| 1. |
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| 2. |
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| 3. |
- Agarwal, Prasoon, et al.
(författare)
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Growth signals employ CGGBP1 to suppress transcription of Alu-SINEs
- 2016
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Ingår i: Cell Cycle. - : Informa UK Limited. - 1538-4101 .- 1551-4005. ; 15:12, s. 1558-1571
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Tidskriftsartikel (refereegranskat)abstract
- CGGBP1 (CGG triplet repeat-binding protein 1) regulates cell proliferation, stress response,cytokinesis, telomeric integrity and transcription. It could affect these processes by modulatingtarget gene expression under different conditions. Identification of CGGBP1-target genes andtheir regulation could reveal how a transcription regulator affects such diverse cellular processes.Here we describe the mechanisms of differential gene expression regulation by CGGBP1 inquiescent or growing cells. By studying global gene expression patterns and genome-wide DNAbindingpatterns of CGGBP1, we show that a possible mechanism through which it affects theexpression of RNA Pol II-transcribed genes in trans depends on Alu RNA. We also show that itregulates Alu transcription in cis by binding to Alu promoter. Our results also indicate thatpotential phosphorylation of CGGBP1 upon growth stimulation facilitates its nuclear retention,Alu-binding and dislodging of RNA Pol III therefrom. These findings provide insights into howAlu transcription is regulated in response to growth signals.
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| 4. |
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| 5. |
- Akanda, Nesar, et al.
(författare)
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Voltage-dependent anion channels (VDAC) in the plasma membrane play a critical role in apoptosis in differentiated hippocampal neurons but not in neural stem cells
- 2008
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Ingår i: Cell Cycle. - : Informa UK Limited. - 1538-4101 .- 1551-4005. ; 7:20, s. 3225-3234
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Tidskriftsartikel (refereegranskat)abstract
- microRNAs (miRNAs) are small non-coding RNAs that regulate a large variety of cellular processes including differentiation, apoptosis and proliferation. Several miRNAs display defective expression patterns in human tumors with the consequent alteration of target oncogene or tumor suppressor genes. Many of these miRNAs modulate the major proliferation pathways through direct interaction with critical regulators such as RAS, PI3K/PTEN or ABL, as well as members of the retinoblastoma pathway, Cyclin-CDK complexes or cell cycle inhibitors of the INK4 or Cip/Kip families. A complex interplay between miRNAs and MYC or E2F family members also exists to modulate cell cycle-dependent transcription during normal or tumoral proliferation. The ability of miRNAs to modulate these proliferation pathways may have relevant implications not only in physiological or developmental processes but also in tumor progression or cancer therapy.
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| 6. |
- Andang, M, et al.
(författare)
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To go or not to go?
- 2015
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Ingår i: Cell cycle (Georgetown, Tex.). - : Informa UK Limited. - 1551-4005 .- 1538-4101. ; 14:8, s. 1136-1137
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Tidskriftsartikel (refereegranskat)
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| 7. |
- Anderberg, C, et al.
(författare)
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On the origin of cancer-associated fibroblasts
- 2009
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Ingår i: Cell cycle (Georgetown, Tex.). - : Informa UK Limited. - 1551-4005 .- 1538-4101. ; 8:10, s. 1461-1462
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 8. |
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| 9. |
- Aufschnaiter, Andreas, Dr. rer. nat. 1988-, et al.
(författare)
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Peroxisomal fission controls yeast life span
- 2015
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Ingår i: Cell Cycle. - : Taylor & Francis. - 1538-4101 .- 1551-4005. ; 14:15, s. 2389-2390
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Tidskriftsartikel (refereegranskat)
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| 10. |
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| 11. |
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| 12. |
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| 13. |
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| 14. |
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| 15. |
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| 16. |
- Bengoechea-Alonso, Maria T., et al.
