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retinoblastoma/− nikotyna

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Tobacco use in adult long-term survivors of retinoblastoma.

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A significant risk of lung cancer was identified among hereditary, but not nonhereditary, retinoblastoma (Rb) patients. Tobacco use was investigated to determine whether differences in smoking prevalence might explain the lung cancer excess and to characterize smoking patterns in adult survivors of

Tobacco retinoblastoma-related protein phosphorylated by a distinct cyclin-dependent kinase complex with Cdc2/cyclin D in vitro.

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The retinoblastoma (Rb) protein was originally identified as a product of a tumour suppressor gene that plays a pivotal role in regulating both the cell cycle and differentiation in mammals. The growth-suppressive activity of Rb is regulated by phosphorylation with cyclin-dependent kinase (CDK), and
BACKGROUND Geminiviruses mainly infect terminally differentiated tissues and cells in plants. They need to reprogramme host cellular machinery for DNA replication. This process is thought to be mediated by inactivation of cell-cycle repressor proteins and by induction of host DNA synthesis protein

Geminivirus-induced gene silencing of the tobacco retinoblastoma-related gene results in cell death and altered development.

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The retinoblastoma-related protein (RBR) is required for cell cycle control and differentiation and is expressed throughout the life of plants and animals. In this study, the tomato golden mosaic virus (TGMV) geminivirus vector was used to silence NbRBR1 in Nicotiana benthamiana by microprojectile

Phosphorylation of retinoblastoma-related protein by the cyclin D/cyclin-dependent kinase complex is activated at the G1/S-phase transition in tobacco.

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In mammals, D-type cyclin-associated kinases mainly regulate the G1/S transition by phosphorylating the retinoblastoma (Rb) protein. We previously demonstrated that in tobacco, cyclin D (Nicta; CycD3;3) is complexed with the PSTAIRE-containing cyclin-dependent kinase (CDKA) from tobacco. Here, we
Evidence is emerging that the E2F family of transcription factors plays an important role in the regulation of gene expression at the G1/S transition in plants. Here, we show that in the tobacco proliferating cell nuclear antigen (PCNA), whose transcript is specifically expressed at G1/S phase, the

Long-term exposure to nicotine, via ras pathway, induces cyclin D1 to stimulate G1 cell cycle transition.

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Nicotine, a major component in tobacco, has been implicated as a potential factor that promotes the development of lung cancer. However, the molecular mechanism of its action is still unclear. In this study, we have shown that, via nicotinic acetylcholine receptors, persistent exposure of mouse
BACKGROUND Tobacco smoke is by far the greatest risk factor for non-small-cell lung cancer (NSCLC). Nicotine, an active alkaloid in tobacco, is unable to initiate tumorigenesis in humans and rodents, but can promote the growth and metastasis of various tumors, including NSCLC, initiated by tobacco

Analysis of putative interactions between potyviral replication proteins and plant retinoblastoma proteins.

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Sequence comparisons suggest that the RNA-dependent RNA polymerase (NIb) of potyviruses and bymoviruses, as well as the viral polymerase of potexviruses may contain a putative retinoblastoma protein (pRb) binding motif. The possibility that the potyviral NIb may function in the nucleus through

Duration but not intensity of alcohol and tobacco exposure predicts p16INK4A homozygous deletion in head and neck squamous cell carcinoma.

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In tobacco-associated solid tumors, evidence suggests that the pattern of carcinogen exposure is related to the nature of somatic gene inactivation within crucial pathways, including the retinoblastoma (Rb) pathway. One somatic event in this pathway, homozygous deletion of the p16INK4A gene, is

Auxin is required for the assembly of A-type cyclin-dependent kinase complexes in tobacco cell suspension culture.

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Although activation of A-type cyclin-dependent kinase (CDKA) is required for plant cell division, little is known about how CDKA is activated before commitment to cell division. Here, we show that auxin is required for the formation of active CDKA-associated complexes, promoting assembly of the

The pro-proliferative effects of nicotine and its underlying mechanism on rat airway smooth muscle cells.

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Recent studies have shown that nicotine, a major component of cigarette smoke, can stimulate the proliferation of non-neuronal cells. Cigarette smoking can promote a variety of pulmonary and cardiovascular diseases, such as chronic obstructive pulmonary disease (COPD), atherosclerosis, and cancer. A

Different susceptibility of increased DNMT1 expression by exposure to tobacco smoke according to histology in primary non-small cell lung cancer.

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OBJECTIVE DNA methyltransferase 1 (DNMT1) is known to play an important role in the development of cancers. However, the underlying mechanisms responsible for the altered expression of DNMT1 in non-small cell lung cancers (NSCLCs) remain to be elucidated. METHODS We investigated the relationships of

On the mechanism of the cell cycle control of suspension-cultured tobacco cells after exposure to static magnetic field.

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One of the main sites of the magnetic fields influence on living cells is the cell cycle. The intensity of this influence however, varies depending on the cell type and the duration of the treatment. Suspension of cultured tobacco cells (Nicotiana tabacum cv. Barley 21) were synchronized via sucrose

Cloning and Expression Profiling of the Polycomb Gene, Retinoblastoma-related Protein from Tomato Solanum lycopersicum L.

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Cell cycle regulation mechanisms appear to be conserved throughout eukaryotic evolution. One of the important proteins involved in the regulation of cell cycle processes is retinoblastoma-related protein (RBR), which is a negative regulator of cell cycle progression, controlling the G1/S transition
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