Nuclear Pore Complex Proteins

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  Subject Areas on Research

  • A nuclear role for the Fragile X mental retardation protein. 
  • A phospholipase C-dependent inositol polyphosphate kinase pathway required for efficient messenger RNA export. 
  • Amino acid permeases require COPII components and the ER resident membrane protein Shr3p for packaging into transport vesicles in vitro. 
  • Analysis of cellular factors that mediate nuclear export of RNAs bearing the Mason-Pfizer monkey virus constitutive transport element. 
  • Association of the kinesin-binding domain of RanBP2 to KIF5B and KIF5C determines mitochondria localization and function. 
  • Characterization of RanBP2-associated molecular components in neuroretina. 
  • Competitive control of independent programs of tumor necrosis factor receptor-induced cell death by TRADD and RIP1. 
  • Cyclophilin-related protein RanBP2 acts as chaperone for red/green opsin. 
  • Differential loss of prolyl isomerase or chaperone activity of Ran-binding protein 2 (Ranbp2) unveils distinct physiological roles of its cyclophilin domain in proteostasis. 
  • Distinct and atypical intrinsic and extrinsic cell death pathways between photoreceptor cell types upon specific ablation of Ranbp2 in cone photoreceptors. 
  • Domain-specific antibodies reveal multiple-site topology of Nup153 within the nuclear pore complex. 
  • Efficiency, selectivity, and robustness of nucleocytoplasmic transport. 
  • Evolutionary biology: Genes to make new species. 
  • Formation of Tap/NXT1 heterodimers activates Tap-dependent nuclear mRNA export by enhancing recruitment to nuclear pore complexes. 
  • Functional consequences of natural sequence variation in the activation domain of HIV-1 Rev. 
  • Genomic organization, expression, and localization of murine Ran-binding protein 2 (RanBP2) gene. 
  • Haploinsufficiency of RanBP2 is neuroprotective against light-elicited and age-dependent degeneration of photoreceptor neurons. 
  • Identification of RanBP2- and kinesin-mediated transport pathways with restricted neuronal and subcellular localization. 
  • Identification of a novel cellular cofactor for the Rev/Rex class of retroviral regulatory proteins. 
  • 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. 
  • Interconversion of red opsin isoforms by the cyclophilin-related chaperone protein Ran-binding protein 2. 
  • Kinesin-1 and mitochondrial motility control by discrimination of structurally equivalent but distinct subdomains in Ran-GTP-binding domains of Ran-binding protein 2. 
  • 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. 
  • Metabolic labeling enables selective photocrosslinking of O-GlcNAc-modified proteins to their binding partners. 
  • Microglial activation in an amyotrophic lateral sclerosis-like model caused by Ranbp2 loss and nucleocytoplasmic transport impairment in retinal ganglion neurons. 
  • 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. 
  • Nuclear export of late HIV-1 mRNAs occurs via a cellular protein export pathway. 
  • Positive and negative phosphorylation regulates RIP1- and RIP3-induced programmed necrosis. 
  • 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. 
  • RANBP2 is an allosteric activator of the conventional kinesin-1 motor protein, KIF5B, in a minimal cell-free system. 
  • RIP3 induces apoptosis independent of pronecrotic kinase activity. 
  • RPGRIP1s with distinct neuronal localization and biochemical properties associate selectively with RanBP2 in amacrine neurons. 
  • RanBP2 modulates Cox11 and hexokinase I activities and haploinsufficiency of RanBP2 causes deficits in glucose metabolism. 
  • 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). 
  • Regulation of myeloid leukaemia by the cell-fate determinant Musashi. 
  • Reprogramming to pluripotency can conceal somatic cell chromosomal instability. 
  • 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. 
  • TNF-induced necroptosis and PARP-1-mediated necrosis represent distinct routes to programmed necrotic cell death. 
  • Targeting the cyclophilin domain of Ran-binding protein 2 (Ranbp2) with novel small molecules to control the proteostasis of STAT3, hnRNPA2B1 and M-opsin. 
  • The COPI complex functions in nuclear envelope breakdown and is recruited by the nucleoporin Nup153. 
  • The cyclophilin-like domain mediates the association of Ran-binding protein 2 with subunits of the 19 S regulatory complex of the proteasome. 
  • The cyclophilin-like domain of Ran-binding protein-2 modulates selectively the activity of the ubiquitin-proteasome system and protein biogenesis. 
  • The docking of kinesins, KIF5B and KIF5C, to Ran-binding protein 2 (RanBP2) is mediated via a novel RanBP2 domain. 
  • The zinc finger cluster domain of RanBP2 is a specific docking site for the nuclear export factor, exportin-1. 
  • Uncoupling phototoxicity-elicited neural dysmorphology and death by insidious function and selective impairment of Ran-binding protein 2 (Ranbp2).