Nuclear Pore Complex Proteins
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Subject Areas on Research
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A high-throughput CRISPR interference screen for dissecting functional regulators of GPCR/cAMP signaling.
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A nuclear role for the Fragile X mental retardation protein.
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A phospholipase C-dependent inositol polyphosphate kinase pathway required for efficient messenger RNA export.
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Allosteric modulation of nucleoporin assemblies by intrinsically disordered regions.
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Amino acid permeases require COPII components and the ER resident membrane protein Shr3p for packaging into transport vesicles in vitro.
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Analysis of cellular factors that mediate nuclear export of RNAs bearing the Mason-Pfizer monkey virus constitutive transport element.
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Association of the kinesin-binding domain of RanBP2 to KIF5B and KIF5C determines mitochondria localization and function.
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Characterization of RanBP2-associated molecular components in neuroretina.
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Cyclophilin-related protein RanBP2 acts as chaperone for red/green opsin.
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Differential loss of prolyl isomerase or chaperone activity of Ran-binding protein 2 (Ranbp2) unveils distinct physiological roles of its cyclophilin domain in proteostasis.
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Distinct and atypical intrinsic and extrinsic cell death pathways between photoreceptor cell types upon specific ablation of Ranbp2 in cone photoreceptors.
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Domain-specific antibodies reveal multiple-site topology of Nup153 within the nuclear pore complex.
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Efficiency, selectivity, and robustness of nucleocytoplasmic transport.
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Evolutionary biology: Genes to make new species.
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Formation of Tap/NXT1 heterodimers activates Tap-dependent nuclear mRNA export by enhancing recruitment to nuclear pore complexes.
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Functional consequences of natural sequence variation in the activation domain of HIV-1 Rev.
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Genomic organization, expression, and localization of murine Ran-binding protein 2 (RanBP2) gene.
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Haploinsufficiency of RanBP2 is neuroprotective against light-elicited and age-dependent degeneration of photoreceptor neurons.
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Identification of RanBP2- and kinesin-mediated transport pathways with restricted neuronal and subcellular localization.
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Identification of a novel cellular cofactor for the Rev/Rex class of retroviral regulatory proteins.
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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 E2I (ubc9) and Ranbp2.
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Inhibition of human immunodeficiency virus Rev and human T-cell leukemia virus Rex function, but not Mason-Pfizer monkey virus constitutive transport element activity, by a mutant human nucleoporin targeted to Crm1.
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Interconversion of red opsin isoforms by the cyclophilin-related chaperone protein Ran-binding protein 2.
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Kinesin-1 and mitochondrial motility control by discrimination of structurally equivalent but distinct subdomains in Ran-GTP-binding domains of Ran-binding protein 2.
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Loss of Ranbp2 in motoneurons causes disruption of nucleocytoplasmic and chemokine signaling, proteostasis of hnRNPH3 and Mmp28, and development of amyotrophic lateral sclerosis-like syndromes.
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Metabolic labeling enables selective photocrosslinking of O-GlcNAc-modified proteins to their binding partners.
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Microglial activation in an amyotrophic lateral sclerosis-like model caused by Ranbp2 loss and nucleocytoplasmic transport impairment in retinal ganglion neurons.
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Necroptosis regulates tumor repopulation after radiotherapy via RIP1/RIP3/MLKL/JNK/IL8 pathway.
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Neuroprotection 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.
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Nuclear export of late HIV-1 mRNAs occurs via a cellular protein export pathway.
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Nuclear pore component Nup98 is a potential tumor suppressor and regulates posttranscriptional expression of select p53 target genes.
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Nucleoporin 153 links nuclear pore complex to chromatin architecture by mediating CTCF and cohesin binding.
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Positive and negative phosphorylation regulates RIP1- and RIP3-induced programmed necrosis.
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Protein sequence requirements for function of the human T-cell leukemia virus type 1 Rex nuclear export signal delineated by a novel in vivo randomization-selection assay.
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RANBP2 is an allosteric activator of the conventional kinesin-1 motor protein, KIF5B, in a minimal cell-free system.
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RIP3 induces apoptosis independent of pronecrotic kinase activity.
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RPGRIP1s with distinct neuronal localization and biochemical properties associate selectively with RanBP2 in amacrine neurons.
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RanBP2 modulates Cox11 and hexokinase I activities and haploinsufficiency of RanBP2 causes deficits in glucose metabolism.
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Ranbp2 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).
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Regulation of myeloid leukaemia by the cell-fate determinant Musashi.
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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.
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TNF-induced necroptosis and PARP-1-mediated necrosis represent distinct routes to programmed necrotic cell death.
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Targeting the cyclophilin domain of Ran-binding protein 2 (Ranbp2) with novel small molecules to control the proteostasis of STAT3, hnRNPA2B1 and M-opsin.
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The COPI complex functions in nuclear envelope breakdown and is recruited by the nucleoporin Nup153.
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The Nuclear Pore Complex in Cell Type-Specific Chromatin Structure and Gene Regulation.
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The SQSTM1-NUP214 fusion protein interacts with Crm1, activates Hoxa and Meis1 genes, and drives leukemogenesis in mice.
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The cyclophilin-like domain mediates the association of Ran-binding protein 2 with subunits of the 19 S regulatory complex of the proteasome.
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The cyclophilin-like domain of Ran-binding protein-2 modulates selectively the activity of the ubiquitin-proteasome system and protein biogenesis.
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The docking of kinesins, KIF5B and KIF5C, to Ran-binding protein 2 (RanBP2) is mediated via a novel RanBP2 domain.
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The zinc finger cluster domain of RanBP2 is a specific docking site for the nuclear export factor, exportin-1.
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Uncoupling phototoxicity-elicited neural dysmorphology and death by insidious function and selective impairment of Ran-binding protein 2 (Ranbp2).