ArticleThe Journal of cell biology1990
Characterization of dominant and recessive assembly-defective mutations in mouse neurofilament NF-M.
Article in The Journal of cell biology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 115 citations in OpenAlex.
- A review and analysis of the clinical literature on Charcot-Marie-Tooth disease caused by mutations in neurofilament protein L.Cytoskeleton (Hoboken, N.J.) · 2021Review
- Splice site, frameshift, and chimeric GFAP mutations in Alexander disease.Human mutation · 2012Article
- Assembly properties of lamprey neurofilament subunits and their expression after spinal cord transection.The Journal of comparative neurology · 2011Article
- Review of the multiple aspects of neurofilament functions, and their possible contribution to neurodegeneration.Molecular neurobiology · 2008Review
- Epidermolysis bullosa simplex-type mutations alter the dynamics of the keratin cytoskeleton and reveal a contribution of actin to the transport of keratin subunits.Molecular biology of the cell · 2004Article
- Mutation in neurofilament transgene implicates RNA processing in the pathogenesis of neurodegenerative disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Epithelial V-like antigen (EVA), a novel member of the immunoglobulin superfamily, expressed in embryonic epithelia with a potential role as homotypic adhesion molecule in thymus histogenesis.The Journal of cell biology · 1998Article
- Specific interaction of HTLV tax protein and a human type IV neuronal intermediate filament protein.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- The function of intermediate filaments in cell shape and cytoskeletal integrity.The Journal of cell biology · 1996Article
- Subunit composition of neurofilaments specifies axonal diameter.The Journal of cell biology · 1996Article
- The 66-kDa neurofilament protein (NF-66): sequence analysis and evolution.Neurochemical research · 1996Article
- Increasing neurofilament subunit NF-M expression reduces axonal NF-H, inhibits radial growth, and results in neurofilamentous accumulation in motor neurons.The Journal of cell biology · 1995Article
- Two distinct functions of the carboxyl-terminal tail domain of NF-M upon neurofilament assembly: cross-bridge formation and longitudinal elongation of filaments.The Journal of cell biology · 1995Article
- The importance of intramolecular ion pairing in intermediate filaments.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Determinants for intracellular sorting of cytoplasmic and nuclear intermediate filaments.The Journal of cell biology · 1994Article
- Differential dynamics of neurofilament-H protein and neurofilament-L protein in neurons.The Journal of cell biology · 1994Article
- Differential organization of desmin and vimentin in muscle is due to differences in their head domains.The Journal of cell biology · 1994Article
- An amino-terminal tetrapeptide specifies cotranslational degradation of beta-tubulin but not alpha-tubulin mRNAs.Molecular and cellular biology · 1994Article
- Intermediate filaments and disease: mutations that cripple cell strength.The Journal of cell biology · 1994Review
- Genetic mutations in the K1 and K10 genes of patients with epidermolytic hyperkeratosis. Correlation between location and disease severity.The Journal of clinical investigation · 1994Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We have generated a set of amino- and carboxy-terminal deletions of the neurofilament NF-M gene and determined the molecular consequences of forced expression of these mutant constructs in mouse fibroblasts. To follow the expression of mutant NF-M subunits in transfected cells, a 12 amino acid epitope (from the human c-myc protein) was expressed at the carboxy terminus of each mutant. We show that NF-M molecules missing up to 90 or 70% of the nonhelical carboxy-terminal tail or amino-terminal head domains, respectively, incorporate readily into an intermediate filament network comprised either of vimentin or NF-L, whereas deletions into either the amino- or carboxy-terminal alpha-helical rod region generate assembly-incompetent polypeptides. Carboxy-terminal deletions into the rod domain invariably yield dominant mutants which rapidly disrupt the array of filaments comprised of NF-L or vimentin. Accumulation of these mutant NF-M subunits disrupts vimentin filament arrays even when present at approximately 1% the level of the wild-type subunits. In contrast, the amino-terminal deletions into the rod produce pseudo-recessive mutants that perturb the wild-type NF-L or vimentin arrays only modestly. The inability of such amino-terminal mutants to disrupt wild-type subunits defines a region near the amino-terminal alpha-helical rod domain (residues 75-126) that is required for the earliest steps in filament assembly.
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