Uptake of Protein by Regenerating Liver Cells

Nature ◽  
1964 ◽  
Vol 204 (4964) ◽  
pp. 1210-1211 ◽  
Author(s):  
T. GHOSE ◽  
S. C. TSO
Keyword(s):  
Liver Cells ◽  
Regenerating Liver

The endoplasmic reticulum in regenerating liver cells

1985 ◽  
Vol 240 (1) ◽  
Author(s):  
Lillemor Lewan ◽  
Hadar Emanuelsson
Keyword(s):  
Endoplasmic Reticulum ◽  
Liver Cells ◽  
Regenerating Liver

1α, 25-Dihydroxyvitamin D3 enables regenerating liver cells to make functional ribonucleotide reductase subunits and replicate DNA in thyroparathyroidectomized rats

1985 ◽  
Vol 63 (5) ◽  
pp. 319-324 ◽  
Author(s):  
T. Youdale ◽  
J. F. Whitfield ◽  
R. H. Rixon
Keyword(s):  
Body Weight ◽  
Dna Replication ◽  
Ribonucleotide Reductase ◽  
Intraperitoneal Injection ◽  
Liver Cells ◽  
Regenerating Liver ◽  
Dihydroxyvitamin D3 ◽  
Dihydroxyvitamin D ◽  
Do So

Between 16 and 20 h after partial (70%) hepatectomy (HPX) in normal rats, the remaining liver cells accumulate ribonucleotide reductase subunits, assemble these into active holoenzyme, and initiate DNA replication. These late prereplicative activities did not occur in most of the liver cells remaining after HPX in rats which had been thyroparathyroidectomized (TPTX) 72 h previously. However, one intraperitoneal injection of 400 or 600 ng 1α, 25-dihydroxyvitamin D3/100 g body weight at the time of HPX enabled the remaining liver cells in such TPTX rats to make functional ribonucleotide reductase subunits, assemble these subunits into active CDP-reducing holoenzymes, and replicate their DNA, though they started to do so 4 to 16 h later than in normal animals.

The gene encoding rat insulinlike growth factor-binding protein 1 is rapidly and highly induced in regenerating liver

1991 ◽  
Vol 11 (3) ◽  
pp. 1393-1401 ◽  
Author(s):  
K L Mohn ◽  
A E Melby ◽  
D S Tewari ◽  
T M Laz ◽  
R Taub
Keyword(s):  
Growth Factor ◽  
Binding Protein ◽  
Normal Liver ◽  
Liver Cells ◽  
Immediate Early ◽  
Cdna Libraries ◽  
Regenerating Liver ◽  
Liver Growth ◽  
Insulinlike Growth Factor ◽  
Igf I

The liver is an epithelioid organ that can regenerate following partial hepatectomy. Although it is composed mainly of hepatocytes, it has a complex, multicellular architecture, implying that intercellular communications must exist during regeneration. As in other mitogen-stimulated cells, immediate-early growth response genes induced in the absence of prior protein synthesis are likely to play an important regulatory role in the regenerative process. Through differential screening of regenerating liver cDNA libraries, we found that one of the most highly expressed immediate-early genes in liver regeneration encodes the rat homolog of the low-molecular-weight insulinlike growth factor (IGF)-binding protein (IGFBP-1). This protein has been implicated in enhancing the mitogenic effect of IGF on tissues. IGFBP-1 gene induction is transcriptionally mediated and specific to regenerating liver, as the gene is not expressed in mitogen-stimulated fibroblasts. IGFBP-1 expression has been shown to increase under low-insulin conditions such as diabetes, and the complex regulation of expression is indicated by our finding that insulin treatment of H35 rat hepatoma cells, which induces proliferation, also causes a rapid decrease in transcription and expression of the IGFBP-1 gene. Of note, IGFBP-1 mRNA is abundant in fetal rat liver, implying that it participates in normal liver growth and development. Although regenerating liver cells continue to produce IGF-I, we did not detect IGF-I receptor mRNA during the first 24 h after hepatectomy. However, some IGFBPs may act to enhance the activity of IGF-I independently of IGF-I receptors. Thus, IGF-1 and IGFBPs may interact with hepatocytes or nonparenchymal liver cells, through either IGF-I or novel receptors. In this way, IGFBP-I and IGF-I could act in a paracrine and/or autocrine fashion in maintaining normal liver architecture during regeneration.

