Cell cycle arrest and morphological alterations following microinjection of NIH3T3 cells with Puraα

Stacey, Dennis W.; Hitomi, Masahiro; Kanovsky, Mechael; Gan, Li; Johnson, Edward M.

doi:10.1038/sj.onc.1202795

Cited by 54 publications

(48 citation statements)

References 40 publications

(32 reference statements)

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“…They participate in cell proliferation, differentiation, and apoptosis as well as cell-specific gene regulation. Cellular levels of PUR proteins fluctuate significantly during the cell cycle, and micro injection of PUR␣ into proliferating NIH3T3 cells during the S phase has been shown to cause cell cycle arrest, thus documenting a critical role of PUR proteins in cell division and growth (30,31). PUR proteins are also highly expressed in cardiac myocytes, and their level changes in diseased hearts; however, except this study we are not aware of any previous report where a role of these proteins in cardiac muscle gene regulation has been reported.…”

Section: Discussionmentioning

confidence: 99%

Single-stranded DNA-binding Proteins PURα and PURβ Bind to a Purine-rich Negative Regulatory Element of the α-Myosin Heavy Chain Gene and Control Transcriptional and Translational Regulation of the Gene Expression

Gupta

Sueblinvong

Raman

et al. 2003

Journal of Biological Chemistry

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The ␣-myosin heavy chain is a principal molecule of the thick filament of the sarcomere, expressed primarily in cardiac myocytes. The mechanism for its cardiacrestricted expression is not yet fully understood. We previously identified a purine-rich negative regulatory (PNR) element in the first intron of the gene, which is essential for its cardiac-specific expression (Gupta, M., Zak, R., Libermann, T. A., and Gupta, M. P.

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Section: Discussionmentioning

confidence: 99%

Single-stranded DNA-binding Proteins PURα and PURβ Bind to a Purine-rich Negative Regulatory Element of the α-Myosin Heavy Chain Gene and Control Transcriptional and Translational Regulation of the Gene Expression

Gupta

Sueblinvong

Raman

et al. 2003

Journal of Biological Chemistry

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“…43 Thirdly, high intracellular levels of Pur␣ have been reported to arrest cell cycle progression. 44 Even modestly increased levels of Pur␣ can reverse certain aspects of ras transformation of NIH3T3 cells (S Barr and EM Johnson, J Cell Biochem 2001, in press). Mutations in the Rb protein are rarely reported in myeloid disorders, 45 whereas deletions of PUR gene family members are relatively common.…”

Section: Discussionmentioning

confidence: 99%

Deletions of PURA, at 5q31, and PURB, at 7p13, in myelodysplastic syndrome and progression to acute myelogenous leukemia

Lezon-Geyda

Najfeld

Em³

2001

Leukemia

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“…We previously developed a method to analyse cell cycle progression without synchronization by combining time lapse, quantitative fluorescent microscopy and microinjection (Hitomi and Stacey, 1999a,b;Stacey et al, 1999Stacey et al, , 2000. This approach revealed that in asynchronous NIH3T3 cell cultures, cyclin D1 is induced in a Ras-dependent manner during cell cycle transition from S to G2 phase.…”

Section: Introductionmentioning

confidence: 99%

“…Cdc6, an E2F target molecule essential for DNA replications, is expressed at very low levels in G1 phase from quiescence, but it is expressed at high levels throughout the cell cycle in proliferating cultures (Yan et al, 1998). Therefore, observations of quiescent cultures reentering the cell cycle may not always be applicable to G1/S transition in rapidly cycling cells.We previously developed a method to analyse cell cycle progression without synchronization by combining time lapse, quantitative fluorescent microscopy and microinjection (Hitomi and Stacey, 1999a,b;Stacey et al, 1999Stacey et al, , 2000. This approach revealed that in asynchronous NIH3T3 cell cultures, cyclin D1 is induced in a Ras-dependent manner during cell cycle transition from S to G2 phase.…”

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confidence: 99%

Post-transcriptional regulation of cyclin D1 expression during G2 phase

2002

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During continuous proliferation, cyclin D1 protein is induced to high levels in a Ras-dependent manner as cells progress from S phase to G2 phase. To understand the mechanism of the Ras-dependent cyclin D1 induction, cyclin D1 mRNA levels were determined by quantitative image analysis following fluorescent in situ hybridization. Although a slight increase in mRNA expression levels was detected during the S/G2 transition, this increase could not explain the more robust induction of cyclin D1 protein levels. This suggested the involvement of posttranscriptional regulation as a mechanism of cyclin D1 protein induction. To directly test this hypothesis, the cyclin D1 transcription rate was determined by run-on assays. The transcription rate of cyclin D1 stayed steady during the synchronous transition from S the G2 phase. We further demonstrated that cyclin D1 protein levels could increase during G2 phase in the absence of new mRNA synthesis. a-Amanitin, a transcription inhibitor, did not suppress cyclin D1 protein elevation as the cells progressed from S to G2 phase, even though the inhibitor was able to completely block cyclin D1 protein induction during reentry into the cell cycle from quiescence. The half life of cyclin D1 protein was shortest during S phase indicating that a change in protein stability might play a role in post-translational induction of cyclin D1 in G2 phase. These data indicate a fundamental difference in the regulation of cyclin D1 production during continuous cell cycle progression and re-initiation of the cell cycle. Oncogene (2002Oncogene ( ) 21, 7545 -7556. doi:10.1038 Keywords: cell cycle; Ras; cyclin D1; in situ hybridization; single cell-based analysis; post-transcriptional regulation IntroductionCell cycle progression consists of multiple coordinated processes, including DNA duplication and chromosome segregation, to ensure accurate transfer of genetic information to daughter cells. To achieve this, cells are equipped with a variety of systems to sense unfavorable conditions for completing the cell cycle, such as lack of mitogens, low nutrient levels, DNA damage, disruption of the mitotic spindles, etc. Under such conditions, check points are activated and cell cycle progression is halted at specific points in the cell cycle (Pardee, 1989;Vogelstein et al., 2000). Some of these reversible checkpoints have been utilized to synchronize cells to study cell cycle regulation. To study the control of G1/S phase transition, for instance, mitogen deprivation-readdition is often employed. When mitogens are removed, mammalian fibroblast cells are arrested in a quiescent state, referred to as G0, with a G1 content of DNA. This withdrawal from the cell cycle may have physiological importance, because forced cell cycle progression in the absence of growth factors often results in apoptosis (Evan and Vousden, 2001). When mitogens are available again, the cells reenter into cell cycle. The reversible nature of this G0 arrest has allowed studies of the molecular events controlling the cell cycle tran...

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Cell cycle arrest and morphological alterations following microinjection of NIH3T3 cells with Puraα

Cited by 54 publications

References 40 publications

Single-stranded DNA-binding Proteins PURα and PURβ Bind to a Purine-rich Negative Regulatory Element of the α-Myosin Heavy Chain Gene and Control Transcriptional and Translational Regulation of the Gene Expression

Single-stranded DNA-binding Proteins PURα and PURβ Bind to a Purine-rich Negative Regulatory Element of the α-Myosin Heavy Chain Gene and Control Transcriptional and Translational Regulation of the Gene Expression

Deletions of PURA, at 5q31, and PURB, at 7p13, in myelodysplastic syndrome and progression to acute myelogenous leukemia

Post-transcriptional regulation of cyclin D1 expression during G2 phase

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