Arginase induction by sodium phenylbutyrate in mouse tissues and human cell lines

2007 ◽  
Vol 90 (1) ◽  
pp. 37-41 ◽  
Author(s):  
R.M. Kern ◽  
Z. Yang ◽  
P.S. Kim ◽  
W.W. Grody ◽  
R.K. Iyer ◽  
...  
Keyword(s):  
Cell Lines ◽  
Human Cell ◽  
Human Cell Lines ◽  
Mouse Tissues ◽  
Sodium Phenylbutyrate

scholarly journals HBO1 (KAT7) Does Not Have an Essential Role in Cell Proliferation, DNA Replication, or Histone 4 Acetylation in Human Cells

2019 ◽  
Vol 40 (4) ◽  
Author(s):  
Andrew J. Kueh ◽  
Samantha Eccles ◽  
Leonie Tang ◽  
Alexandra L. Garnham ◽  
Rose E. May ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Adhesion ◽  
Dna Replication ◽  
Cell Lines ◽  
Human Cell ◽  
Human Cells ◽  
Human Cell Lines ◽  
Hela Cell Lines ◽  
Mouse Tissues ◽  
Sirna Knockdown

ABSTRACT HBO1 (MYST2/KAT7) is essential for histone 3 lysine 14 acetylation (H3K14ac) but is dispensable for H4 acetylation and DNA replication in mouse tissues. In contrast, previous studies using small interfering RNA (siRNA) knockdown in human cell lines have suggested that HBO1 is essential for DNA replication. To determine if HBO1 has distinctly different roles in immortalized human cell lines and normal mouse cells, we performed siRNA knockdown of HBO1. In addition, we used CRISPR/Cas9 to generate 293T, MCF7, and HeLa cell lines lacking HBO1. Using both techniques, we show that HBO1 is essential for all H3K14ac in human cells and is unlikely to have a direct effect on H4 acetylation and only has minor effects on cell proliferation. Surprisingly, the loss of HBO1 and H3K14ac in HeLa cells led to the secondary loss of almost all H4 acetylation after 4 weeks. Thus, HBO1 is dispensable for DNA replication and cell proliferation in immortalized human cells. However, while cell proliferation proceeded without HBO1 and H3K14ac, HBO1 gene deletion led to profound changes in cell adhesion, particularly in 293T cells. Consistent with this phenotype, the loss of HBO1 in both 293T and HeLa principally affected genes mediating cell adhesion, with comparatively minor effects on other cellular processes.

Mirror expression of adrenoleukodystrophy and adrenoleukodystrophy related genes in mouse tissues and human cell lines

1998 ◽  
Vol 75 (3) ◽  
pp. 254-264 ◽  
Author(s):  
Nathalie Troffer-Charlier ◽  
Nathalie Doerflinger ◽  
Elisabeth Metzger ◽  
Françoise Fouquet ◽  
Jean-Louis Mandel ◽  
...  
Keyword(s):  
Cell Lines ◽  
Human Cell ◽  
Human Cell Lines ◽  
Mouse Tissues

scholarly journals A cross-organism framework for supervised enhancer prediction with epigenetic pattern recognition and targeted validation

2018 ◽  
Author(s):  
Anurag Sethi ◽  
Mengting Gu ◽  
Emrah Gumusgoz ◽  
Landon Chan ◽  
Koon-Kiu Yan ◽  
...  
Keyword(s):  
Cell Lines ◽  
Human Cell ◽  
Mammalian Species ◽  
Machine Learning Algorithms ◽  
Supervised Machine Learning ◽  
Support Vector ◽  
Human Cell Lines ◽  
Mouse Tissues

AbstractEnhancers are important noncoding elements, but they have been traditionally hard to characterize experimentally. Only a few mammalian enhancers have been validated, making it difficult to train statistical models for their identification properly. Instead, postulated patterns of genomic features have been used heuristically for identification. The development of massively parallel assays allows for the characterization of large numbers of enhancers for the first time. Here, we developed a framework that uses Drosophila STARR-seq data to create shape-matching filters based on enhancer-associated meta-profiles of epigenetic features. We combined these features with supervised machine learning algorithms (e.g., support vector machines) to predict enhancers. We demonstrated that our model could be applied to predict enhancers in mammalian species (i.e., mouse and human). We comprehensively validated the predictions using a combination of in vivo and in vitro approaches, involving transgenic assays in mouse and transduction-based reporter assays in human cell lines. Overall, the validations involved 153 enhancers in 6 mouse tissues and 4 human cell lines. The results confirmed that our model can accurately predict enhancers in different species without re-parameterization. Finally, we examined the transcription-factor binding patterns at predicted enhancers and promoters in human cell lines. We demonstrated that these patterns enable the construction of a secondary model effectively discriminating between enhancers and promoters.

