Expression of vimentin and glial fibrillary acidic protein in human developing spinal cord
Jazyk angličtina Země Nizozemsko Médium print
Typ dokumentu časopisecké články
PubMed
2482269
DOI
10.1007/bf01002834
Knihovny.cz E-zdroje
- MeSH
- barvení a značení MeSH
- elektroforéza v polyakrylamidovém gelu MeSH
- exprese genu MeSH
- fluorescenční mikroskopie MeSH
- fluorescenční protilátková technika MeSH
- gestační stáří MeSH
- gliový fibrilární kyselý protein genetika imunologie MeSH
- lidé MeSH
- mícha embryologie metabolismus MeSH
- monoklonální protilátky MeSH
- těhotenství MeSH
- vimentin genetika imunologie MeSH
- Check Tag
- lidé MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- gliový fibrilární kyselý protein MeSH
- monoklonální protilátky MeSH
- vimentin MeSH
Expression of intermediate filament proteins was studied in human developing spinal cord using immunoperoxidase and double-label immunofluorescence methods with monoclonal antibodies to vimentin and glial fibrillary acidic protein (GFAP). Vimentin was found in the processes of radial glial cells in 6-week embryos, while GFAP appeared in vimentin-positive astroglial cells at 8-10 weeks. GFAP and vimentin were present in approximately equal amounts in differentiating astrocytes in 23-week spinal cord. In 30-week fetuses, astrocytes reacted strongly for GFAP, while both the reaction intensity and the number of vimentin-positive cells fluctuated predominantly in the grey matter. No clear-cut transition from vimentin to GFAP was noticed during the development of astrocytes. The majority of ependymal cells in 23-week fetuses contained vimentin but only a few of them reacted for GFAP. The expression of vimentin continued during the whole development of the ependymal layer, in contrast to the reactivity for GFAP which disappeared between the 30th week and term.
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Folia Biol (Praha). 1986;32(5):295-303 PubMed
Lab Invest. 1984 Sep;51(3):307-16 PubMed
Ann Neurol. 1982 Feb;11(2):203-6 PubMed
Nature. 1970 Aug 15;227(5259):680-5 PubMed
Proc Natl Acad Sci U S A. 1973 Mar;70(3):765-8 PubMed
Eur J Cell Biol. 1981 Dec;26(1):68-82 PubMed
Brain Res. 1983 Aug;285(2):189-95 PubMed
Histochemistry. 1988;89(5):485-92 PubMed
Brain Res. 1979 Nov 16;177(2):219-29 PubMed
Differentiation. 1981;19(3):161-7 PubMed
J Cell Biol. 1979 Aug;82(2):577-84 PubMed
Brain Res. 1980 Oct 27;200(1):13-21 PubMed
Science. 1984 Jan 27;223(4634):407-9 PubMed
J Neurochem. 1987 Aug;49(2):348-54 PubMed
J Neurosci Res. 1981;6(6):741-8 PubMed
Brain Res. 1976 Feb 27;103(3):613-6 PubMed
J Comp Neurol. 1980 Oct 1;193(3):815-40 PubMed
Am J Surg Pathol. 1984 Aug;8(8):615-24 PubMed
Acta Neuropathol. 1986;70(3-4):308-13 PubMed
J Cell Biol. 1981 Jan;88(1):115-26 PubMed
Anal Biochem. 1985 Mar;145(2):315-21 PubMed
Cesk Patol. 1987 Sep;23(3):169-73 PubMed
Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 PubMed
Cold Spring Harb Symp Quant Biol. 1982;46 Pt 1:317-29 PubMed
Dev Biol. 1983 Apr;96(2):472-84 PubMed
Cell Biol Int Rep. 1982 Aug;6(8):725-31 PubMed
Eur J Cell Biol. 1981 Jun;24(2):191-6 PubMed
Brain Res. 1981 Apr;227(2):249-67 PubMed
Med Biol. 1984;62(1):38-48 PubMed
Nature. 1980 Jan 17;283(5744):249-256 PubMed
Exp Neurol. 1981 Aug;73(2):496-506 PubMed
Dev Biol. 1982 Jun;91(2):286-95 PubMed
Arch Pathol Lab Med. 1987 Sep;111(9):796-812 PubMed
J Neurosci. 1984 Aug;4(8):2080-94 PubMed
Histochemistry. 1988;88(3-6):575-81 PubMed
Cold Spring Harb Symp Quant Biol. 1982;46 Pt 1:413-29 PubMed
Cell. 1982 Nov;31(1):11-24 PubMed
Nature. 1979 Jan 25;277(5694):303-5 PubMed
Scand J Immunol. 1973;2(3):273-90 PubMed
J Cell Biol. 1981 Aug;90(2):435-47 PubMed
