Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.108 (TAT)
 2,389 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lethal myocardial ischemia-reperfusion (I/R) injury has been attributed in part to mitochondrial respiratory dysfunction (including damage to complex I) and the resultant excessive production of reactive oxygen species. Recent evidence has shown that reduced nicotinamide adenine dinucleotide-quinone internal oxidoreductase (Ndi1; the single-subunit protein that in yeast serves the analogous function as complex I), transduced by addition of the TAT-conjugated protein to culture media and perfusion buffer, can preserve mitochondrial function and attenuate I/R injury in neonatal rat cardiomyocytes and Langendorff-perfused rat hearts. However, this novel metabolic strategy to salvage ischemic-reperfused myocardium has not been tested in vivo. In this study, TAT-conjugated Ndi1 and placebo-control protein were synthesized using a cell-free system. Mitochondrial uptake and functionality of TAT-Ndi1 were demonstrated in mitochondrial preparations from rat hearts after intraperitoneal administration of the protein. Rats were randomized to receive either TAT-Ndi1 or placebo protein, and 2 hours later all animals underwent 45-minute coronary artery occlusion followed by 2 hours of reperfusion. Infarct size was delineated by tetrazolium staining and normalized to the volume of at-risk myocardium, with all analysis conducted in a blinded manner. Risk region was comparable in the 2 cohorts. Preischemic administration of TAT-Ndi1 was profoundly cardioprotective. These results demonstrate that it is possible to target therapeutic proteins to the mitochondrial matrix and that yeast Ndi1 can substitute for complex I to ameliorate I/R injury in the heart. Moreover, these data suggest that cell-permeable delivery of mitochondrial proteins may provide a novel molecular strategy to treat mitochondrial dysfunction in patients.
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PMID:Reduction of infarct size by the therapeutic protein TAT-Ndi1 in vivo. 2436 6

The complete mitogenome of the potato tuber moth Tecia solanivora (Lepidoptera: Gelechiidae) was sequenced, annotated, characterized and compared with 140 species of the order Lepidoptera. The circular genome is 15,251 bp, containing 37 genes (13 protein-coding genes (PCGs), two rRNA genes, 22 tRNA genes and an A+T-rich region). The gene arrangement was identical to other lepidopteran mitogenomes but different from the ancestral arrangement found in most insects for the tRNA-Met gene (A+T-region, tRNA-I, tRNA-Q, tRNA-M). The mitogenome of T. solanivora is highly A+T-biased (78.2%) and exhibits negative AT- and GC-skews. All PCGs are initiated by canonical ATN start codons, except for Cytochrome Oxidase subunit 1 (COI), which is initiated by CGA. Most PCGs have a complete typical stop codon (TAA). Only NAD1 has a TAG stop codon and the COII and NAD5 genes have an incomplete stop codon consisting of just a T. The A+T-rich region is 332 bp long and contains common features found in lepidopteran mitogenomes, including the 'ATAGA' motif, a 17 bp poly (T) stretch and a (AT)8 element preceded by the 'ATTTA' motif. Other tandem repeats like (TAA)4 and (TAT)7 were found, as well as (T)6 and (A)10 mononucleotide repeat elements. Finally, this mitogenome has 20 intergenic spacer regions. The phylogenetic relationship of T. solanivora with 28 other lepidopteran families (12 superfamilies) showed that taxonomic classification by morphological features coincides with the inferred phylogeny. Thus, the Gelechiidae family represents a monophyletic group, suggesting that T. solanivora and Pectinophora gossypiella have a recent common ancestor.
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PMID:Mitochondrial genome characterization of Tecia solanivora (Lepidoptera: Gelechiidae) and its phylogenetic relationship with other lepidopteran insects. 2680 72