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The protein encoded by INPP5E is an inositol 1,4,5-trisphosphate (InsP3) 5-phosphatase. Additionally we are shipping INPP5E Proteins (5) and many more products for this protein.
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Therefore our study identifies a compartmentalized PtdIns(3,4,5)P3/AKT (show AKT1 Antibodies)/GSK3beta signaling axis at cilia in SHH (show SHH Antibodies)-dependent medulloblastoma that is regulated by INPP5E to maintain tumor cell cilia, promote SHH (show SHH Antibodies) signaling and thereby medulloblastoma progression.
we identify Inpp5e as an essential inhibitor of the PI3K/Akt (show AKT1 Antibodies)/mTORC1 signaling axis in renal epithelial cells, and demonstrate a critical role for Inpp5e-dependent mTORC1 regulation in Polycystic kidney disease (PKD (show PRKD1 Antibodies)) 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 Antibodies) and phosphoinositide signaling at cilia that maintains transition zone function and Hedgehog (show SHH Antibodies)-dependent embryonic development.
the affinity to PDE6delta and the release by Arl2 (show ARL2 Antibodies)/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 Antibodies) on the phagosome, activates Rab5 (show RAB5A Antibodies), which, in turn, increases PtdIns3P and delays phagosome acidification.
Inpp5e and SHIP1 (show INPP5D Antibodies) exhibit specificity in regulating FcgammaR- versus CR3 (show ITGAM Antibodies)-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.
INPP5E associates with the N-terminus of RPGR (show RPGR Antibodies) and trafficking of INPP5E to cilia is dependent upon the ciliary localization of RPGR (show RPGR Antibodies).
we identify Inpp5e as an essential inhibitor of the PI3K (show PIK3CA Antibodies)/Akt (show AKT1 Antibodies)/mTORC1 signaling axis in renal epithelial cells, and demonstrate a critical role for Inpp5e-dependent mTORC1 regulation in Polycystic kidney disease (PKD (show PRKD1 Antibodies)) suppression
ARL13B (show ARL13B Antibodies) 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 Antibodies) 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 Antibodies) and phosphoinositide signaling and suggest that the function of INPP5E in cilia is at least partly mediated by its interactions with AURKA (show AURKA Antibodies)
Proteomic analysis identified INPP5E, whose mutations also lead to Joubert syndrome as novel prenyl-dependent cargo of PDE6D (show PDE6D Antibodies). Mutant PDE6D (show PDE6D Antibodies) shows reduced binding to INPP5E, which fails to localize to primary cilia in patient fibroblasts and tissues.
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