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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
Here we show that OCRL1 is part of the membrane-trafficking machinery operating at the trans-Golgi network (TGN (show TG Proteins))/endosome interface.
Authors propose that the precise spatial and temporal activation of Rab35 (show RAB35 Proteins) 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 (show INPP5B Proteins)-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.
The crystal structures of human OCRL in complex with phosphoinositide substrate analogs revealed a membrane interaction patch likely to assist in sequestering substrates from the lipid bilayer.
Implications of OCRL and TRPV4 (show TRPV4 Proteins) in primary cilia function may also shed light on mechanosensation in other organ systems.
Dent disease is caused by mutations in at least two genes, i.e. CLCN5 (show CLCN5 Proteins) and OCRL1, and its genetic background and phenotypes are common among European countries and the USA.
Three Chinese children were diagnosed with Lowe syndrome through clinical and genetic analyses. And two novel mutations in the OCRL gene were identified
a role of OCRL in cilia maintenance and suggest the involvement of ciliary dysfunction in the manifestation of Lowe syndrome.
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 (show INPP5B Proteins) 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