Stable overexpression of arginase I and ornithine transcarbamylase in HepG2 cells improves its ammonia detoxification

2012 ◽  
Vol 113 (2) ◽  
pp. 518-527 ◽  
Author(s):  
Nanhong Tang ◽  
Yan Wang ◽  
Xiaoqian Wang ◽  
Liangyi Zhou ◽  
Feiyuan Zhang ◽  
...  
Keyword(s):  
Hepg2 Cells ◽  
Ornithine Transcarbamylase ◽  
Ammonia Detoxification ◽  
Arginase I

Comprehensive characterization of ureagenesis in the spf ash mouse, a model of human ornithine transcarbamylase deficiency, reveals age‐dependency of ammonia detoxification

2019 ◽  
Vol 42 (6) ◽  
pp. 1064-1076 ◽  
Author(s):  
Gabriella Allegri ◽  
Sereina Deplazes ◽  
Nicole Rimann ◽  
Benjamin Causton ◽  
Tanja Scherer ◽  
...  
Keyword(s):  
Ornithine Transcarbamylase ◽  
Ornithine Transcarbamylase Deficiency ◽  
Age Dependency ◽  
Ammonia Detoxification ◽  
Comprehensive Characterization

Promoter and 11-kilobase upstream enhancer elements responsible for hepatoma cell-specific expression of the rat ornithine transcarbamylase gene

1990 ◽  
Vol 10 (3) ◽  
pp. 1180-1191
Author(s):  
T Murakami ◽  
A Nishiyori ◽  
M Takiguchi ◽  
M Mori
Keyword(s):  
Transient Expression ◽  
Expression Analysis ◽  
Base Pair ◽  
Cho Cells ◽  
Hepg2 Cells ◽  
Hepatoma Cell ◽  
Regulatory Elements ◽  
Ornithine Transcarbamylase ◽  
Footprint Analysis ◽  
Flanking Region

The gene for ornithine transcarbamylase (OTC; EC 2.1.3.3), a urea cycle enzyme, is expressed almost exclusively in the liver and small intestine. To identify DNA elements regulating transcription of the OTC gene in the liver, transient expression analysis was carried out by using hepatoma (HepG2) and nonhepatic (CHO) cell lines. The 1.3-kilobase 5'-flanking region of the rat OTC gene directed expression of the fused chloramphenicol acetyltransferase gene in HepG2 cells much more efficiently than in CHO cells. Analysis of deletion mutants of the 5'-flanking region in HepG2 cells revealed that there are at least one negative and two positive regulatory elements within the about 220-base-pair immediate 5'-flanking region. DNase I footprint analysis showed the presence of factors binding to these regulatory elements in nuclear extracts of rat liver and brain, and footprint profiles at the two positive elements exhibited liver-specific features. Transient expression analysis also revealed the existence of an enhancer region located 11 kilobases upstream of the transcription start site. The OTC enhancer was able to activate both its own and heterologous promoters in HepG2 but not in CHO cells. The enhancer was delimited to an about 230-base-pair region, and footprint analysis of this region revealed four protected areas. Footprint profiles at two of the four areas exhibited liver-specific features, and gel shift competition analysis showed that a factor(s) binding to the two liver-specific sites is related to C/EBP. These results suggest that both liver-specific promoter and enhancer elements regulate expression of the OTC gene through interaction with liver-specific factors binding to these elements.

Ornithine transcarbamylase and arginase I deficiency are responsible for diminished urea cycle function in the human hepatoblastoma cell line HepG2

2007 ◽  
Vol 39 (3) ◽  
pp. 555-564 ◽  
Author(s):  
Demetra Mavri-Damelin ◽  
Simon Eaton ◽  
Leonard H. Damelin ◽  
Myrddin Rees ◽  
Humphrey J.F. Hodgson ◽  
...  
Keyword(s):  
Cell Line ◽  
Urea Cycle ◽  
Ornithine Transcarbamylase ◽  
Arginase I ◽  
Hepatoblastoma Cell Line

scholarly journals Promoter and 11-kilobase upstream enhancer elements responsible for hepatoma cell-specific expression of the rat ornithine transcarbamylase gene.

1990 ◽  
Vol 10 (3) ◽  
pp. 1180-1191 ◽  
Author(s):  
T Murakami ◽  
A Nishiyori ◽  
M Takiguchi ◽  
M Mori
Keyword(s):  
Transient Expression ◽  
Expression Analysis ◽  
Base Pair ◽  
Cho Cells ◽  
Hepg2 Cells ◽  
Hepatoma Cell ◽  
Regulatory Elements ◽  
Ornithine Transcarbamylase ◽  
Footprint Analysis ◽  
Flanking Region