(författare)
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Cdk1/cyclin B-mediated phosphorylation stabilizes SREBP1 during mitosis
- 2006
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Ingår i: Cell Cycle. - 1538-4101 .- 1551-4005. ; 5:15, s. 1708-1718
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Tidskriftsartikel (refereegranskat)abstract
- Members of the sterol regulatory element-binding protein (SREBP) family of transcription factors control the biosynthesis of cholesterol and other lipids, and lipid synthesis is critical for cell growth and proliferation. We recently found that the mature forms of SREBP1a and SREBP1c are hyperphosphorylated in mitotic cells, giving rise to a phosphoepitope recognized by the mitotic protein monoclonal-2 (MPM-2) antibody. In addition, we found that mature SREBP1 was stabilized in a phosphorylation-dependent manner during mitosis. We have now mapped the major MPM-2 epitope to a serine residue, S439, in the C terminus of mature SREBP1. Using phosphorylation-specific antibodies, we demonstrate that endogenous SREBP1 is phosphorylated on S439 specifically during mitosis. Mature SREBP1 interacts with the Cdk1/cyclin B complex in mitotic cells and we demonstrate that Cdk1 phosphorylates S439, both in vitro and in vivo. Our results suggest that Cdk1-mediated phosphorylation of S439 stabilizes mature SREBP1 during mitosis, thereby preserving a critical pool of active transcription factors to support lipid synthesis. Taken together with our previous work, the current study suggests that SREBP1 may provide a link between lipid synthesis, proliferation and cell growth. This hypothesis was supported by our observation that siRNA-mediated inactivation of SREBP1 arrested cells in the G(1) phase of the cell cycle, thereby attenuating cell growth.
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| 17. |
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| 18. |
- Berglund, Pontus, et al.
(författare)
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Cyclin e overexpression reduces infiltrative growth in breast cancer - Yet another link between proliferation control and tumor invasion
- 2006
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Ingår i: Cell Cycle. - 1551-4005. ; 5:6, s. 606-609
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Tidskriftsartikel (refereegranskat)abstract
- Overexpression of cyclin E is strongly linked to an aggressive phenotype and poor prognosis in breast cancer. Unexpectedly, it has been shown that cyclin E overexpression decreases mobility and invasiveness of breast cancer cells. In fact, in a study of 985 breast cancers, cyclin E correlated with less infiltrative growth. This suggests a novel function for cyclin E in breast cancer tumorigenesis and a mutual control of proliferation and invasive behavior.
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| 19. |
- Bergström, Rosita, et al.
(författare)
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CTCF Regulates Asynchronous Replication of the Imprinted H19/Igf2 Domain
- 2007
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Ingår i: Cell Cycle. - : Informa UK Limited. - 1538-4101 .- 1551-4005. ; 6:4, s. 450-454
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Tidskriftsartikel (refereegranskat)abstract
- Asynchronous replication during S phase is a universal characteristic of genomically imprinted genes. Replication timing in imprinted domains is determined epigenetically, as it is parent of origin specific, and is seen in the absence of sequence divergence between the two alleles. At the imprinted H19/lgf2 domain, the methylated paternal allele replicates early while the CTCF-bound maternal allele replicates late during S phase. CTCF regulates the allele-specific epigenetic characteristics of this domain, including methylation, transcription and chromosome conformation. Here we show that maternal, but not paternal inheritance of a mutated H19 imprinting control region, lacking functional CTCF binding sites, underlies a late to early switch in replication timing of the maternal H19/ lgf2 domain.
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| 20. |
- Bernander, Rolf, et al.
(författare)
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Comparative and functional analysis of the archaeal cell cycle
- 2010
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Ingår i: Cell Cycle. - : Informa UK Limited. - 1538-4101 .- 1551-4005. ; 9:4, s. 795-806
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Tidskriftsartikel (refereegranskat)abstract
- The temporal and spatial organization of the chromosome replication, genome segregation and cell division processes is less well understood in species belonging to the Archaea, than in those from the Bacteria and Eukarya domains. Novel insights into the regulation and key components of the Sulfolobus acidocaldarius cell cycle have been obtained through genome-wide analysis of cell cycle-specific gene expression, followed by cloning and characterization of gene products expressed at different cell cycle stages. Here, the results of the transcript profiling are further explored, and potential key players in archaeal cell cycle progression are highlighted in an evolutionary context, by comparing gene expression patterns and gene conservation between three selected microbial species from different domains of life. We draw attention to novel putative nucleases and helicases implicated in DNA replication, recombination and repair, as well as to potential genome segregation factors. Focus is also placed upon regulatory features, including transcription factors and protein kinases inferred to be involved in the execution of specific cell cycle stages, and regulation through metabolic coupling is discussed.
