation of OCI/AML-2 (Montrer RUNX3 Kits ELISA), OCI/AML-3 (Montrer RUNX2 Kits ELISA), and THP-1 (Montrer GLI2 Kits ELISA) cells. In addition, IRF2 (Montrer IRF2 Kits ELISA) knockdown induces apoptosis of acute myeloid leukemia (Montrer BCL11A Kits ELISA) (AML (Montrer RUNX1 Kits ELISA)) cells by regulating apoptotic effectors. Further mechanism analysis shows that INPP4B contributes to the effects of IRF2 (Montrer IRF2 Kits ELISA) on apoptosis and growth of AML (Montrer RUNX1 Kits ELISA) cells. Thus, IRF2 (Montrer IRF2 Kits ELISA) serves as an important regulator in AML (Montrer RUNX1 Kits ELISA) by targeting INPP4B.
Immunohistochemical assessment of nestin (Montrer NES Kits ELISA) 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 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 cell survival, potentially by regulating EMT (Montrer ITK Kits ELISA) through the PI3K (Montrer PIK3CA Kits ELISA)/Akt (Montrer AKT1 Kits ELISA) signaling pathway
Mechanism analyses found polyphosphate 4-phosphatase type II (INPP4B) was the target of miR (Montrer MLXIP Kits ELISA)-937, miR (Montrer MLXIP Kits ELISA)-937 directly bound to the 3'UTR (Montrer UTS2R Kits ELISA) of INPP4B, knockdown of INPP4B in A549 with miR (Montrer MLXIP Kits ELISA)-937 inhibitor promoted anchorage -dependent and -independent growth, suggesting miR (Montrer MLXIP Kits ELISA)-937 contributed to cell proliferation of lung cancer
INPP4B expression is associated with enhanced ATM (Montrer ATM Kits ELISA)-dependent DNA double strand break repair, which could be mediated by p65 nuclear translocation.
Studies indicate that phosphatidylinositol 4-phosphate phosphatase (INPP4B) that acting as tumor suppressors by antagonizing AKT (Montrer AKT1 Kits ELISA) signaling at endosomes.
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