about
RanBP2 modulates Cox11 and hexokinase I activities and haploinsufficiency of RanBP2 causes deficits in glucose metabolismSpecies-specific subcellular localization of RPGR and RPGRIP isoforms: implications for the phenotypic variability of congenital retinopathies among speciesEvidence for RPGRIP1 gene as risk factor for primary open angle glaucomaRANBP2 is an allosteric activator of the conventional kinesin-1 motor protein, KIF5B, in a minimal cell-free systemHaploinsufficiency of RanBP2 is neuroprotective against light-elicited and age-dependent degeneration of photoreceptor neuronsLimited proteolysis differentially modulates the stability and subcellular localization of domains of RPGRIP1 that are distinctly affected by mutations in Leber's congenital amaurosisInterconversion of red opsin isoforms by the cyclophilin-related chaperone protein Ran-binding protein 2The zinc finger cluster domain of RanBP2 is a specific docking site for the nuclear export factor, exportin-1Neuroprotection resulting from insufficiency of RANBP2 is associated with the modulation of protein and lipid homeostasis of functionally diverse but linked pathways in response to oxidative stress.Loss of Ranbp2 in motoneurons causes disruption of nucleocytoplasmic and chemokine signaling, proteostasis of hnRNPH3 and Mmp28, and development of amyotrophic lateral sclerosis-like syndromesIdentification of RanBP2- and kinesin-mediated transport pathways with restricted neuronal and subcellular localization.Selective impairment of a subset of Ran-GTP-binding domains of ran-binding protein 2 (Ranbp2) suffices to recapitulate the degeneration of the retinal pigment epithelium (RPE) triggered by Ranbp2 ablation.Distinct and atypical intrinsic and extrinsic cell death pathways between photoreceptor cell types upon specific ablation of Ranbp2 in cone photoreceptors.Targeting the cyclophilin domain of Ran-binding protein 2 (Ranbp2) with novel small molecules to control the proteostasis of STAT3, hnRNPA2B1 and M-opsin.Selective loss of RPGRIP1-dependent ciliary targeting of NPHP4, RPGR and SDCCAG8 underlies the degeneration of photoreceptor neuronsRanbp2 haploinsufficiency mediates distinct cellular and biochemical phenotypes in brain and retinal dopaminergic and glia cells elicited by the Parkinsonian neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).Insights into X-linked retinitis pigmentosa type 3, allied diseases and underlying pathomechanismsUncoupling phototoxicity-elicited neural dysmorphology and death by insidious function and selective impairment of Ran-binding protein 2 (Ranbp2).RPGRIP1 is essential for normal rod photoreceptor outer segment elaboration and morphogenesis.Differential loss of prolyl isomerase or chaperone activity of Ran-binding protein 2 (Ranbp2) unveils distinct physiological roles of its cyclophilin domain in proteostasis.Gene and protein expression pilot profiling and biomarkers in an experimental mouse model of hypertensive glaucoma.Kinesin-1 and mitochondrial motility control by discrimination of structurally equivalent but distinct subdomains in Ran-GTP-binding domains of Ran-binding protein 2.Impairments in age-dependent ubiquitin proteostasis and structural integrity of selective neurons by uncoupling Ran GTPase from the Ran-binding domain 3 of Ranbp2 and identification of novel mitochondrial isoforms of ubiquitin-conjugating enzyme E2IRPGRIP1s with distinct neuronal localization and biochemical properties associate selectively with RanBP2 in amacrine neurons.The docking of kinesins, KIF5B and KIF5C, to Ran-binding protein 2 (RanBP2) is mediated via a novel RanBP2 domain.Bovine phospholipase C highly homologous to the norpA protein of Drosophila is expressed specifically in cones.The cyclophilin-like domain mediates the association of Ran-binding protein 2 with subunits of the 19 S regulatory complex of the proteasome.Characterization of RanBP2-associated molecular components in neuroretinaIsolation of retinal proteins that interact with retinitis pigmentosa GTPase regulator by interaction trap screen in yeastThe coming-of-age of nucleocytoplasmic transport in motor neuron disease and neurodegenerationCorrection to: The coming-of-age of nucleocytoplasmic transport in motor neuron disease and neurodegenerationMicroglial activation in an amyotrophic lateral sclerosis-like model caused by Ranbp2 loss and nucleocytoplasmic transport impairment in retinal ganglion neurons
P50
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P50
description
hulumtues
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Paulo A Ferreira
@nl
Paulo A Ferreira
@sl
Paulo A. Ferreira
@en
Paulo A. Ferreira
@es
type
label
Paulo A Ferreira
@nl
Paulo A Ferreira
@sl
Paulo A. Ferreira
@en
Paulo A. Ferreira
@es
prefLabel
Paulo A Ferreira
@nl
Paulo A Ferreira
@sl
Paulo A. Ferreira
@en
Paulo A. Ferreira
@es
P1053
S-4209-2016
P106
P21
P31
P3829
P496
0000-0003-4585-1717