Intracellular ribonucleic acid composition in regenerating liver cells

1958 ◽  
Vol 27 ◽  
pp. 395-401 ◽  
Author(s):  
Gaston de Lamirande ◽  
Claude Allard ◽  
Antonio Cantero
Keyword(s):  
Acid Composition ◽  
Ribonucleic Acid ◽  
Liver Cells ◽  
Regenerating Liver

Changes in the cytoplasmic and nuclear activities of the ribonucleotide reductase holoenzyme and its subunits in regenerating liver cells in normal and thyroparathyroidectomized rats

1984 ◽  
Vol 62 (9) ◽  
pp. 914-919 ◽  
Author(s):  
T. Youdale ◽  
L. Frappier ◽  
J. F. Whitfield ◽  
R. H. Rixon
Keyword(s):  
Dna Synthesis ◽  
Ribonucleotide Reductase ◽  
Maximum Level ◽  
Liver Cells ◽  
Synthetic Activity ◽  
Regenerating Liver ◽  
Nuclear Level ◽  
Rat Liver Cells ◽  
Specific Effector ◽  
High Level

The level of the cytoplasmic ribonucleotide reductase nonheme-iron-containing L2 subunit in regenerating rat liver cells began rising about 2 h before the onset of DNA synthesis, rose sharply to a maximum level about 4 h before the DNA-synthetic activity reached its peak, and then stayed at this high level even after the cells had finished replicating their DNA. The cytoplasmic level of the CDP-specific, effector-binding L1 subunit and the holoenzyme activity began rising together about 2 h after the L2 subunit began increasing and at the same time as the DNA-synthetic activity, but subsequently rose much more slowly than the L2 subunit and continued rising even after the cells had finished making DNA. The nuclear level of the L2 subunit did not rise in the regenerating liver cells, but the nuclear level of the L1 subunit and the holoenzyme activity began rising together about the same time as the DNA-synthetic activity, peaked briefly 4–6 h before the peak DNA-synthetic activity, and dropped sharply back to the basal levels by the time the DNA-synthetic activity reached its peak, but then rose again slowly as the cells finished making DNA. Thyroparathyroidectomy 72 h before partial hepatectomy prevented the cytoplasmic and nuclear subunits and holoenzyme activity from rising and prevented most of the remaining liver cells from initiating DNA synthesis.

scholarly journals p21 Inhibits Cdk1 in the Absence of Cdk2 to Maintain the G1/S Phase DNA Damage Checkpoint

2008 ◽  
Vol 19 (1) ◽  
pp. 65-77 ◽  
Author(s):  
Ande Satyanarayana ◽  
Mary Beth Hilton ◽  
Philipp Kaldis
Keyword(s):  
Dna Damage ◽  
Liver Cells ◽  
S Phase ◽  
Dna Damage Checkpoint ◽  
Regenerating Liver ◽  
Γ Irradiation ◽  
Embryonic Fibroblasts ◽  
Repair Activity ◽  
Lethal Irradiation

Cdk1 was proposed to compensate for the loss of Cdk2. Here we present evidence that this is possible due to premature translocation of Cdk1 from the cytoplasm to the nucleus in the absence of Cdk2. We also investigated the consequence of loss of Cdk2 on the maintenance of the G1/S DNA damage checkpoint. Cdk2−/− mouse embryonic fibroblasts in vitro as well as regenerating liver cells after partial hepatectomy (PH) in Cdk2−/− mice, arrest promptly at the G1/S checkpoint in response to γ-irradiation due to activation of p53 and p21 inhibiting Cdk1. Furthermore re-entry into S phase after irradiation was delayed in Cdk2−/− cells due to prolonged and impaired DNA repair activity. In addition, Cdk2−/− mice were more sensitive to lethal irradiation compared to wild-type and displayed delayed resumption of DNA replication in regenerating liver cells. Our results suggest that the G1/S DNA damage checkpoint is intact in the absence of Cdk2, but Cdk2 is important for proper repair of the damaged DNA.

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