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anti-Rat (Rattus) OCRL Antikörper:
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Human Polyclonal OCRL Primary Antibody für IHC, IHC (p) - ABIN4341304
Bohdanowicz, Balkin, De Camilli, Grinstein: Recruitment of OCRL and Inpp5B to phagosomes by Rab5 and APPL1 depletes phosphoinositides and attenuates Akt signaling. in Molecular biology of the cell 2012
OCRL1 is required for renal tubular endocytosis.
Knockdown of OCRL1 in zebrafish caused developmental defects consistent with disruption of ciliary function.
results indicate a novel role for OCRL1 in neural development, and support a model whereby dysregulation of phosphoinositide metabolism and clathrin-mediated membrane traffic leads to the neurological symptoms of Lowe syndrome
OCRL1 gene mutation is responsible in the development od Lowe syndrome in Chinese families.
docrl ( phosphatidylinositol-5-phosphatase OCRL)regulation of endosomal traffic maintains hemocytes in a poised, but quiescent state, suggesting mechanisms by which endosomal misregulation of signaling may contribute to symptoms of Lowe syndrome
We discuss how studies of OCRL have led to important discoveries about the basic mechanisms of membrane trafficking and describe the key features and limitations of the currently available animal models of Lowe syndrome. Mutations in OCRL can also give rise to a milder pathology, Dent disease 2, which is characterized by renal Fanconi syndrome in the absence of extrarenal pathologies.
A diagnosis of Dent disease was established in 19 boys from 16 families by the presence of loss of function/deleterious mutations in CLCN5 (zeige CLCN5 Antikörper) or OCRL1.
Depleting or inhibiting OCRL leads to an accumulation of lysosomal PtdIns(4,5)P2, an inhibitor of the calcium channel mucolipin-1 (zeige MCOLN1 Antikörper) that controls autophagosome-lysosome fusion
Here we show that OCRL1 is part of the membrane-trafficking machinery operating at the trans-Golgi network (TGN (zeige TG Antikörper))/endosome interface.
Authors propose that the precise spatial and temporal activation of Rab35 (zeige RAB35 Antikörper) acts as a major switch for OCRL recruitment on newborn endosomes, post-scission PtdIns(4,5)P2 hydrolysis, and subsequent endosomal trafficking.
OCRL mRNA and protein were downregulated in osteoarthritis knee cartilage. OCRL inhibits Rac1 activation in OA.
OCRL-mutated fibroblasts from patients with Dent-2 disease exhibit INPP5B (zeige INPP5B Antikörper)-independent phenotypic variability relatively to Lowe syndrome cells.
Results indicate that inositol 5-phosphatase OCRL acts as an uncoating factor and that defects in clathrin-mediated endocytosis likely contribute to pathology in patients with OCRL mutations.
These results suggest that the functions of OCRL/INPP5B (zeige INPP5B Antikörper) and proton-chloride exchange transporter 5 converge on shared mechanisms, the impairment of which has a dramatic effect on proximal tubule endocytosis
Implications of OCRL and TRPV4 (zeige TRPV4 Antikörper) in primary cilia function may also shed light on mechanosensation in other organ systems.
Bcl10 was required to locally deliver the vesicular OCRL phosphatase that regulates PI(4,5)P(2) and F-actin turnover, both crucial for the completion of phagosome closure.
These results indicate a functional overlap of Ocrl and Inpp5b (zeige INPP5B Antikörper) in most cell lineages, especially in extraembryonic tissues.
The results indicate that OCRL1 restricts intracellular growth of L. pneumophila and binds to Legionella-containing vacuoles in association with Legionella LpnE.
This gene encodes a phosphatase enzyme that is involved in actin polymerization and is found in the trans-Golgi network. Mutations in this gene cause oculocerebrorenal syndrome of Lowe and also Dent disease.
inositol polyphosphate 5-phosphatase OCRL-1
, phosphatidylinositol polyphosphate 5-phosphatase
, phosphatidylinositol polyphosphate 5-phosphotase
, oculocerebrorenal syndrome of Lowe
, phosphatidylinositol polyphosphate 5-phosphatase-like
, inositol polyphosphate 5-phosphatase OCRL-1-like
, Lowe oculocerebrorenal syndrome protein