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L1cam  -  L1 cell adhesion molecule

Rattus norvegicus

Synonyms: Caml1, Hsas, Hyd, N-CAM-L1, NCAM-L1, ...
 
 
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Disease relevance of L1cam

  • Moreover, antibodies to Ng-CAM inhibited fasciculation of neurites, a functional property shared with NILE [1].
  • Immunoprecipitation with L1 and NILE antibodies of [3H]fucose-labeled material from culture supernatants and detergent extracts of NGF-treated rat PC12 pheochromocytoma cells yielded comigrating bands by SDS-PAGE [2].
  • M21 melanoma cells displayed significant Ca(++)-dependent adhesion and spreading on immunopurified rat L1 (NILE) [3].
  • To understand the basis of L1CAM function in adhesion and migration, we quantified directly the diffusion characteristics of L1CAM on the upper surface of ND-7 neuroblastoma hybrid cells as an indication of receptor-cytoskeleton interactions [4].
  • Other activities present in the original sera are not specifically retained by recombinant fusion proteins, and Escherichia coli lysates made with nonrecombinant lambda gt11 do not absorb the anti-NILE activity.(ABSTRACT TRUNCATED AT 250 WORDS)[5]
 

Psychiatry related information on L1cam

 

High impact information on L1cam

 

Chemical compound and disease context of L1cam

  • In the presence of nerve growth factor (NGF), PC12 pheochromocytoma cells undergo neuronal differentiation with a concomitant 3- to 5-fold increase in the specific level of an Mr = 230,000 cell surface component named the NGF-inducible large external, or NILE, glycoprotein [10].
  • The findings suggest that D-NAP and 1-octanol selectively interact with NMDA receptors in an ethanol-dependent manner, further implicating the L1 cell adhesion molecule in alcohol-related brain disorders [11].
  • We investigated temporal and spatial changes of free cholesterol (FC) and neutral lipids (NLs) after brain ischemia with filipin complex staining to detect mainly FC and Nile Red staining for NLs such as cholesteryl ester (CE) and triacylglyceride (TAG) [12].
 

Biological context of L1cam

  • This released NILE is 15-20 kDa smaller than the detergent-extracted NILE and, in addition to lacking the anti-NILE-beta-gal epitope, does not contain the cytoplasmic site(s) of phosphorylation [13].
  • Exposed on the cell surface of sympathetic neurons in culture is a family of high molecular weight glycoproteins (B1, B2, B3, and B4, related to the NILE protein) which undergoes post-translational modification (Sweadner, K. J. (1983) J. Neurosci. 3: 2504-2517) [14].
  • Indirect excitation spectra for these components are distinct and the 4.5-ns component exhibits tryptophan to Nile Red energy transfer [15].
  • Since the soluble NILE and other released GPs had somewhat faster mobilities on SDS-polyacrylamide gels than their apparent membrane-bound correspondents, release could either be due to, or accompanied by, minor changes in molecular structure [16].
  • Photoreceptor organization and rhythmic phagocytosis in the nile rat Arvicanthis ansorgei: a novel diurnal rodent model for the study of cone pathophysiology [17].
 

Anatomical context of L1cam

 

Associations of L1cam with chemical compounds

  • Characterization of a partial cDNA clone for the NILE glycoprotein and identification of the encoded polypeptide domain [13].
  • The phosphate moiety of NILE GP is almost completely alkali labile, suggesting that phosphoserine groups predominate [10].
  • Concomitant with this is a significant induction in the incorporation of radiolabeled fucose or glucosamine into a 230,000-dalton cell surface glycoprotein named the NGF-Inducible Large External, or NILE, glycoprotein (GP) (McGuire, J. C., L. A. Greene, and A. V. Furano (1978) Cell 15: 357-365) [21].
  • The AO vesicular staining pattern was similar in cells labeled with the lamellar body marker phosphine 3R and the phospholipid dye nile red [22].
  • Nile Red does not alter tubulin polymerization, and polymerization in 2-(N-morpholino)ethanesulfonic acid (Mes) buffer does not alter the spectrum of the Nile Red-tubulin complex [15].
 

Other interactions of L1cam

 

Analytical, diagnostic and therapeutic context of L1cam

  • Both immunoprecipitation and immunofluorescence experiments indicate that the anti-NILE-beta-gal epitope is not exposed on the cell surface but is accessible only after cells are treated with detergent [18].
  • Both immunoprecipitation and immunofluorescence experiments indicate that the anti-NILE-beta-gal epitope is not exposed on the cell surface but is accessible only after cells are treated with detergent [13].
  • Finally, by sequential immunoprecipitation from detergent extracts of [35S]methionine-labeled early post-natal cerebellar cell cultures or [3H]fucose-labeled NGF-treated PC12 cells, all immunoreactivity for NILE antibody could be removed by pre-clearing with L1 antibody and vice versa [2].
  • Using quantitative immunoelectrophoresis, the action of NGF on NILE GP was represent an increase in the amount of protein, rather than a selective increase in carbohydrate incorporation [21].
  • In the current studies NILE GP was purified from PC12 cells using wheat germ agglutinin-agarose affinity chromatography and SDS-polyacrylamide gel electrophoresis (PAGE) [21].

