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The protein encoded by INPP5E is an inositol 1,4,5-trisphosphate (InsP3) 5-phosphatase. Additionally we are shipping INPP5E Antibodies (19) and and many more products for this protein.
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The expression levels of the INPP5E gene in NTD mouse embryos were significantly lower compared with control embryos, at the time of neural tube closure (gestational day 11.5). The INPP5E gene regulates the process of embryonic neural development. Abnormal levels of expression of the INPP5E gene may contribute to NTDs.
Therefore our study identifies a compartmentalized PtdIns(3,4,5)P3/AKT (show AKT1 Proteins)/GSK3beta signaling axis at cilia in SHH (show SHH Proteins)-dependent medulloblastoma that is regulated by INPP5E to maintain tumor cell cilia, promote SHH (show SHH Proteins) signaling and thereby medulloblastoma progression.
we identify Inpp5e as an essential inhibitor of the PI3K/Akt (show AKT1 Proteins)/mTORC1 signaling axis in renal epithelial cells, and demonstrate a critical role for Inpp5e-dependent mTORC1 regulation in Polycystic kidney disease (PKD (show PRKD1 Proteins)) suppression
INPP5E localizes to centrosomes, chromosomes, and kinetochores in early mitosis and shuttles to the midzone spindle at mitotic exit.
INPP5E is an essential point of convergence between Hedgehog (show SHH Proteins) and phosphoinositide signaling at cilia that maintains transition zone function and Hedgehog (show SHH Proteins)-dependent embryonic development.
the affinity to PDE6delta and the release by Arl2 (show ARL2 Proteins)/3 in addition to a retention signal are the determinants for cargo sorting and enrichment at its destination.
PIPKIgamma and INPP5E localize to the centrosome and coordinate the initiation of ciliogenesis.
Inpp5e, through functional interactions with Rab20 (show RAB20 Proteins) on the phagosome, activates Rab5 (show RAB5A Proteins), which, in turn, increases PtdIns3P and delays phagosome acidification.
Inpp5e and SHIP1 (show INPP5D Proteins) exhibit specificity in regulating FcgammaR- versus CR3 (show ITGAM Proteins)-stimulated phagocytosis by controlling the amplitude and duration of PtdIns(3,4,5)P(3) at the phagocytic cup.
Inpp5e mutations cause primary cilium signaling defects, ciliary instability and ciliopathies in the mouse.
miR598 contributed to cell proliferation and cell cycle progression in colorectal carcinoma by targeting INPP5E.
INPP5E associates with the N-terminus of RPGR (show RPGR Proteins) and trafficking of INPP5E to cilia is dependent upon the ciliary localization of RPGR (show RPGR Proteins).
we identify Inpp5e as an essential inhibitor of the PI3K (show PIK3CA Proteins)/Akt (show AKT1 Proteins)/mTORC1 signaling axis in renal epithelial cells, and demonstrate a critical role for Inpp5e-dependent mTORC1 regulation in Polycystic kidney disease (PKD (show PRKD1 Proteins)) suppression
ARL13B (show ARL13B Proteins) regulates IFT-A-mediated retrograde protein trafficking within cilia through its interaction with INPP5E.
In neuronal cells, INPP5E knockdown strongly inhibited autophagy by impairing the autophagosome-lysosome fusion step.
MKS1 (show MKS1 Proteins) functions in the transition zone at the base of the cilium to regulate ciliary INPP5E content.
These findings establish the first direct link between AURKA (show AURKA Proteins) and phosphoinositide signaling and suggest that the function of INPP5E in cilia is at least partly mediated by its interactions with AURKA (show AURKA Proteins)
The protein encoded by this gene is an inositol 1,4,5-trisphosphate (InsP3) 5-phosphatase. InsP3 5-phosphatases hydrolyze Ins(1,4,5)P3, which mobilizes intracellular calcium and acts as a second messenger mediating cell responses to various stimulation. Studies of the mouse counterpart suggest that this protein may hydrolyze phosphatidylinositol 3,4,5-trisphosphate and phosphatidylinositol 3,5-bisphosphate on the cytoplasmic Golgi membrane and thereby regulate Golgi-vesicular trafficking. Mutations in this gene cause Joubert syndrome\; a clinically and genetically heterogenous group of disorders characterized by midbrain-hindbrain malformation and various associated ciliopathies that include retinal dystrophy, nephronophthisis, liver fibrosis and polydactyly.
72 kDa inositol polyphosphate 5-phosphatase
, inositol polyphosphate-5-phosphatase, 72 kDa
, phosphatidylinositol 4,5-bisphosphate 5-phosphatase
, phosphatidylinositol polyphosphate 5-phosphatase type IV
, phosphatidylinositol-4,5-bisphosphate 5-phosphatase
, 5-phosphatase that induces arborization
, inositol polyphosphate 5-phosphatase
, phosphatidylinositol (4,5) bisphosphate 5-phosphatase
, inositol polyphosphate-5-phosphatase E
, peptidase (mitochondrial processing) alpha