Unscheduled cyclin B expression and p34 cdc2 activation in T lymphocytes from HIV-infected patients

Piedimonte, Giuseppe; Corsi, Dario; Paiardini, Mirco; Cannavò, Giuseppe; Ientile, Riccardo; Picerno, Isa; Montroni, M; Silvestri, Guido; Magnani, Mauro

doi:10.1097/00002030-199907090-00003

Cited by 37 publications

(68 citation statements)

References 28 publications

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“…Thus, cyclin B has been found to be overexpressed in circulating T lymphocytes from HIV-1 carriers, and this upregulation disappears upon successful antiretroviral therapy. 71,72 Similarly, mTOR and the phosphoneoepitope indicating phosphorylation of p53 on serine 15 were found to be overexpressed among a fraction of peripheral blood mononuclear cells, correlating with viral load, 55,62 as well as with the frequency of cells expressing tissue transglutaminase-2, a marker of preapoptosis. 73 Highly active antiretroviral therapy (HAART) corrected the abnormally high mTOR and p53S15P levels of the patients.…”

Section: Syncytial Apoptosis Induced By Envmentioning

confidence: 97%

Mechanisms of apoptosis induction by the HIV-1 envelope

et al. 2005

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The envelope glycoprotein complex (Env) of human immunodeficiency virus-1 (HIV-1) can induce apoptosis by a cornucopia of distinct mechanisms. A soluble Env derivative, gp120, can kill cells through signals that are transmitted by chemokine receptors such as CXCR4. Cell surface-bound Env (gp120/gp41), as present on the plasma membrane of HIV-1-infected cells, can kill uninfected bystander cells expressing CD4 and CXCR4 (or similar chemokine receptors, depending on the Env variant) by at least three different mechanisms.

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Section: Syncytial Apoptosis Induced By Envmentioning

confidence: 97%

Mechanisms of apoptosis induction by the HIV-1 envelope

et al. 2005

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“…These alterations return to normal after successful antiretroviral therapy. 44,45 The increased expression of cyclin B has been correlated with an enhanced half-life of the cyclin B protein and is associated with a decreased level of cyclin B ubiquitination. 45 In vitro, CD4 + T cells exposed to cells expressing the HIV-1 envelope (Env) gene can undergo cell death while arresting in the G2/M-phase without any significant formation of syncytia.…”

Section: Cdk1 In Mitotic Catastrophementioning

confidence: 99%

Cyclin-dependent kinase-1: linking apoptosis to cell cycle and mitotic catastrophe

et al. 2002

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The cyclin-dependent kinase 1 (Cdk1), formerly called Cdc2 (or p34 Cdc2 ), interacts with cyclin B1 to form an active heterodimer. The activity of Cdk1 is subjected to a complex spatiotemporary regulation, required to guarantee its scheduled contribution to the mitotic prophase and metaphase. Moreover, the activation of Cdk1 may be required for apoptosis induction in some particular pathways of cell killing. This applies to several clinically important settings, for instance to paclitaxel-induced killing of breast cancer cells, in which the ErbB2 receptor kinase can mediate apoptosis inhibition through inactivation of Cdk1. The activation of Cdk1 participates also in HIV-1-induced apoptosis, upstream of the p53-dependent mitochondrial permeabilization step. An unscheduled Cdk1 activation may contribute to neuronal apoptosis occurring in neurodegenerative diseases. Finally, the premature activation of Cdk1 can lead to mitotic catastrophe, for instance after irradiation-induced DNA damage. Thus, a cell type-specific modulation of Cdk1 might be taken advantage of for the therapeutic correction of pathogenic imbalances in apoptosis control.

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“…Cytokines, in contrast, prevented both the apoptotic phenotype and the cell death by preserving mitochondrial membrane potential staining for the argyrophilic Nucleolar Organizing Regions (AgNOR) and the subcellular localization of nucleolin in confocal microscopy. [122][123][124][125][126][127] Importantly, the HIV-associated cell cycle dysregulation is exacerbated by in vitro treatment with mitogens and appears to be correlated with induction of T-cell apoptosis; 122,123,126 however, these cell cycle perturbations and apoptosis are reduced after exogenous administration of IL-2 in vitro. 122 In mitogen-activated lymphocytes from HIV-infected patients, the inappropriate activation of the cyclin B1/p34 cdc2 kinase complex is temporally associated with increased threonine phosphorylation, augmented fragmentation, and prominent extranuclear and cell surface localization of nucleolin.…”

Section: Cell Cycle Dysregulationmentioning

confidence: 99%