References

  1. Nerve growth factor enhances expression of neuron-glia cell adhesion molecule in PC12 cells. Friedlander, D.R., Grumet, M., Edelman, G.M. J. Cell Biol. (1986) [Pubmed]
  2. Demonstration of immunochemical identity between the nerve growth factor-inducible large external (NILE) glycoprotein and the cell adhesion molecule L1. Bock, E., Richter-Landsberg, C., Faissner, A., Schachner, M. EMBO J. (1985) [Pubmed]
  3. Human neural cell adhesion molecule L1 and rat homologue NILE are ligands for integrin alpha v beta 3. Montgomery, A.M., Becker, J.C., Siu, C.H., Lemmon, V.P., Cheresh, D.A., Pancook, J.D., Zhao, X., Reisfeld, R.A. J. Cell Biol. (1996) [Pubmed]
  4. Ankyrin binding mediates L1CAM interactions with static components of the cytoskeleton and inhibits retrograde movement of L1CAM on the cell surface. Gil, O.D., Sakurai, T., Bradley, A.E., Fink, M.Y., Cassella, M.R., Kuo, J.A., Felsenfeld, D.P. J. Cell Biol. (2003) [Pubmed]
  5. Isolation of NILE glycoprotein-related cDNA probes. Sajovic, P., Ennulat, D.J., Shelanski, M.L., Greene, L.A. J. Neurochem. (1987) [Pubmed]
  6. Individual differences in rhythms of behavioral sleep and its neural substrates in Nile grass rats. Schwartz, M.D., Smale, L. J. Biol. Rhythms (2005) [Pubmed]
  7. Variability of diurnality in laboratory rodents. Refinetti, R. Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology. (2006) [Pubmed]
  8. Spatial regulation of axonal glycoprotein expression on subsets of embryonic spinal neurons. Dodd, J., Morton, S.B., Karagogeos, D., Yamamoto, M., Jessell, T.M. Neuron (1988) [Pubmed]
  9. The neuronal chondroitin sulfate proteoglycan neurocan binds to the neural cell adhesion molecules Ng-CAM/L1/NILE and N-CAM, and inhibits neuronal adhesion and neurite outgrowth. Friedlander, D.R., Milev, P., Karthikeyan, L., Margolis, R.K., Margolis, R.U., Grumet, M. J. Cell Biol. (1994) [Pubmed]
  10. Biochemical properties of the nerve growth factor-inducible large external (NILE) glycoprotein. Salton, S.R., Shelanski, M.L., Greene, L.A. J. Neurosci. (1983) [Pubmed]
  11. Synergistic effects of the peptide fragment D-NAPVSIPQ on ethanol inhibition of synaptic plasticity and NMDA receptors in rat hippocampus. Zhang, T.A., Hendricson, A.W., Wilkemeyer, M.F., Lippmann, M.J., Charness, M.E., Morrisett, R.A. Neuroscience (2005) [Pubmed]
  12. Changes of free cholesterol and neutral lipids after transient focal brain ischemia in rats. Kamada, H., Sato, K., Iwai, M., Ohta, K., Nagano, I., Shoji, M., Abe, K. Acta Neurochir. Suppl. (2003) [Pubmed]
  13. Characterization of a partial cDNA clone for the NILE glycoprotein and identification of the encoded polypeptide domain. Prince, J.T., Milona, N., Stallcup, W.B. J. Neurosci. (1989) [Pubmed]
  14. Size, shape, and solubility of a class of releasable cell surface proteins of sympathetic neurons. Sweadner, K.J. J. Neurosci. (1983) [Pubmed]
  15. Hydrophobic surfaces of tubulin probed by time-resolved and steady-state fluorescence of nile red. Sackett, D.L., Knutson, J.R., Wolff, J. J. Biol. Chem. (1990) [Pubmed]
  16. Release of the NILE and other glycoproteins from cultured PC12 rat pheochromocytoma cells and sympathetic neurons. Richter-Landsberg, C., Lee, V.M., Salton, S.R., Shelanski, M.L., Greene, L.A. J. Neurochem. (1984) [Pubmed]
  17. Photoreceptor organization and rhythmic phagocytosis in the nile rat Arvicanthis ansorgei: a novel diurnal rodent model for the study of cone pathophysiology. Bobu, C., Craft, C.M., Masson-Pevet, M., Hicks, D. Invest. Ophthalmol. Vis. Sci. (2006) [Pubmed]
  18. Characterization of a partial cDNA clone for the NILE glycoprotein and identification of the encoded polypeptide domain. Prince, J.T., Milona, N., Stallcup, W.B. J. Neurosci. (1989) [Pubmed]
  19. Involvement of the nerve growth factor-inducible large external glycoprotein (NILE) in neurite fasciculation in primary cultures of rat brain. Stallcup, W.B., Beasley, L. Proc. Natl. Acad. Sci. U.S.A. (1985) [Pubmed]
  20. Antibody against nerve growth factor-inducible large external (NILE) glycoprotein labels nerve fiber tracts in the developing rat nervous system. Stallcup, W.B., Beasley, L.L., Levine, J.M. J. Neurosci. (1985) [Pubmed]
  21. Nerve growth factor-inducible large external (NILE) glycoprotein: studies of a central and peripheral neuronal marker. Salton, S.R., Richter-Landsberg, C., Greene, L.A., Shelanski, M.L. J. Neurosci. (1983) [Pubmed]
  22. Inhibition of cellular processing of surfactant protein C by drugs affecting intracellular pH gradients. Beers, M.F. J. Biol. Chem. (1996) [Pubmed]
  23. A new activity of doublecortin in recognition of the phospho-FIGQY tyrosine in the cytoplasmic domain of neurofascin. Kizhatil, K., Wu, Y.X., Sen, A., Bennett, V. J. Neurosci. (2002) [Pubmed]
  24. Functional regeneration of chronically injured sensory afferents into adult spinal cord after neurotrophin gene therapy. Romero, M.I., Rangappa, N., Garry, M.G., Smith, G.M. J. Neurosci. (2001) [Pubmed]
 
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