TAA Cyprus
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ABSTRACT:
PROVIDER: PRJEB29481 | ENA |
REPOSITORIES: ENA
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Project description:The aim is to characterize rat liver fibrosis induced by thioacetamide (TAA). To induce hepatic fibrosis, Male Sprague Dawley rats (9-12 weeks of age and 380-420 g of weight upon arrival, supplied by Beijing Vital River laboratory animal Co., Ltd.) were treated with thioacetamide (TAA). Rat liver samples were collected from five groups of rats at week 1, 2, 4, 8 and 13 after TAA (300 mg/kg) administration three times per week while five control groups receive the same volume of 0.9% normal saline. Four biological replicates were used for each group.
2021-09-29 | E-MTAB-10547 | biostudies-arrayexpress
Project description:Acidobacteriaceae bacterium TAA 166
| PRJNA190839 | ENA
Project description:Velcrin compounds kill cancer cells expressing high levels of phosphodiesterase 3A (PDE3A) and Schlafen family member 12 (SLFN12) by inducing complex formation between these two proteins, but the mechanism of cancer cell killing by the PDE3A–SLFN12 complex is not fully understood. Here, we report that the physiological substrate of SLFN12 RNase is tRNALeu(TAA). SLFN12 selectively digests tRNALeu(TAA), and velcrin treatment promotes the cleavage of tRNALeu(TAA) by inducing PDE3A–SLFN12 complex formation in vitro. We found that distinct sequences in the variable loop and acceptor stem of tRNALeu(TAA) are required for substrate digestion. Velcrin treatment of sensitive cells results in downregulation of tRNALeu(TAA), ribosome pausing at Leu-TTA codons and global inhibition of protein synthesis. Velcrin-induced cleavage of tRNALeu(TAA) by SLFN12 and the concomitant global inhibition of protein synthesis thus define a new mechanism of apoptosis initiation.
2022-09-01 | GSE185827 | GEO
Project description:Velcrin compounds kill cancer cells expressing high levels of phosphodiesterase 3A (PDE3A) and Schlafen family member 12 (SLFN12) by inducing complex formation between these two proteins, but the mechanism of cancer cell killing by the PDE3A–SLFN12 complex is not fully understood. Here, we report that the physiological substrate of SLFN12 RNase is tRNALeu(TAA). SLFN12 selectively digests tRNALeu(TAA), and velcrin treatment promotes the cleavage of tRNALeu(TAA) by inducing PDE3A–SLFN12 complex formation in vitro. We found that distinct sequences in the variable loop and acceptor stem of tRNALeu(TAA) are required for substrate digestion. Velcrin treatment of sensitive cells results in downregulation of tRNALeu(TAA), ribosome pausing at Leu-TTA codons and global inhibition of protein synthesis. Velcrin-induced cleavage of tRNALeu(TAA) by SLFN12 and the concomitant global inhibition of protein synthesis thus define a new mechanism of apoptosis initiation.
2022-09-01 | GSE185826 | GEO
Project description:Velcrin compounds kill cancer cells expressing high levels of phosphodiesterase 3A (PDE3A) and Schlafen family member 12 (SLFN12) by inducing complex formation between these two proteins, but the mechanism of cancer cell killing by the PDE3A–SLFN12 complex is not fully understood. Here, we report that the physiological substrate of SLFN12 RNase is tRNALeu(TAA). SLFN12 selectively digests tRNALeu(TAA), and velcrin treatment promotes the cleavage of tRNALeu(TAA) by inducing PDE3A–SLFN12 complex formation in vitro. We found that distinct sequences in the variable loop and acceptor stem of tRNALeu(TAA) are required for substrate digestion. Velcrin treatment of sensitive cells results in downregulation of tRNALeu(TAA), ribosome pausing at Leu-TTA codons and global inhibition of protein synthesis. Velcrin-induced cleavage of tRNALeu(TAA) by SLFN12 and the concomitant global inhibition of protein synthesis thus define a new mechanism of apoptosis initiation.
2022-09-01 | GSE185822 | GEO
Project description:Purpose: The goal of this study is to investigate the effect of recombinant human Cytoglobin (rhCYGB) on liver fibrosis induced by TAA in mice. Method: mRNA profiles of liver tissues from TAA-control mice and TAA-rhCYGB treated mice were generated by deep sequencing. Results: The RNA-seq data confirmed that extracellular matrix-encoding genes and fibrosis-related genes were down-regulated by the rhCYGB treatment.
2020-08-25 | GSE156777 | GEO
Project description:Zebrafish transgenic lines Tg(fabp10a:dsRed), Tg(hand2:EGFP) and Tg(kdrl:ras-mCherry) in AB wild-type background were anesthetized with MS-222 and adult females were injected intraperitoneally with 500 mg/kg thioacetamide (TAA) or sterile water as a control 6 times over the course of 2 weeks. We have characterized chromatin accessibility profiles of FACS-isolated hepatocytes (dsRed+), stellate cells (EGFP+) and liver endothelial cells (mCherry+) from fishes treated with TAA or sterile water. Cells negative for the fluorescence were used as a control.
2021-12-23 | GSE145563 | GEO
Project description:Terriglobus sp. TAA 43 Genome sequencing and assembly
| PRJNA208396 | ENA
Project description:Zebrafish transgenic lines Tg(fabp10a:dsRed), Tg(hand2:EGFP) and Tg(kdrl:ras-mCherry) in AB wild-type background were anesthetized with MS-222 and adult females were injected intraperitoneally with 500 mg/kg thioacetamide (TAA) or sterile water as a control 6 times over the course of 2 weeks. We have characterized transcriptomic profiles of FACS-isolated hepatocytes (dsRed+), stellate cells (EGFP+) and liver endothelial cells (mCherry+) from fishes treated with TAA or sterile water. Cells negative for the fluorescence were used as a control.
2021-12-23 | GSE145564 | GEO
Project description:C/D box small nucleolar RNAs (snoRNAs) transcribed from the DLK1-DIO3 locus are associated with vascular remodelling and cardiovascular disease. None of these snoRNAs has any known targets yet, except for one, AF357425 in mice and SNORD113-6 in humans. We previously showed that this snoRNA targets mRNAs of the integrin signalling pathway and affects arterial fibroblast function. Here, we aimed to identify whether AF357425/SNORD113-6 can also target small RNAs. We overexpressed or inhibited AF357425 in murine fibroblasts and performed small RNA sequencing. Expression of tRNA fragments (tRFs) was predominantly regulated. Compared to overexpression, AF357425 knockdown led to an overall decrease in tRFs, but with an enrichment in smaller tRFs (<30 nucleotides). We focused on tRNA Leucine anti-codon TAA (tRNALeu(TAA)), that has a conserved predicted binding site for AF357425/SNORD113-6. Adjacent to this site, the tRNA is cleaved to form tRFLeu 47-64, in both primary murine fibroblasts and human arterial fibroblasts. We show that AF357425/SNORD113-6 methylates tRNALeu(TAA) and thereby prevents the formation of tRFLeu 47-64. Exposing fibroblasts to oxidative or hypoxic stress, increased AF357425/SNORD113-6 and tRNALeu(TAA) expression, but AF357425/SNORD113-6 knockdown did not lead to an additional formation of tRFLeu 47-64. Thus, independent of cellular stress, AF357425/SNORD113-6 directs site-specific fragmentation of tRNALeu(TAA) via 2’O-ribose-methylation.
2021-12-11 | GSE190537 | GEO