Disease relevance of ENO2

• Myelin-associated glycoprotein (MAG) immunoreactivity was used to characterize the subpopulation of small B ganglion cells, whereas neuron-specific enolase (NSE) immunoreactivity acted as a general neuronal cell marker [1].

High impact information on ENO2

• Primary cell cultures of diencephalon astrocytes that express glial fibrillary acidic protein (GFAP), but not neuron-specific enolase (NSE) immunoreactivity, were employed to determine the cellular distribution and physiological role for the three known receptor subtypes [2].
• Using chicken brain mRNAs, alpha and gamma enolase precursors were synthesized in the rabbit reticulocyte cell-free translation system [3].
• Double-labelling with NSE and S100 revealed PKC alpha beta/S100-positive glial cells present in the paleostriatal region only [4].
• Furthermore, a computer-assisted three-dimensional imaging technique allowed to clarify the reverse distributional pattern of both elements: NSE-positive pinealocytes displayed a dense distribution especially in the vesicular portion of the gland, whereas NSE-immunoreactive nerve cells were mainly found in the pineal stalk [5].
• Immunohistochemistry for neuron-specific enolase (NSE) revealed that NSE is localized in both a limited number of pinealocytes and intrinsic afferent neurons in the pineal organ of the domestic fowl [5].

Anatomical context of ENO2

• Northern blot analysis has revealed that the mRNA for gamma-enolase (2.3 kb) is expressed in the brain and, to much less but significant extents, in the pituitary and adrenal gland of the chicken [6].
• Our results suggest that NNE and NSE are regulated separately by various factors involved in nerve cell maturation [7].
• Developmental changes of the neuron-specific enolase (NSE) and the non-neuronal enolase (NNE) were determined in pure neuronal, or mixed cultures of neuronal and glial cells, prepared from brains of 8-day-old chick embryos, as a function of cellular development with time in culture [8].
• Antibodies to neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP), and S-100 protein variably stained nerves, but melanocytes were only rarely immunolabelled by NSE antibodies and there was no specific staining of these cells for S-100 or GFAP [9].
• In normal fetuses, immunostained elements positive for NSE first appeared in the spinal gray matter on postincubation day 16 and increased in intensity during the fetal period [10].

Associations of ENO2 with chemical compounds

• Hydrocortisone and diBcAMP had no effect on NSE [7].

Analytical, diagnostic and therapeutic context of ENO2

• Similar immunoprecipitation of reticulocyte lysates programmed with total RNA derived from embryonic chick heart failed to indicate the synthesis of NSE [11].
• Autoradiography indicated the synthesis of a product that comigrated with purified NSE and was recognized only by the anti-NSE antisera [11].

References