Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.28 (chloramphenicol acetyltransferase)
 5,100 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Creatine kinase (EC 2.7.3.2) (CK) isoenzymes are crucial to energy metabolism, particularly in tissues with high energy requirements. Nuclear genes encode four known CK subunits: cytoplasmic muscle, cytoplasmic brain, ubiquitous mitochondrial (uMtCK), and sarcomeric mitochondrial (sMtCK). Herein, we report the isolation and complete structural characterization of the human sMtCK gene. It contains 11 exons and encompasses more than 37 kilobase pairs (kb). The sites of exon localization in the sMtCK-coding region and their precise sizes are identical with the human uMtCK gene. The translation start codon is in the third exon and lies 17 kb from the transcription start site. The human sMtCK gene is located on chromosome 5. Sequence analysis of the sMtCK genomic upstream sequences reveals a typical TATAA box within the 80 base pairs (bp) that, by transfection experiments, are sufficient to promote expression of chimeric plasmids with the chloramphenicol acetyltransferase reporter. Cis-acting sequences in a fragment containing 3360 bp of upstream sequence, the first exon, and 750 bp of the first intron are sufficient to mediate tissue-specific expression. However, these sequences only partially regulate induction of sMtCK expression in differentiating mouse myoblasts. MEF1/MYOD and MEF2 sequence motifs present in the sMtCK gene are not sufficient to regulate differentiation-specific expression. The sMtCK gene contains sequences homologous to several motifs that are shared among some nuclear genes encoding mitochondrial proteins and that may be essential for the coordinated activation of these genes during mitochondrial biogenesis.
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PMID:Regulatory element analysis and structural characterization of the human sarcomeric mitochondrial creatine kinase gene. 191 43

We have isolated an avian muscle cell line (QM) which has the essential features of established mammalian muscle cell lines. The experiments reported here were undertaken to determine the suitability of QM cells for the introduction and analysis of cloned transgenes. The promoter of the cardiac troponin T (cTNT) gene has been previously shown to contain sequence elements which govern muscle-specific expression of the chloramphenicol acetyltransferase (CAT) gene in transiently transfected primary cell cultures. We show here that QM cells stably harboring cTNT promoter-CAT fusion genes up-regulate CAT expression in concert with myogenic differentiation, and that as few as 110 upstream nucleotides are sufficient for such differentiation-dependent regulation. In addition, both transient and stable transfection experiments demonstrate that differentiated QM cells possess trans-acting factors necessary for the expression of the skeletal alpha-actin promoter, despite the absence of mRNA or protein product from the endogenous sarcomeric actin genes in these cells. Finally, to follow the developmental potential of QM cells in vivo, we created a clone, QM2ADH, which constitutively expresses the histochemical marker transgene encoding Drosophila alcohol dehydrogenase. When surgically inserted into the limb buds of developing chick embryos, QM2ADH cells are incorporated into endogenous developing muscles, indicating that QM cells are capable of recognizing and responding to host cues governing muscle morphogenesis. Thus, QM cells are versatile as recipients of transgenes for the in vitro and in vivo analysis of molecular events in muscle development.
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PMID:Transgene expression in the QM myogenic cell line. 198 14