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| 21. |
- Bhattacharya, D, et al.
(författare)
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Rapid lymphocyte reconstitution of unconditioned immunodeficient mice with non-self-renewing multipotent hematopoietic progenitors
- 2006
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Ingår i: Cell Cycle. - 1551-4005. ; 5:11, s. 1135-1139
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Tidskriftsartikel (refereegranskat)abstract
- The replacement of abnormal hematopoietic stem cells (HSCs) with normal transplanted HSCs can correct a wide range of hematologic disorders. Here, we provide evidence that transplantation of more differentiated progenitor cells can be used to more rapidly correct lymphoid deficiencies in unconditioned immunocompromised mice. Transplantation of flk2+ multipotent progenitors led to robust B and T cell reconstitution that was maintained for at least 16 weeks. Antigenic challenge at 16 weeks post-transplantation revealed that reconstituted lymphocytes maintained a functional repertoire. In contrast to the persistent lymphocytic engraftment, myeloid chimerism was lost by 12 weeks post-transplantation consistent with the fact that flk2+ progenitors are non-self-renewing. Thus, while more differentiated progenitors are capable of rescuing lymphoid deficiencies, transplantation of HSCs must be used for the correction of non-lymphoid disorders, and, we propose, very long-term immune reconstitution. Based on recent evidence, we discuss novel strategies to achieve the replacement of abnormal HSCs without the use of cytotoxic conditioning regimens.
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| 22. |
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| 23. |
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| 24. |
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| 25. |
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| 26. |
- Carrera, Ana, et al.
(författare)
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SADB kinases license centrosome replication
- 2009
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Ingår i: Cell Cycle. - : Informa UK Limited. - 1551-4005 .- 1538-4101. ; 8:24, s. 4005-4006
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 27. |
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| 28. |
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| 29. |
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| 30. |
- Dudgeon, Crissy, et al.
(författare)
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Genetic variants and mutations of PPM1D control the response to DNA damage
- 2013
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Ingår i: Cell Cycle. - : Informa UK Limited. - 1538-4101 .- 1551-4005. ; 12:16
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Tidskriftsartikel (refereegranskat)abstract
- The Wip1 phosphatase is an oncogene that is overexpressed in a variety of primary human cancers. We were interested in identifying genetic variants that could change Wip1 activity. We identified 3 missense SNPs of the human Wip1 phosphatase, L120F, P322Q, and I496V confer a dominant-negative phenotype. On the other hand, in primary human cancers, PPM1D mutations commonly result in a gain-of-function phenotype, leading us to identify a hot-spot truncating mutation at position 525. Surprisingly, we also found a significant number of loss-of-function mutations of PPM1D in primary human cancers, both in the phosphatase domain and in the C terminus. Thus, PPM1D has evolved to generate genetic variants with lower activity, potentially providing a better fitness for the organism through suppression of multiple diseases. In cancer, however, the situation is more complex, and the presence of both activating and inhibiting mutations requires further investigation to understand their contribution to tumorigenesis.
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| 31. |
- Eigeliene, Natalija, et al.
