Exploring the molecular etiology of dominant-negative mutations.
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Crystal Structure and Molecular Imaging of the Nav Channel 3 Subunit Indicates a Trimeric AssemblySorghum mutant RG displays antithetic leaf shoot lignin accumulation resulting in improved stem saccharification propertiesSuppressor of sessile spikelets1 functions in the ramosa pathway controlling meristem determinacy in maize.Characterising and predicting haploinsufficiency in the human genome.A small basic protein from the brz-brb operon is involved in regulation of bop transcription in Halobacterium salinarum.Severe anemia in the Nan mutant mouse caused by sequence-selective disruption of erythroid Kruppel-like factor.The genetic control of growth rate: a systems biology study in yeast.Tempo and mode of gene duplication in mammalian ribosomal protein evolution.P0S63del impedes the arrival of wild-type P0 glycoprotein to myelin in CMT1B mice.Convergent gene loss following gene and genome duplications creates single-copy families in flowering plantsGene expression regulation in the context of mouse interspecific mosaic genomesDissecting disease inheritance modes in a three-dimensional protein network challenges the "guilt-by-association" principle.Systematic morphological profiling of human gene and allele function via Cell Painting.A new look at sodium channel β subunitsDominant-negative proteins in herpesviruses - from assigning gene function to intracellular immunization.Mutagenesis of ARS2 Domains To Assess Possible Roles in Cell Cycle Progression and MicroRNA and Replication-Dependent Histone mRNA Biogenesis.Overexpression of a functional calcium-sensing receptor dramatically increases osteolytic potential of MDA-MB-231 cells in a mouse model of bone metastasis through epiregulin-mediated osteoprotegerin downregulation.AIRE is a critical spindle-associated protein in embryonic stem cells.Decoding disease-causing mechanisms of missense mutations from supramolecular structures.Dosage-sensitive genes in evolution and disease.KLHL3 Knockout Mice Reveal the Physiological Role of KLHL3 and the Pathophysiology of Pseudohypoaldosteronism Type II Caused by Mutant KLHL3.On gene dosage balance in protein complexes: a comment on Semple JI, Vavouri T, Lehner B. A simple principle concerning the robustness of protein complex activity to changes in gene expression.Phosphate regulation of lipid biosynthesis in Arabidopsis is independent of the mitochondrial outer membrane DGS1 complex.A dominant mutation in the light-oxygen and voltage2 domain vicinity impairs phototropin1 signaling in tomato.The LCB2 subunit of the sphingolip biosynthesis enzyme serine palmitoyltransferase can function as an attenuator of the hypersensitive response and Bax-induced cell death.Fibronectin type III and intracellular domains of Toll-like receptor 4 interactor with leucine-rich repeats (Tril) are required for developmental signaling.Multiple PPR protein interactions are involved in the RNA editing system in Arabidopsis mitochondria and plastids.The tobacco BLADE-ON-PETIOLE2 gene mediates differentiation of the corolla abscission zone by controlling longitudinal cell expansion.Molecular Evolution and Functional Characterization of a Bifunctional Decarboxylase Involved in Lycopodium Alkaloid Biosynthesis.Mechanisms of Mendelian dominance.Heterozygous Truncating Variants in POMP Escape Nonsense-Mediated Decay and Cause a Unique Immune Dysregulatory Syndrome.
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P2860
Exploring the molecular etiology of dominant-negative mutations.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 14 December 2007
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Exploring the molecular etiology of dominant-negative mutations.
@en
Exploring the molecular etiology of dominant-negative mutations.
@nl
type
label
Exploring the molecular etiology of dominant-negative mutations.
@en
Exploring the molecular etiology of dominant-negative mutations.
@nl
prefLabel
Exploring the molecular etiology of dominant-negative mutations.
@en
Exploring the molecular etiology of dominant-negative mutations.
@nl
P2860
P356
P1433
P1476
Exploring the molecular etiology of dominant-negative mutations.
@en
P2093
Reiner A Veitia
P2860
P304
P356
10.1105/TPC.107.055053
P577
2007-12-14T00:00:00Z