An in vivo study on the synchronizing effect of hydroxyurea

Maurer‐Schultze, B.; Siebert, Michael; Bassukas, Ioannis D.

doi:10.1016/0014-4827(88)90157-7

Cited by 51 publications

(23 citation statements)

References 30 publications

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“…Cell-cycle inhibitors mimic the effect of MV on lymphoproliferation and p24 antigen production Cell-cycle blocking agents were used to induce phase-specific inhibition of the cell cycle and simulate the effect of MV on lymphoproliferation and p24 antigen production. Thapsigargin induces a block in G 0 (Furuya et al, 1994), nbutyrate at G 1a (Darzynkiewicz et al, 1981;Korin & Zack, 1998) and hydroxyurea in G 1 /S (Maurer-Schultze et al, 1988). Thapsigargin failed to produce consistent dosedependent reductions in either lymphoproliferation or p24 antigen production (Fig.…”

Section: Blocks Hiv-1 Reverse Transcription In Hiv-1-infected Pbmcsmentioning

confidence: 86%

“…The effects of MV on lymphoproliferation and p24 antigen production were simulated by hydroxyurea, a drug that blocks the cell cycle in G 1 /S phase (Maurer-Schultze et al, 1988), and by n-butyrate, which blocks the cell cycle at G 1a (Darzynkiewicz et al, 1981;Korin & Zack, 1998). Thapsigargin, which blocks the cell cycle at G 0 , did not consistently reduce lymphoproliferation or p24 antigen production.…”

Section: Discussionmentioning

confidence: 99%

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Measles virus inhibits human immunodeficiency virus type 1 reverse transcription and replication by blocking cell-cycle progression of CD4+ T lymphocytes

Garcia

Griffin

et al. 2008

Journal of General Virology

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Acute measles virus (MV) infection results in a decrease in plasma human immunodeficiency virus type 1 (HIV-1) RNA levels in co-infected children. An in vitro peripheral blood mononuclear cell (PBMC) culture system was used to assess the mechanisms by which MV blocks HIV-1 replication. MV inhibited proliferation of CD4 + T lymphocytes, the target cell for HIV-1 replication. In the presence of MV, cells did not progress to G 1b and S phases, steps critical for the completion of HIV-1 reverse transcription and productive replication. This block in cell-cycle progression was characterized by an increased proportion of CD4 + and HIV-1-infected cells retained in the parental generation in PBMCs co-cultured with MV and HIV-1, and decreased levels of cyclins and RNA synthesis. Early HIV-1 replication was also inhibited in the presence of MV, as measured by reduced expression of a luciferase reporter gene and lower levels of both early (LTR) and late (LTR-gag) DNA intermediates of HIV-1 reverse transcription in the presence of CCR5-tropic HIV-1. The effects of MV on lymphoproliferation and p24 antigen production were reproduced by n-butyrate and hydroxyurea, drugs that block the cell cycle in G 1a and G 1 /S, respectively. It was concluded that MV inhibits HIV-1 productive replication in part by blocking the proliferation of CD4 + T lymphocytes.

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Section: Blocks Hiv-1 Reverse Transcription In Hiv-1-infected Pbmcsmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Measles virus inhibits human immunodeficiency virus type 1 reverse transcription and replication by blocking cell-cycle progression of CD4+ T lymphocytes

Garcia

Griffin

et al. 2008

Journal of General Virology

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“…29 In the second part of our study, we sought to confirm our results by assessing the effect of the tyrosine kinase inhibitor STI571 on the cell cycle status of CML CD34 + HPC. It should be noted that all patients treated with STI571 had received antineoplastic therapies prior to inclusion in this study, as requested by the study protocols, including hydroxyurea, which is known to cause cell cycle arrest in early S phase, 30 in nine of 13 cases. Thus, the lower proliferation rates of CD34 + HPC from these patients as compared to the patients with newly diagnosed CML are explained by this pretreatment.…”

Section: Discussionmentioning

confidence: 99%

Proliferating status of peripheral blood progenitor cells from patients with BCR/ABL-positive chronic myelogenous leukemia

et al. 2001

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“…The latter folate is used in the production of purines, required for synthesis of the RNA primers during initiation of DNA replication, as well as for general DNA synthesis (reviewed by Rosenblatt and Fenton, 2001). These drugs have been reported to arrest cells at different phases of the cell cycle: mimosine at late G 1 (Biard et al, 2003;Lalande, 1990;Krek and DeCaprio, 1995) and during S-phase (Gilbert et al, 1995), and HU at the onset of S-phase (Maurer-Schultze et al, 1988;Merrill, 1998). A double cell-cycle block, using thymidine and then either mimosine or HU, arrested the cells either in late G 1 (Fig.…”

Section: Discussionmentioning

confidence: 99%

Decreased origin usage and initiation of DNA replication in haploinsufficient HCT116 Ku80+/- cells

Sibani

Price

Zannis‐Hadjopoulos

2005

Journal of Cell Science

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One of the functions of the abundant heterodimeric nuclear protein, Ku (Ku70/Ku80), is its involvement in the initiation of DNA replication through its ability to bind to chromosomal replication origins in a sequence-specific and cell cycle dependent manner. Here, using HCT116 Ku80+/- cells, the effect of Ku80 deficiency on cell cycle progression and origin activation was examined. Western blot analyses revealed a 75% and 36% decrease in the nuclear expression of Ku80 and Ku70, respectively. This was concomitant with a 33% and 40% decrease in chromatin binding of both proteins, respectively. Cell cycle analysis of asynchronous and late G1 synchronized Ku80+/- cells revealed a prolonged G1 phase. Furthermore, these Ku-deficient cells had a 4.5-, 3.4- and 4.3-fold decrease in nascent strand DNA abundance at the lamin B2, β-globin and c-myc replication origins, respectively. Chromatin immunoprecipitation (ChIP) assays showed that the association of Ku80 with the lamin B2, β-globin and c-myc origins was decreased by 1.5-, 2.3- and 2.5-fold, respectively, whereas that of Ku70 was similarly decreased (by 2.1-, 1.5- and 1.7-fold, respectively) in Ku80+/- cells. The results indicate that a deficiency of Ku80 resulted in a prolonged G1 phase, as well as decreased Ku binding to and activation of origins of DNA replication.

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An in vivo study on the synchronizing effect of hydroxyurea

Cited by 51 publications

References 30 publications

Measles virus inhibits human immunodeficiency virus type 1 reverse transcription and replication by blocking cell-cycle progression of CD4+ T lymphocytes

Measles virus inhibits human immunodeficiency virus type 1 reverse transcription and replication by blocking cell-cycle progression of CD4+ T lymphocytes

Proliferating status of peripheral blood progenitor cells from patients with BCR/ABL-positive chronic myelogenous leukemia

Decreased origin usage and initiation of DNA replication in haploinsufficient HCT116 Ku80+/- cells

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