The gene for ornithine transcarbamylase (OTC; EC 2.1.3.3), a urea cycle enzyme, is expressed almost exclusively in the liver and small intestine. To identify DNA elements regulating transcription of the OTC gene in the liver, transient expression analysis was carried out by using hepatoma (HepG2) and nonhepatic (CHO) cell lines. The 1.3-kilobase 5'-flanking region of the rat OTC gene directed expression of the fused chloramphenicol acetyltransferase gene in HepG2 cells much more efficiently than in CHO cells. Analysis of deletion mutants of the 5'-flanking region in HepG2 cells revealed that there are at least one negative and two positive regulatory elements within the about 220-base-pair immediate 5'-flanking region. DNase I footprint analysis showed the presence of factors binding to these regulatory elements in nuclear extracts of rat liver and brain, and footprint profiles at the two positive elements exhibited liver-specific features. Transient expression analysis also revealed the existence of an enhancer region located 11 kilobases upstream of the transcription start site. The OTC enhancer was able to activate both its own and heterologous promoters in HepG2 but not in CHO cells. The enhancer was delimited to an about 230-base-pair region, and footprint analysis of this region revealed four protected areas. Footprint profiles at two of the four areas exhibited liver-specific features, and gel shift competition analysis showed that a factor(s) binding to the two liver-specific sites is related to C/EBP. These results suggest that both liver-specific promoter and enhancer elements regulate expression of the OTC gene through interaction with liver-specific factors binding to these elements.

Differenzial diagnosis of acute encephalopathy: Acute decompensation in ornithine transcarbamylase (OTC) deficiency in a seven year old girl

2011 ◽  
Vol 42 (S 01) ◽  
Author(s):  
C Abels ◽  
B Fiedler ◽  
W Weimer ◽  
F Rutsch ◽  
G Kurlemann
Keyword(s):  
Ornithine Transcarbamylase ◽  
Acute Encephalopathy ◽  
Acute Decompensation ◽  
Otc Deficiency

Linalool Effect on HepG2 cells: Structure Function Relation

Planta Medica ◽  
2011 ◽  
Vol 77 (12) ◽  
Author(s):  
J Usta ◽  
K Racha ◽  
K Boushra ◽  
S Shatha ◽  
B Yolla ◽  
...  
Keyword(s):  
Structure Function ◽  
Hepg2 Cells ◽  
Function Relation

Transcriptome analysis in HepG2 cells revealed multiple activity mechanisms of a Tibetan polyherbal formula

2012 ◽  
Vol 33 (S 01) ◽  
Author(s):  
K Becker ◽  
A Klein ◽  
OA Wrulich ◽  
P Gruber ◽  
D Fuchs ◽  
...  
Keyword(s):  
Transcriptome Analysis ◽  
Hepg2 Cells

Impact of soluble Endoglin on TGF-β1 mediated immediate early responses in HepG2 cells

2014 ◽  
Vol 52 (01) ◽  
Author(s):  
M Neß ◽  
SK Meurer ◽  
E Borkham-Kamphorst ◽  
R Weiskirchen
Keyword(s):  
Hepg2 Cells ◽  
Immediate Early ◽  
Soluble Endoglin ◽  
Tgf Β1

The Effects of Vitamin K1 and Warfarin on Prothrombin Expression in Human Hepatoblastoma (HepG2) Cells

1992 ◽  
Vol 68 (01) ◽  
pp. 040-047 ◽  
Author(s):  
C Scott Jamison ◽  
Bryan F Burkey ◽  
Sandra J Friezner Degen
Keyword(s):  
Total Protein ◽  
Hepg2 Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Response Analysis ◽  
Secreted Protein ◽  
Mrna Levels ◽  
Vitamin K1 ◽  
Maximal Increase ◽  
Protein Levels ◽  
Warfarin Treatment

SummaryCultures of human hepatoblastoma (HepG2) cells were treated with vitamin K1 or warfarin and prothrombin antigen and mRNA levels were determined. With 3 and 6 h of 10 µg vitamin K1 treatment secreted prothrombin antigen levels, relative to total secreted protein levels, were increased 1.5-fold and 2.1-fold, respectively, over ethanol-treated control levels as determined by an enzyme-linked immunosorbent assay. Dose-response analysis with 3 h of 25 µg/ml vitamin K1 treatment demonstrated a maximal increase of 2.0-fold in secreted prothrombin antigen levels, relative to total secreted protein levels, over ethanol-treated control levels. Pulse-chase analysis with 35S-methionine and immunoprecipitation of 35S-labelled prothrombin demonstrated that, with vitamin K1 treatment (25 µg/ml, 3 h), the rate of prothrombin secretion increased approximately 2-fold and the total amount (intra- and extracellular) of prothrombin synthesized increased approximately 50% over ethanol-treated control levels. Warfarin treatment (1, 5, or 10 µg/ml, 24 h) resulted in decreases in secreted prothrombin antigen levels, relative to total protein levels to approximately 85%, 87% or 81% of ethanol-treated control levels. Analysis of total RNA isolated from these cultures by Northern and solution hybridization techniques demonstrated that prothrombin mRNA was approximately 2.1 kb and that neither vitamin K1 nor warfarin treatment affected the quantity of prothrombin mRNA (ranging from 240–350 prothrombin mRNA molecules per cell). These results demonstrate that vitamin K1 and warfarin, in addition to effects on γ-carboxylation, affect prothrombin synthesis post-transcriptionally, perhaps influencing translation, post-translational processing and/or secretion mechanisms.

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