(författare)
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Effects of estradiol and medroxyprogesterone acetate on expression of the cell cycle proteins cyclin D1, p21 and p27 in cultured human breast tissues
- 2008
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Ingår i: Cell Cycle. - 1551-4005. ; 7:1, s. 71-80
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Tidskriftsartikel (refereegranskat)abstract
- Estrogen and progesterone are key regulators of normal breast epithelial cell proliferation and differentiation. They are also involved in the initiation and progression of breast tumorigenesis. Several experimental studies have demonstrated that steroid hormones affect cell cycle proteins associated with tumor initiation and progression. Hormone replacement therapy (HT) is widely used to alleviate climacteric symptoms among postmenopausal women. Little is known, however, about cell cycle protein regulation during hormonal treatment of human breast tissue (HBT). In this study we aimed to evaluate the effects of 17 beta-estradiol (E-2) and medroxyprogesterone acetate (MPA) on cultured HBTs representing samples from reduction mammoplasty of premenopausal (pre-HBT) and postmenopausal (postm-HBT) women, and from peritumoral tissue (peritum-HBT) after breast tumor surgery among postmenopausal patients. Explants of HBT were cultured for 14 days in medium supplemented with E-2, MPA or E-2 + MPA. Expression of cyclin D1, p21 and p27 was assessed by immunohistochemical staining of explants cultured for 2 and 14 days. Further, Ki-67 staining was performed to evaluate correlation between proliferation and cell cycle regulatory protein expression. Our results showed that HBTs studied were positive for ER alpha, ER beta and PR (>= 10% of the cells stained). The level of p21 was lower (p < 0.001) in pre-HBT than in postm-HBT, whereas p27 levels were higher (p < 0.05) in pre-HBT than in postm-and peritum-HBT. The level of Ki-67 positive cells was higher in pre-HBT than in post-HBT. Interestingly, level of p21 positive cells showed an opposite pattern. Treatment with E-2 increased the relative number of cyclin D1-staining cells and decreased that of p27-staining cells in postm-HBT (p < 0.05), but not in pre-HBT. All hormone regimens (E-2, MPA, E-2 + MPA) increased the number of p21-positive cells in postm-HBTs at 14 days and E-2 even at 2 days. In pre-HBT p21 staining was increased (p < 0.05) in explants cultured with E-2 for 14 days but no response was observed in cyclin D1 and p27. The number of cyclin D1-staining cells was clearly higher (p < 0.05) in peritum-HBT than in non-tumorous pre-or postm-HBT, but the response cyclin D1 to all hormonal treatments in peritum-HBT was the same as in postm-HBT. Moreover, we found that E-2, MPA, E-2 + MPA in vitro increased numbers of Ki-67 positive cells in post-HBTs at 14 days and E-2 also in pre-HBT. Stimulated proliferation rate was associated with increase of cyclin D1 and p21-positive cells and reduced numbers of p27, especially in post-HBTs. Taken together, our results suggest that cell cycle regulatory proteins are more sensitive to exogenous hormone treatment in postm-HBT than in pre-HBT.
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| 32. |
- Fard, Shahrzad Shirazi, et al.
(författare)
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The heterogenic final cell cycle of chicken retinal Lim1 horizontal cells is not regulated by the DNA damage response pathway
- 2014
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Ingår i: Cell Cycle. - : Informa UK Limited. - 1538-4101 .- 1551-4005. ; 13:3, s. 408-417
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Tidskriftsartikel (refereegranskat)abstract
- Cells with aberrations in chromosomal ploidy are normally removed by apoptosis. However, aneuploid neurons have been shown to remain functional and active both in the cortex and in the retina. Lim1 horizontal progenitor cells in the chicken retina have a heterogenic final cell cycle, producing some cells that enter S-phase without proceeding into M-phase. The cells become heteroploid but do not undergo developmental cell death. This prompted us to investigate if the final cell cycle of these cells is under the regulation of an active DNA damage response. Our results show that the DNA damage response pathway, including gamma-H2AX and Rad51 foci, is not triggered during any phase of the different final cell cycles of horizontal progenitor cells. However, chemically inducing DNA adducts or double-strand breaks in Lim1 horizontal progenitor cells activated the DNA damage response pathway, showing that the cells are capable of a functional response to DNA damage. Moreover, manipulation of the DNA damage response pathway during the final cell cycle using inhibitors of ATM/ATR, Chk1/2, and p38MAPK, neither induced apoptosis nor mitosis in the Lim1 horizontal progenitor cells. We conclude that the DNA damage response pathway is functional in the Lim1 horizontal progenitor cells, but that it is not directly involved in the regulation of the final cell cycle that gives rise to the heteroploid horizontal cell population.
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| 33. |
- Farnebo, M
(författare)
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Wrap53, a novel regulator of p53
- 2009
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Ingår i: Cell cycle (Georgetown, Tex.). - : Informa UK Limited. - 1551-4005 .- 1538-4101. ; 8:15, s. 2343-2346
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Tidskriftsartikel (refereegranskat)
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| 34. |
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| 35. |
- Fernandez-Capetillo, O
(författare)
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The (elusive) role of the SMC5/6 complex
- 2016
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Ingår i: Cell cycle (Georgetown, Tex.). - : Informa UK Limited. - 1551-4005 .- 1538-4101. ; 15:6, s. 775-776
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Tidskriftsartikel (refereegranskat)
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| 36. |
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| 37. |
- Fülöp, Katalin, et al.
