Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The N-myc cellular oncogene is frequently amplified and expressed at a high level in neuroectodermal tumor cells such as neuroblastoma and retinoblastoma. We examined N-myc expression in NCB-20 hybrid (N18TG2 neuroblastoma x embryonic Chinese Hamster brain) cells. After five days of culture, cells treated with 1 mM db cAMP show extensive neurite outgrowth and secrete acetylcholinesterase into the media at a level three times higher than untreated control. In situ hybridizations, dot blots, and Northern analyses reveal four- to eight-fold higher levels of N-myc mRNA in the treated, differentiated cells than in the untreated, undifferentiated controls. Our results show that the highly differentiated state is not incompatible with a high level of N-myc mRNA.
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PMID:Increased N-myc mRNA expression associated with dibutyryl cyclic AMP induced neuroblastoma differentiation. 256 Apr 82

Following the treatment with dibutyryl cyclic AMP (dbcAMP) in the absence of serum, a proportion of cultured human embryo retinoblasts will differentiate rapidly. This is characterized by cell rounding and the extension of neuritic-type processes. A transformed cell line (Ad 12 HER 10), developed by transfection of human embryo retinoblasts with adenovirus 12 (Ad 12) early region 1 (E1) DNA, forms retinoblastoma-like tumours in athymic nude mice and retains the ability to extend neuritic-like processes after treatment with dbcAMP in the absence of serum. This response, which occurs in almost all cells (over 98%), is accompanied by growth arrest and reverses rapidly after re-exposure to serum. Other agents known to increase intracellular cAMP also mediate differentiation. Ad 12 HER 10 cells were shown to contain the neuronal markers, neurone-specific enolase and protein gene product 9.5, but not the glial cell marker glial fibrillary acidic protein (GFAP). Activity of the neurotransmitter enzyme acetylcholinesterase was also detected and found to increase after differentiation. Interestingly, the expression of the Ad 12 E1 transforming proteins did not change throughout differentiation. These results show first, that the Ad 12 HER 10 cell line can differentiate in a similar manner to that observed in a proportion of primary retinoblasts and second, that the expression of transforming proteins does not preclude at least part of that differentiative capacity. This is the first demonstration of in vitro differentiation in an adenovirus-transformed human cell line, as well as offering a useful system for the study of factors controlling growth and differentiation of tumorigenic human retinoblasts.
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PMID:Differentiation of normal and adenovirus-12 E1 transformed human embryo retinal cells. 284 75

The gene encoding human esterase D (EsD), a member of the nonspecific esterase family, is a useful genetic marker for retinoblastoma (RB) and Wilson's disease. Previously we identified a cDNA clone from this gene and determined its chromosomal location. In this report, we present the complete cDNA sequence of the human EsD gene. A long open reading frame encoded a predicted protein of 282 amino acids with molecular weight of 30 kD. A computer-assisted search of a protein sequence data base revealed homology with two other esterases, acetylcholinesterase of Torpedo and esterase-6 of Drosophila. Homologous region were centered around presumptive active sites, suggesting that the catalytic domains of the esterases are conserved during evolution. Three genomic clones of this gene were also isolated and characterized by restriction mapping. At least ten exons were distributed over a 35-kb (kilobase pair) region; each exon contained an average of 100 basepairs (bp). A polymorphic site for Apa I, located within an intron of the esterase D gene, can be used to identify chromosome 13 carrying defective RB alleles within retinoblastoma families.
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PMID:Human esterase D gene: complete cDNA sequence, genomic structure, and application in the genetic diagnosis of human retinoblastoma. 316 2