Disease relevance of TERT

• As a result of this study, derivatives 7 and 26, which are substituted with tert-butyl groups at N-1, were found to possess excellent in vitro and in vivo potency, particularly against Staphylococcus aureus, comparable to that of norfloxacin or ciprofloxacin [1].

High impact information on TERT

• In comparison with guancydine, which is the de-3-pyridyl analogue of 20, a 150-fold increase of potency in spontaneously hypertensive rats was obtained with 20 and its tert-butyl analogue 19 [2].
• The protective effect of D-glucose was much less marked in tert-butyl hydroperoxide-cytotoxicity [3].
• Sample pretreatment involved liquid-liquid extraction with tert-butyl methyl ether [4].
• Samples were analysed by positive ion electrospray ionisation LC/MS on two different instruments and the unknown compound was identified as an N-oxide of the tert. nitrogen atom of the 2-(diethylamino)ethyl substituent on N7 of the theophylline nucleus [5].
• Expression of TERT mRNA was examined by reverse transcription (RT)-PCR assay [6].

Biological context of TERT

• RESULTS: The canine TERT cDNA clone was 237 base pairs in length and contained a central region encoding the reverse transcriptase motif 2 [6].
• Still another metabolite is formed by hydroxylation in the tert-butyl group to N-(2-hydroxymethyl-2-propyl)-4,4-diphenyl-2-butylamine [7].

Anatomical context of TERT

• Expression of TERT mRNA was detected in canine tumor cell lines that had telomerase activity but not in telomerase-negative canine primary fibroblasts [6].
• The TERT mRNA was detected in 13 of 16 canine tumor tissues and several normal tissues such as liver, ovary, lymph node, and thymus [6].

Associations of TERT with chemical compounds

• A series of procaterol derivatives having a tert-amino group was synthesized [8].
• During development of the extraction procedure, degradation of desbutylhalofantrine was observed under non-acidic conditions in the extraction solvent (tert-butyl methyl ether) and we also report the structural elucidation of the breakdown product and the conditions required to avoid this degradation [9].
• Oxidative metabolism (phase 1 reactions) mediated by the microsomal monooxygenase system is the major route for BHT degradation; oxidation of the ring methyl group predominates in the rat, rabbit and monkey, and oxidation of the tert-butyl groups in man [10].
• Diltiazem, clentiazem and their acidic and basic metabolites extractable with tert-butyl methyl ether, which are all 2,3,5-trisubstituted-1,5-benzothiazepines, were analysed by positive ion electron ionization (PIEI) mass spectrometry, and the structures of fragment ions and their fragmentation pathways were investigated [11].
• New tert-butyl, picolyl and fluorinated analogues of capromorelin (3), a short-acting growth hormone secretagogue (GHS), were prepared as part of a program to identify long-acting GHSs that increase 24-h plasma IGF-1 levels [12].

Analytical, diagnostic and therapeutic context of TERT

• Canine TERT complementary DNA (cDNA) was amplified by use of polymerase chain reaction (PCR) and sequenced [6].
• Molecular cloning of the canine telomerase reverse transcriptase gene and its expression in neoplastic and non-neoplastic cells [6].
• In this present study we analysed 93 canine brain tumours for telomerase reverse transcriptase (TERT) expression by immunohistochemistry [13].

References