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The protein encoded by INPP5E is an inositol 1,4,5-trisphosphate (InsP3) 5-phosphatase. Zusätzlich bieten wir Ihnen INPP5E Proteine (5) und viele weitere Produktgruppen zu diesem Protein an.
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Therefore our study identifies a compartmentalized PtdIns(3,4,5)P3/AKT (zeige AKT1 Antikörper)/GSK3beta signaling axis at cilia in SHH (zeige SHH Antikörper)-dependent medulloblastoma that is regulated by INPP5E to maintain tumor cell cilia, promote SHH (zeige SHH Antikörper) signaling and thereby medulloblastoma progression.
we identify Inpp5e as an essential inhibitor of the PI3K/Akt (zeige AKT1 Antikörper)/mTORC1 signaling axis in renal epithelial cells, and demonstrate a critical role for Inpp5e-dependent mTORC1 regulation in Polycystic kidney disease (PKD (zeige PRKD1 Antikörper)) 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 (zeige SHH Antikörper) and phosphoinositide signaling at cilia that maintains transition zone function and Hedgehog (zeige SHH Antikörper)-dependent embryonic development.
the affinity to PDE6delta and the release by Arl2 (zeige ARL2 Antikörper)/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 (zeige RAB20 Antikörper) on the phagosome, activates Rab5 (zeige RAB5A Antikörper), which, in turn, increases PtdIns3P and delays phagosome acidification.
Inpp5e and SHIP1 (zeige INPP5D Antikörper) exhibit specificity in regulating FcgammaR- versus CR3 (zeige ITGAM Antikörper)-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 (zeige RPGR Antikörper) and trafficking of INPP5E to cilia is dependent upon the ciliary localization of RPGR (zeige RPGR Antikörper).
we identify Inpp5e as an essential inhibitor of the PI3K (zeige PIK3CA Antikörper)/Akt (zeige AKT1 Antikörper)/mTORC1 signaling axis in renal epithelial cells, and demonstrate a critical role for Inpp5e-dependent mTORC1 regulation in Polycystic kidney disease (PKD (zeige PRKD1 Antikörper)) suppression
ARL13B (zeige ARL13B Antikörper) 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 (zeige MKS1 Antikörper) 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 (zeige AURKA Antikörper) and phosphoinositide signaling and suggest that the function of INPP5E in cilia is at least partly mediated by its interactions with AURKA (zeige AURKA Antikörper)
Proteomic analysis identified INPP5E, whose mutations also lead to Joubert syndrome as novel prenyl-dependent cargo of PDE6D (zeige PDE6D Antikörper). Mutant PDE6D (zeige PDE6D Antikörper) 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