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| 17015226 | NF-M | NF-M | 1.9 | obligate heteropolymers of NF light (NF-L), NF-L NF medium (NF-M), NF-M and NF heavy (NF-H) NF-H subunits and interestingly transgenic mice | |  |
| 17015226 | NF-M | NF-M | 1.9 | gene replacement to remove the phosphorylated _amp_#x201c tail_amp_#x201d domains of NF-M and NF-H that normally provide intra-axonal crosslinking of adjacent filaments | | |
| 17015226 | NF-M | NF-M | 1.9 | and volume after elimination of the tail domains of the NF-M and NF-H subunits Lobsiger et_amp_#xa0 al. 2005 provide extended survival | | |
| 17015226 | nf m | nf m | 1.0 | neurofilaments are obligate heteropolymers of nf light nf l nf medium nf m and nf heavy nf h subunits and interestingly transgenic mice expressing a point mutation in nf l develop motor neuron disease lee et_amp_#xa0;al. 1994 . | | |
| 17015226 | nf m | nf m | 1.0 | this was demonstrated to be the case by use of gene replacement to remove the phosphorylated _amp_#x201c;tail_amp_#x201d; domains of nf m and nf h that normally provide intra axonal crosslinking of adjacent filaments. | | |
| 17015226 | nf m | nf m | 1.0 | hin neurons i.e. gene disruption to remove all neurofilaments [ williamson et_amp_#xa0;al. 1998 ] or gene replacement to alter axonal structure and volume after elimination of the tail domains of the nf m and nf h subunits [ lobsiger et_amp_#xa0;al. 2005 ] provide extended survival of sod1 mutant mice but only by slowing disease onset. | | |