Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.4.37 (CNPase)
539 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

L-3,5,3'-Triiodothyronine (T3) has been shown to influence the synthesis of myelin-associated lipids in cultures of cells dissociated from brains of embryonic mice (Bhat, N. R., Sarlieve, L., Subba Rao, G., and Pieringer, R. A. (1979) J. Biol. Chem. 254, 9342-9344). This culture system was used in the present study to gain additional information on the regulation of the synthesis of myelin lipids by thyroid hormone. The rate of synthesis of the myelin associated sulfolipids remained drastically diminished throughout a 70-day developmental period when cells were grown in the presence of hypothyroid calf serum (T3 < 25 ng/100 ml; thyroxine (T4), 1.2 microgram/ml). However, the activity could be restored to normal levels after 72 h of exposure to deficient medium supplemented with exogenous T3. Half-maximal effects were obtained with 2 X 10(-9) M T3 and 6.25 X 10(-7) M T4. T3 does not alter the synthesis of sulfated mucopolysaccharides, which share adenosine 3'-phosphate, 5'-phosphosulfate (PAPS), as a common precursor, with sulfolipids. This observation argues against the hormone altering the entry of sulfate or the synthesis of PAPS. Rather, T3 acts by changing the activity of the glycolipid:PAPS sulfotransferase(s) in direct proportion to the concentration of T3 in the growth medium. The activity of 2',3'-cyclic nucleotide 3'-phosphohydrolase, another myelin marker was also found to be T3 dependent. The response of sulfolipid synthesis to varying amounts of T3 was also observed in a serum-free medium, which suggests that T3 can function independently of other hormones and serum factors in exerting a relatively specific effect on the regulation of myelination.
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PMID:Investigations on myelination in vitro. Regulation of sulfolipid synthesis by thyroid hormone in cultures of dissociated brain cells from embryonic mice. 625 88

Progenitors that migrate through the white matter of the postnatal cerebellum give rise to cortical interneurons, astroglia, and oligodendroglia. To determine whether this progenitor population is heterogeneous with respect to specific lineage markers, we infected progenitors in vivo with a retrovirus encoding the green fluorescent protein on postnatal day 4/5 and labeled them in situ with various antibodies 2 days postviral injection: the neuronal marker was the transcription factor SOX1; early oligodendroglial markers were chondroitin sulfate proteoglycan antigen and platelet-derived growth factor receptor-alpha. Markers for astroglial progenitors were vimentin, nestin, zebrin II, and the astroglial-specific glutamate transporter subtype GLAST. None of the progenitors was doubly labeled with any combination of markers characteristic for different cell lineages. Most progenitors were not labeled with any of the various combinations of antibodies used. Progenitors did not express markers characteristic for mature astroglia (GFAP), oligodendroglia (CNPase), or neurons (MAP2). Thus, although these progenitors are morphologically indistinguishable, a minority expresses markers of early neuronal or glial lineages, suggesting that they begin to differentiate during migration.
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PMID:Progenitors in the postnatal cerebellar white matter are antigenically heterogeneous. 1227 92


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