Disease relevance of Eno3

• Serum from mice also contained an enzyme (referred to as MSE) which cleaved the trypsin inhibitor 4-methylumbelliferyl-p-guanidinobenzoate as a true substrate, but there was no relationship with weight loss or the presence or absence of tumour and the level of this serum enzyme [1].

High impact information on Eno3

• Analysis of myogenic cell lines shows that beta enolase gene is expressed at the myoblast stage [2].
• It is known that a progressive transition from alpha alpha to beta beta enolase occurs in developing skeletal muscle [2].
• The MSE restrictive element was found to prohibit inappropriate up-regulation of the M promoter by selectively sequestering it from H promoter elements in both myoblasts and myotubes [3].
• Another muscle-specific enhancer and a restrictive element, MEN2/MSE, were found in the interval -1100 to -350 [3].
• A basic carboxypeptidase appears to be involved in generating an acidic beta-enolase variant, and may regulate plasminogen binding by this subunit [4].

Biological context of Eno3

• During murine myogenesis, beta enolase transcripts are detected early in the forming muscles, and the beta gene is further upregulated at specific stages of muscle development [5].
• We have previously shown that the beta-enolase gene belongs to a small subset of muscle-specific genes showing transcriptional activity in cultured myoblasts, prior to withdrawal from the cell cycle [6].
• It is concluded that the up-regulation of beta-enolase as well as IGF-II gene expression in differentiating muscle cells reflects an increased rate of entry of newly synthesized mRNAs into the general pool of transcripts without changes in their respective half-lives [6].

Anatomical context of Eno3

• Our data show that the appearance of beta enolase transcripts temporally correlates with the formation of the second generation of muscle fibers and suggest that the developmental transition from alpha to beta enolase is linked to a developmental program which takes place in fetal but not in embryonic muscle [7].
• Modulation of embryonic and muscle-specific enolase gene products in the developing mouse hindlimb [8].

Associations of Eno3 with chemical compounds

• Polyunsaturated fatty acids (PUFAs) were shown to be inhibitors of MSE at microM concentrations and one PUFA, eicosapentaenoic acid (EPA) was found to be a non-competitive inhibitor of both MSE and GB [1].

Regulatory relationships of Eno3

• The beta-enolase gene is expressed only in striated muscles [9].

Other interactions of Eno3

• Fibre-type distribution and subcellular localisation of alpha and beta enolase in mouse striated muscle [10].
• This gradient parallels the ATPase activity associated to MHC isoforms, indicating that the expression of beta enolase in myofibres is finely regulated as a function of energetic requirements [10].
• The enolase beta subunit (beta-enolase) and the M subunit of CK (CK-M) were present in the RFM at levels increased several-fold compared to levels in the SOL of the same mice [11].
• In the RFM of 3-week-old dystrophic mice, S-100 alpha and beta-enolase levels were similar to those in the RFM of control littermates, but a significant increase of CK-B and a decrease of CK-M were already observed in this early stage of dystrophy [11].

References