Example sentences for: decarboxylase

How can you use “decarboxylase” in a sentence? Here are some example sentences to help you improve your vocabulary:

  • Many genes that are known to amplify in response to selection, primarily during anticancer drug treatments, were found to be present in multiple copies in mammalian genomes as well, in particular, aminoacyl-tRNA synthetases, glutamine synthetase and other anabolic enzymes, adenosine deaminase, ornithine decarboxylase, AMP deaminase, and N -acetyl glucosaminyltransferase [ 34, 46].

  • Many studies have shown that chronic intravenous infusion of norepinephrine is sufficient to cause hypertrophy, and that various forms of hypertrophy are linked to a decrease in either beta-adrenergic receptor density or a decreased responsiveness to beta-adrenergic stimulation [ 46 48 49 56 57 58 59 60 61 62 63 ] . Barth, for example, showed that norepinephrine infusion induced left ventricular hypertrophy that could be prevented by an adrenergic-receptor blocker [ 58 ] . It has been suggested that ornithine decarboxylase is a link between beta-adrenoreceptors and stimulation of tissue growth factor, which results in hypertrophy [ 64 ] . However, recent studies have focused on alpha-adrenergic reception as a mediator of cardiac hypertrophy [ 35 ] , although some question the role of the alpha-adrenergic receptor as a hypertrophic mediator in vivo [ 34 ] . To date, no published studies of which we are aware have examined alpha-adrenergic reception and the development of cardiac hypertrophy with iron deficiency.

  • The mouse gene encoding the 67 kDa isoform of glutamate decarboxylase ( Gad1 ) is expressed in the tail bud mesenchyme, vibrissal placodes, pharyngeal arches and pouches and the apical ectodermal ridge (AER), mesenchyme and ectoderm of the limb buds in mouse embryos from E9.

  • GABA is a well-documented neurotrophic agent involved in brain development [ 27 28 29 30 ] . Most of the work done on the effects of GABA and neural development has been done on embryos and embryonic tissue well past the neural tube stage [ 27 31 32 ] . However, there is evidence of glutamic acid decarboxylase (GAD) and GABA receptor expression about the time of neural tube formation [ 27 ] . Given that GABA is important to neural development, and the early developmental time frame of the GABA system, it is logical that agents active at the GABA receptor (ethanol, BDZs) can have adverse consequences on CNS development.

  • T1DM susceptibility in the NOD mouse is linked to I-A g7, the murine MHC class II gene that encodes a histidine at position 56 and a serine at position 57 in the β chain, in place of the more frequent proline 56β and aspartic acid 57β [ 3 ] . The development of diabetes is prevented in NOD.PD mice (which are NOD mice with I-A g7) that carry a β chain transgene with site-specific mutations that restore proline and aspartic acid at positions 56β and 57β, respectively [ 4 ] . Furthermore, because of the two amino acid changes in the additional (transgenic) MHC class II allele β chain in NOD.PD mice, NOD.PD mice recognize three additional peptide epitopes in the glutamic acid decarboxylase 65 (GAD65) autoantigen [ 5 ] .


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