(författare)
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Arabidopsis anaphase-promoting complexes : multiple activators and wide range of substrates might keep APC perpetually busy
- 2005
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Ingår i: Cell Cycle. - Austin : Landes bioscience. - 1538-4101 .- 1551-4005. ; 4:8, s. 1084-1092
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Tidskriftsartikel (refereegranskat)abstract
- The anaphase-promoting complex (APC), a multisubunit E3 ubiquitin ligase, is an essential regulator of the cell cycle from metaphase until S phase in yeast and metazoans. APC mediates degradation of numerous cell cycle-related proteins, including mitotic cyclins and its activation and substrate-specificity are determined by two adaptor proteins, Cdc20 and Cdh1. Plants have multiple APC activators and the Cdh1-type proteins, in addition, are represented by two subclasses, known as Ccs52A and Ccs52B. The Arabidopsis genome contains five cdc20 genes as well as ccs52A1, ccs52A2 and ccs52B.In Schizosaccharomyces pombe, expression of the three Atccs52 genes elicited distinct phenotypes supporting nonredundant function of the AtCcs52 proteins. Consistent with these activities, the AtCcs52 proteins were able to bind both to the yeast and the Arabidopsis APCs. In synchronized Arabidopsis cell cultures the cdc20 transcripts were present from early G2 until the M-phase exit, ccs52B from G2/M to M while ccs52A1 and ccs52A2 were from late M until early G2, suggesting consecutive action of these APC activators in the plant cell cycle. The AtCcs52 proteins interacted with different subsets of mitotic cyclins, in accordance with their expression profiles, either in free- or CDK-bound forms. Expression of most APC subunits was constitutive, whereas cdc27a and cdc27b, corresponding to two forms of apc3, and ubc19 and ubc20 encoding E2-C type ubiquitin-conjugating enzymes displayed differences in their cell cycle regulation. These data indicate the existence of numerous APC(Cdc20/Ccs52/Cdc27) forms in Arabidopsis, which in conjunction with different E2 enzymes might have distinct or complementary functions at distinct stages of the cell cycle.
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| 38. |
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| 39. |
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| 40. |
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| 41. |
- Gisselsson Nord, David
(författare)
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Aneuploidy in cancer: Sudden or sequential?
- 2011
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Ingår i: Cell Cycle. - : Informa UK Limited. - 1551-4005 .- 1538-4101. ; 10:3, s. 359-361
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Tidskriftsartikel (refereegranskat)abstract
- Comment on: Gisselsson D, et al. Proc Natl Acad Sci USA 2010; 107:20489-93.
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| 42. |
- Gisselsson Nord, David
(författare)
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Mitotic instability in cancer - Is there method in the madness?
- 2005
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Ingår i: Cell Cycle. - 1551-4005. ; 4:8, s. 1007-1010
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Tidskriftsartikel (refereegranskat)abstract
- It has been known for more than a century that neoplastic cells often exhibit disturbances of the mitotic process, but the causes have only recently been thoroughly explored. In many cancers, a combination of cell cycle checkpoint deficiency and abnormal shortening of telomeres predisposes to unbalanced chromosome segregation at cell division and the development of complex genomic rearrangements. Shortening of telomeric repeats beyond normal limits leads to fusion of chromosome ends and the formation of chromatin bridges at anaphase. In turn, these bridges may trigger at least three types of chromosomes mutation: ( 1) structural rearrangements of chromosomes through extensive chromatin fragmentation beyond the centromeric sequences, typically leading to the formation of isochromosomes and whole-arm translocations, ( 2) loss of whole chromosomes through mechanical detachment from the mitotic spindle machinery, and ( 3) failure of cytokinesis, leading to polyploidisation and supernumerary centrosomes, which may in turn orchestrate multipolar spindle configurations at a subsequent mitosis. Anaphase bridging rarely hinders further survival of tumor daughter cells. In contrast, multipolar mitoses may lead to extensive reshuffling of chromosome copies that compromise further clonal expansion. The telomere-dependent instability can be partly counteracted by expression of telomerase during tumor progression, but genomic stabilisation is rarely, if ever, complete.
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| 43. |
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| 44. |
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| 45. |
- Gubanova, Evgenia, et al.
