Structural analysis of the GAP-related domain from neurofibromin and its implications
about
Structural basis for activation and non-canonical catalysis of the Rap GTPase activating protein domain of plexinCrystal structure of the GTPase-activating protein-related domain from IQGAP1Regulation of small GTPases by GEFs, GAPs, and GDIsCrystal structure of the GAP domain of Gyp1p: first insights into interaction with Ypt/Rab proteinsStructure of the ExoS GTPase activating domainStructure of a fast kinesin: implications for ATPase mechanism and interactions with microtubules.Crystal structure of the plexin A3 intracellular region reveals an autoinhibited conformation through active site sequestrationCrystal structure of a truncated urease accessory protein UreF from Helicobacter pyloriStructural and biochemical consequences of NF1 associated nontruncating mutations in the Sec14-PH module of neurofibrominTfs1p, a member of the PEBP family, inhibits the Ira2p but not the Ira1p Ras GTPase-activating protein in Saccharomyces cerevisiaeNeurofibromatosis type 1 alternative splicing is a key regulator of Ras signaling in neuronsThe semaphorin 3A receptor may directly regulate the activity of small GTPases.Ca2+-dependent GTPase, extra-large G protein 2 (XLG2), promotes activation of DNA-binding protein related to vernalization 1 (RTV1), leading to activation of floral integrator genes and early flowering in Arabidopsis.NF1 gene mutations represent the major molecular event underlying neurofibromatosis-Noonan syndrome.Structure-energy-based predictions and network modelling of RASopathy and cancer missense mutationsGenetic effects on human cognition: lessons from the study of mental retardation syndromesA Homogenous Bioluminescent System for Measuring GTPase, GTPase Activating Protein, and Guanine Nucleotide Exchange Factor Activities.Structural mechanisms of plexin signalingDirect evidence that a conserved arginine in RuvB AAA+ ATPase acts as an allosteric effector for the ATPase activity of the adjacent subunit in a hexamer.A method to determine 18 O kinetic isotope effects in the hydrolysis of nucleotide triphosphates.Interaction between a Domain of the Negative Regulator of the Ras-ERK Pathway, SPRED1 Protein, and the GTPase-activating Protein-related Domain of Neurofibromin Is Implicated in Legius Syndrome and Neurofibromatosis Type 1.Mapping the functional versatility and fragility of Ras GTPase signaling circuits through in vitro network reconstitution.A novel stem loop control element-dependent UGA read-through system without translational selenocysteine incorporation in Drosophila.The neurofibromin recruitment factor Spred1 binds to the GAP related domain without affecting Ras inactivationTransition state structures and the roles of catalytic residues in GAP-facilitated GTPase of Ras as elucidated by (18)O kinetic isotope effects.Genetic basis of cognitive disability.Connections between constitutional mismatch repair deficiency syndrome and neurofibromatosis type 1.Site-specific monoubiquitination activates Ras by impeding GTPase-activating protein functionMinor lesion mutational spectrum of the entire NF1 gene does not explain its high mutability but points to a functional domain upstream of the GAP-related domain.Neurofibromin physically interacts with the N-terminal domain of focal adhesion kinaseNeurofibromin GTPase-activating protein-related domains restore normal growth in Nf1-/- cells.The Structural Basis for Cdc42-Induced Dimerization of IQGAPs.The spectrum of NF1 mutations in Korean patients with neurofibromatosis type 1.Screening in silico predicted remotely acting NF1 gene regulatory elements for mutations in patients with neurofibromatosis type 1.NF1 modulates the effects of Ras oncogenes: evidence of other NF1 function besides its GAP activity.GTPase stimulation in shrimp Ras(Q(61)K) with geranylgeranyl pyrophosphate but not mammalian GAP.Fluoride complexes of oncogenic Ras mutants to study the Ras-RasGap interaction.Functional analysis of a duplication (p.E63_D69dup) in the switch II region of HRAS: new aspects of the molecular pathogenesis underlying Costello syndrome.Neurofibromin is actively transported to the nucleus.New model for the interaction of IQGAP1 with CDC42 and RAC1.
P2860
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P2860
Structural analysis of the GAP-related domain from neurofibromin and its implications
description
1998 nî lūn-bûn
@nan
1998 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
1998 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
name
Structural analysis of the GAP-related domain from neurofibromin and its implications
@ast
Structural analysis of the GAP-related domain from neurofibromin and its implications
@en
type
label
Structural analysis of the GAP-related domain from neurofibromin and its implications
@ast
Structural analysis of the GAP-related domain from neurofibromin and its implications
@en
prefLabel
Structural analysis of the GAP-related domain from neurofibromin and its implications
@ast
Structural analysis of the GAP-related domain from neurofibromin and its implications
@en
P2093
P2860
P356
P1433
P1476
Structural analysis of the GAP-related domain from neurofibromin and its implications
@en
P2093
Ahmadian MR
Scheffzek K
Wiesmüller L
Wittinghofer A
P2860
P304
P356
10.1093/EMBOJ/17.15.4313
P407
P577
1998-08-01T00:00:00Z