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Protein neurofilament

The leucine zipper DNA-binding proteins, described in Chapter 10, are examples of globular proteins that use coiled coils to form both homo- and heterodimers. A variety of fibrous proteins also have heptad repeats in their sequences and use coiled coils to form oligomers, mainly dimers and trimers. Among these are myosin, fibrinogen, actin cross-linking proteins such as spectrin and dystrophin as well as the intermediate filament proteins keratin, vimentin, desmin, and neurofilament proteins. [Pg.287]

Multiple sclerosis The 150-kDa calpain specific degradation product of a-spectrin increases 50% in human MS plaques.44 Degradation of the 68-kDa neurofilament protein is inhibited by a synthetic calpain inhibitor45... [Pg.313]

Takahashi S., Iwanaga T Takahashi Y., Nakano Y., et al. (1984). Neuron-specific enolase, neurofilament protein and S-100 protein protein in the olfactory mucosa of human fetuses an immunohistochemical study. Cell Tiss Res 238, 231-234. [Pg.251]

The reaction of anti-neurofilament antibodies with high molecular weight aggregates from rat neuronal cytoskeletal proteins provided direct evidence for neurofilament cross-linking after 2,5-hexanedione administration (Lapadula et al. 1986). Immunoblotting with antibodies specific for phosphorylated forms of cytoskeletal proteins has demonstrated a reduction of phosphorylation in neurofilament proteins and microtubule-associated-protein 2 (MAP-2) after 2,5-hexanedione treatment (Abou-Donia et al. 1988). [Pg.121]

Lapadula DM, Irwin RD, Suwita E et al. 1986. Cross-linking of neurofilament proteins of rat spinal cord in vivo after administration of 2,5-hexanedione. J Neurochem 46 1843-1850. [Pg.239]

Rats given 2mmol/kg allyl chloride by subcutaneous injection 5 days/week for 3 months showed clinical signs of neurotoxicity after the treatment period and biochemical evidence of neurofilament protein accumulation in both the central and peripheral nervous systems. However, no evidence of neurofilament protein cross-linking was found, suggesting that allyl chloride may not share a common mechanism for the accumulation of neurofilaments with other neurotoxins such as 2, 5-hexanedione. [Pg.33]

Nagano M, Yamamoto H, Harada K, et ah Comparative study of modification and degradation of neurofilament proteins in rats subchronically treated with allyl chloride, acrylamide or 2, 5-hexanedione. Environ Res 63 229-240, 1993... [Pg.34]

Other research being conducted at Case Western Reserve University under the direction of Dr. Lawrence Sayre is a study in which analogs of 2,5-hexanedione will be synthesized, studied chemically, and biologically evaluated in an effort to clarify the structural basis of toxicity, particularly in respect to the direct chemical modification of neurofilament proteins by these analogs or any of their metabolites. [Pg.52]

Selkoe, D. J., Abraham, C., and Ihara, Y. (1982). Brain transglutaminase In vitro crosslinking of human neurofilament proteins into insoluble polymers. Proc. Natl. Acad. Sci. USA 79, 6070-6074. [Pg.149]

Beitner-Johnson D., Guitart X., and Nestler E.J. (1992) Neurofilament proteins and the mesolimbic dopamine system common regulation by chronic morphine and chronic cocaine in the rat ventral tegmental area./ Neurosci 12(6) 2165-2176. [Pg.42]

Vaidya V.A., Terwilliger R.Z., and Duman R.S. (2000) Alterations in heavy and light neurofilament proteins in hippocampus following chronic ECS administration. Synapse 35(2) 137-43. [Pg.43]

Guitart, Xavier, Dana Bcitner-Johnson, David W. Marby, Therese A. Kosten, and Eric J. Nestler. 1992. "Fischer and Lewis Rat Strains Differ in Basal Levels of Neurofilament Proteins and Their Regulation by Chronic Morphine in the Mesolimbic Dopamine System." Synapse 12 242-53. [Pg.101]

More recent work suggested that one of four 4.1 proteins—4.1R—may associate with neurofilament proteins in forebrain postsynaptic densities, thus regulating the associated spectrin-rich cortex (Scott et al, 2001). Blot overlay analyses demonstrated that, in addition to spectrin and actin, postsynaptic density polypeptides included NF-L and o-internexin as interacting partners for 4.1R. Collectively, these studies emphasize that common themes are used in different cell types to both strengthen plasma membrane domains enriched in actin and IF polypeptides and to coordinate these sites with cytoplasmic architecture. [Pg.168]

Yabe,J. T.,Jung, C., Chan, W. K., and Shea, T. B. (2000). Phospho-dependent association of neurofilament proteins with kinesin in situ. Cell Motil. Cytoskeleton 45,... [Pg.202]

Yabe, J. T., Pimenta, A., and Shea, T. B. (1999). Kinesin-mediated transport of neurofilament protein oligomers in growing axons./ Cell Sri. 112(Pt 21), 3799-3814. [Pg.202]

Bajo, M., Yoo, B. C., Cairns, N., Geatzer M., Lubec, G. (2001). Neurofilament proteins NF-L, NF-M and NF-H in brain of patients with Down syndrome and Alzheimer s disease. Amino Acids 21, 293-301. [Pg.294]

Millecamps S, Robertson J, Laiiviere R, MaUet J, Juhen JP (2006) Defective axonal transport of neurofilament proteins in neurons overexpressing peripherin. J Neurochem 98 926-938... [Pg.94]

Table 7 lists S-100-positive tumors and their positivity with additional markers. Myelin basic protein (MBP) (30) is a single-chain polypeptide associated with the central and peripheral nervous system. Glial fibrillary acidic protein (GFAP) and neurofilament proteins (NFP) are intermediate filaments associated with glial cells and neural cells, respectively. HMB-45 is a mouse monoclonal antibody that reacts with an antigen present in premelanosomes. It is highly sensitive and specific for melanomas and certain nevi (junctional, congenital, blue nevi). EMA has been discussed in Section 3.1.3.1. [Pg.420]

Prahlad V, Helfand BT, Langford GM, Vale RD, Goldman RD. 2000. Fast transport of neurofilament protein along microtubules in squid axoplasm. J. Cell Sci. 113 3939—46... [Pg.144]

Evidence of selective oxidative damage, resulting from redox imbalance, involving neurons tied to AD is accumulating. The advanced gly-cation end products, nitration, lipid peroxidation adduction products, carbonyl-modified neurofilament protein, and free carbonyls belong to the list (200). The question remains whether the oxidative damage is caused by A)3, known to possess oxidative and hydrolytic properties (286, 287), or by other factors, whereas Aj3 is released as an antioxidant in response to oxidative stress (200). As in other groups of potential AD therapeutics there is a noticeable difference between their behavior in vitro and in vivo. A number of potential antioxidants are or have been in clinical trials... [Pg.767]

Savory J, Huang Y, Herman MM, Wills MR. Quantitative image analysis of temporal changes in tau and neurofilament proteins during the course of acute experimental neurofibrillary degeneration Non-phosphorylated epitopes precede phosphorylation. Brain Res 1996 707 272-81. [Pg.1389]

Immunoreactivity for parvalbumin and the neurofilament protein SMl-32 identifies the ventral pallidum (Paxinos etal., in press [a]). We retained the term substantia innominata and identified dorsal, ventral (as in Grove, 1988), and basal components with the assistance of G. Alheid. The basal component is marked by some positivity in tyrosine hydroxylase but is negative for SMl-32 (although surrounding areas are positive). [Pg.130]


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Neurofilaments

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