(författare)
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SMG-1 suppresses CDK2 and tumor growth by regulating both the p53 and Cdc25A signaling pathways
- 2013
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Ingår i: Cell Cycle. - : Informa UK Limited. - 1538-4101 .- 1551-4005. ; 12:24, s. 3770-3780
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Tidskriftsartikel (refereegranskat)abstract
- The DNA damage response is coordinated by phosphatidylinositol 3-kinase-related kinases, ATM, ATR, and DNA-PK. SMG-1 is the least studied stress-responsive member of this family. Here, we show that SMG-1 regulates the G 1/S checkpoint through both a p53-dependent, and a p53-independent pathway. We identify Cdc25A as a new SMG-1 substrate, and show that cells depleted of SMG-1 exhibit prolonged Cdc25A stability, failing to inactivate CDK2 in response to radiation. Given an increased tumor growth following depletion of SMG-1, our data demonstrate a novel role for SMG-1 in regulating Cdc25A and suppressing oncogenic CDK2 driven proliferation, confirming SMG-1 as a tumor suppressor.
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| 46. |
- Gururaj, Anupama E, et al.
(författare)
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Breast cancer-amplified sequence 3, a target of metastasis-associated protein 1, contributes to tamoxifen resistance in premenopausal patients with breast cancer
- 2006
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Ingår i: Cell Cycle. - 1551-4005. ; 5:13, s. 1407-1410
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Tidskriftsartikel (refereegranskat)abstract
- Lysine acetylation occurs in many protein targets, including core histones, transcription factors, and other proteins. Metastasis-associated protein 1 (MTA1) is implicated in the progression and metastasis of various epithelial tumors. Because MTA1 functions as a transcriptional coregulator, much of its role in cancer promoting processes are likely to involve its ability to regulate the transcription of downstream target genes that encode effector proteins. We recently showed that MTA1 could be post-translationally modified by acetylation, which modulates its function as a coregulator molecule. We also defined a chromatin target of MTA1, namely, breast cancer-amplified sequence 3 (BCAS3), in the context of which MTA1 behaves as a transcriptional coactivator in breast cancer cells. Because the phenotypic effect of BCAS3 overexpression in tumors has not been defined, we investigated the consequence of increased expression of BCAS3 in human breast tumors. Here, we report that BCAS3 overexpression in hormone receptor-positive premenopausal breast cancer seemed to be associated with impaired responses to tamoxifen. Our findings have implications for endocrine therapy.
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| 47. |
- Hedblom, Andreas, et al.
(författare)
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CDK1 interacts with RARγ and plays an important role in treatment response of acute myeloid leukemia
- 2013
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Ingår i: Cell Cycle. - : Taylor & Francis. - 1538-4101 .- 1551-4005. ; 12:8, s. 1251-1266
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Tidskriftsartikel (refereegranskat)abstract
- Alterations in cell cycle pathways and retinoic acid signaling are implicated in leukemogenesis. However, little is known about the roles of cyclin-dependent kinases (CDKs) in treatment response of leukemia. In this study, we observed that CDK1 expression was significantly higher in bone marrow from 42 patients with acute myeloid leukemia (AML) at recurrence than that at first diagnosis (p = 0.04). AML patients had higher level of nuclear CDK1 in their leukemic blasts tended to have poorer clinical outcome compared with those with lower levels. We showed that CDK1 function is required for all-trans retinoic acid (ATRA) to achieve the optimal effect in U-937 human leukemic cells. CDK1 modulates the levels of P27(kip) and AKT phosphorylation in response to ATRA treatment. Further, we show, for the first time, that RARγ in concert with ATRA regulates protein levels of CDK1 and its subcellular localization. The regulation of the subcellular content of CDK1 and RARγ by ATRA is an important process for achieving an effective response in treatment of leukemia. RARγ and CDK1 form a reciprocal regulatory circuit in the nucleus and influence the function and protein stability of each other and the level of P27(kip) protein. In addition, expression of wee1 kinase and Cdc25A/C phosphatases also coincide with CDK1 expression and its subcellular localization in response to ATRA treatment. Our study reveals a novel mechanism by which CDK1 and RARγ coordinate with ATRA to influence cell cycle progression and cellular differentiation.
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| 48. |
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| 49. |
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