scholarly journals Nucleocytoplasmic human O-GlcNAc transferase is sufficient for O-GlcNAcylation of mitochondrial proteins

2016 ◽  
Vol 473 (12) ◽  
pp. 1693-1702 ◽  
Author(s):  
Riccardo Trapannone ◽  
Daniel Mariappa ◽  
Andrew T. Ferenbach ◽  
Daan M.F. van Aalten
Keyword(s):  
Cell Lines ◽  
Human Cell ◽  
Neuronal Development ◽  
Mitochondrial Proteins ◽  
Human Cell Lines ◽  
Post Translational Modification ◽  
Mitochondrial Proteome ◽  
Mouse Tissues ◽  
Dependent Protein ◽  
Glcnac Transferase

O-linked N-acetylglucosamine modification (O-GlcNAcylation) is a nutrient-dependent protein post-translational modification (PTM), dynamically and reversibly driven by two enzymes: O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) that catalyse the addition and the removal of the O-GlcNAc moieties to/from serine and threonine residues of target proteins respectively. Increasing evidence suggests involvement of O-GlcNAcylation in many biological processes, including transcription, signalling, neuronal development and mitochondrial function. The presence of a mitochondrial O-GlcNAc proteome and a mitochondrial OGT (mOGT) isoform has been reported. We explored the presence of mOGT in human cell lines and mouse tissues. Surprisingly, analysis of genomic sequences indicates that this isoform cannot be expressed in most of the species analysed, except some primates. In addition, we were not able to detect endogenous mOGT in a range of human cell lines. Knockdown experiments and Western blot analysis of all the predicted OGT isoforms suggested the expression of only a single OGT isoform. In agreement with this, we demonstrate that overexpression of the nucleocytoplasmic OGT (ncOGT) isoform leads to increased O-GlcNAcylation of mitochondrial proteins, suggesting that ncOGT is necessary and sufficient for the generation of the O-GlcNAc mitochondrial proteome.

Complex expression pattern of the Barth syndrome gene product tafazzin in human cell lines and murine tissues

2004 ◽  
Vol 82 (5) ◽  
pp. 569-576 ◽  
Author(s):  
Biao Lu ◽  
Marguerite R Kelher ◽  
Douglas P Lee ◽  
Tal M Lewin ◽  
Rosalind A Coleman ◽  
...  
Keyword(s):  
Cell Lines ◽  
Human Cell ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Barth Syndrome ◽  
In Vitro Translation ◽  
Human Cell Lines ◽  
Mouse Tissues ◽  
Species Specific

Tafazzins, a group of proteins that are defective in patients with Barth syndrome, are produced by alternate splicing of the gene G4.5 or TAZ. RT-PCR and transcription-coupled in vitro translation analysis were undertaken to determine the expression of alternatively spliced TAZ mRNA in mouse tissues and human cell lines. Only two tafazzin transcripts, both lacking exon 5, were expressed in murine tissues, whereas four tafazzin transcripts, all lacking exon 5, were observed in human umbilical vein vascular endothelial cells and U937 human monoblasts indicating a species-specific difference in the expression of TAZ mRNAs in mouse and humans. Only TAZ lacking exon 5 was expressed in murine heart. Differentiation of U937 human monoblasts into macrophages did not alter expression of the tafazzin transcripts indicating that TAZ expression is independent of monocyte differentiation. Cloning and in vitro expression of both murine and human tafazzin cDNA revealed two prominent protein bands that corresponded to the expected sizes of alternative translation. A novel fifth motif, identified as critical for the glycerolphosphate acyltransferase family, was observed in human tafazzin. The presence of a mutation in this region in Barth syndrome patients indicates that this motif is essential for tafazzin function.Key words: cardiolipin, murine, heart, Barth Syndrome, phospholipid, acyltransferase, tafazzin.

Investigations of the influence of microgravity on the state of human cell lines

2004 ◽  
Vol 10 (5-6) ◽  
pp. 226-228
Author(s):  
L.M. Nosach ◽  
◽  
O.Yu. Povnitsa ◽  
V.L. Zhovnovata ◽  
◽  
...  
Keyword(s):  
Cell Lines ◽  
Human Cell ◽  
The State ◽  
Human Cell Lines
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