Complete structure of the human gene encoding neuron-specific enolase

Oliva, Daniele; Calı̀, Larissa; Feo, Salvatore; Giallongo, Agata

doi:10.1016/0888-7543(91)90496-2

Cited by 52 publications

(31 citation statements)

References 32 publications

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“…Immunogenic epitopes within human NSE have not been characterized, making the search for a common epitope difficult. The α-subunit of NNE is 336 amino acids residues in length (65), whereas the γ-subunit of NSE is 434 amino acids long (66). The polypeptide sequences of these subunits align together with the first 98 residues of NSE being unique to that molecule.…”

Section: Discussionmentioning

confidence: 92%

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

et al. 2007

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Introduction-Although myelin autoimmunity is known to be a major factor in the pathogenesis of multiple sclerosis (MS), the role of nonmyelin antigens is less clear. Given the complexity of this disease, it is possible that autoimmunity against nonmyelin antigens also has a pathogenic role. Autoantibodies against enolase and arrestin have previously been reported in MS patients. The Tcell response to these antigens, however, has not been established.

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Section: Discussionmentioning

confidence: 92%

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

et al. 2007

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“…DNA fragments spanning the entire p enolase gene were isolated from the B.21 3, phage and subcloned into the KS' or KSBluescript vectors (Stratagene). The Bluescript clones were used directly or after progressive digestion with exonuclease I11 (Boehringer) for nucleotide sequencing according to Sanger et al [17], as previously described [6]. The nucleotide sequence was determined on both strands (90%) or at least twice on the same strand routinely using T7 DNA polymerase (Sequenase) and Tuq I polymerase (Promega) in case of the presence of G+C-rich regions of DNA.…”

Section: Materials and Methods Isolation And Nucleotide Sequencing Ofmentioning

confidence: 99%

Structural features of the human gene for muscle‐specific enolase

Giallongo

Venturella

Oliva

et al. 1993

European Journal of Biochemistry

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We report here the isolation and characterization of the human gene for the p or muscle-specific isoform of the glycolytic enzyme enolase. The nucleotide sequence analysis revealed structural features, such as organization as 11 coding exons, the first exon consisting of an untranslated sequence and hence resembling sequences of the other two members of the gene family, the a and y enolase genes. The p enolase locus spans about 6 kbp genomic DNA. Sequences matching the consensus sequence for muscle-specific regulatory factors are present in the 5'-flanking region and within the first intron. A combination of primer extension, S1 nuclease protection and RNA-sequencing experiments indicates that the gene has a unique transcriptional start site, 26 bp downstream of a TATA-like box; the differential usage of two donor sites within the untranslated exon I generates two alternatively spliced transcripts. The existence of the two mRNA, differing from one another in the presence or absence of a 42-nucleotide fragment in the leader sequence, was confirmed by cloning the corresponding cDNA using the rapid amplification of cDNA ends strategy. Secondarystructure predictions indicated that the leader sequences of the spliced forms could form hairpin structures with different free energies of formation, suggesting translational control.

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“…Compared to LNCaP cells, the CRE sites (40,42,(44)(45)(46), suggesting a direct regulation by the transcription factor pCREB. In addition to gene expression, our data indicated high protein levels of SYP (another marker of NE differentiation) and VEGF in ISO-stimulated prostate tumors.…”

Section: Discussionmentioning

confidence: 99%

Triiodothyronine Attenuates Prostate Cancer Progression Mediated by β-Adrenergic Stimulation

Delgado‐González

Sánchez-Tusié

Morales

et al. 2016

Mol Med

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Prostate cancer cells are responsive to adrenergic and thyroid stimuli. It is well established that β-adrenergic activation (protein kinase A [PKA]/cAMP response element binding protein [CREB]) promotes cancer progression, but the role of thyroid hormones is poorly understood. We analyzed the effects of β-adrenergic stimulation (isoproterenol [ISO]) and/or thyroid hormone on neuroendocrine (NE) differentiation and cell invasion, using in vivo (LNCaP tumor) and in vitro models (LNCaP and DU145 human cells). Nude mice were inoculated with LNCaP cells and were treated for 6 wks with ISO (200 μg/d), triiodothyronine (T3, 2.5 μg/d) or both. ISO alone reduced tumor growth but increased tumor expression of cAMP response element (CRE)-dependent genes (real-time polymerase chain reaction, chromogranin A, neuron-specific enolase, survivin, vascular endothelial growth factor [VEGF], urokinase plasmin activator [uPA] and metalloproteinase-9 [MMP-9]) and some proteins related to NE differentiation and/or invasiveness (synaptophysin, VEGF, pCREB). T3 reduced tumor growth and prevented the overexpression of ISO-stimulated factors through a pCREB-independent mechanism. In low invasive LNCaP cells, 50 μmol/L ISO or 100 nmol/L thyroxine (T4) induced the acquisition of NE-like morphology (phase-contrast microscopy), increased VEGF secretion (ELISA) and invasive capacity (Transwell assay), but no synergistic effects were observed after the coadministration of ISO + T4. In contrast, 10 nmol/L T3 alone had no effect, but it prevented the NE-like morphology and invasiveness stimulated by ISO. None of these treatments had any effect on highly invasive DU145 cells. In summary, this study showed that ISO and T4 increase cancer progression, and T3 attenuates ISO-stimulated progression. Further studies are required to determine if changes in the ratio of T4/T3 could be relevant for prostate cancer progression.

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Complete structure of the human gene encoding neuron-specific enolase

Cited by 52 publications

References 32 publications

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

Enolase and Arrestin are Novel Nonmyelin Autoantigens in Multiple Sclerosis

Structural features of the human gene for muscle‐specific enolase

Triiodothyronine Attenuates Prostate Cancer Progression Mediated by β-Adrenergic Stimulation

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