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  • 1.
    Akanda, Nesar
    et al.
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi.
    Tofighi, Roshan
    Karolinska Inst, Dept Neurosci, SE-17177 Stockholm, Sweden .
    Brask, Johan
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi.
    Tamm, Christoffer
    Karolinska Inst, Dept Neurosci, SE-17177 Stockholm, Sweden .
    Elinder, Fredrik
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Ceccatelli, Sandra
    Karolinska Inst, Dept Neurosci, SE-17177 Stockholm, Sweden .
    Voltage-dependent anion channels (VDAC) in the plasma membrane play a critical role in apoptosis in differentiated hippocampal neurons but not in neural stem cells2008Inngår i: Cell Cycle, ISSN 1538-4101, E-ISSN 1551-4005, Vol. 7, nr 20, s. 3225-3234Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    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.

  • 2.
    Jensen, Lasse Dahl
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Hälsouniversitetet. Karolinska Institute, Stockholm, Sweden.
    Cao, Yihai
    Linköpings universitet, Institutionen för medicin och hälsa, Avdelningen för kardiovaskulär medicin. Linköpings universitet, Hälsouniversitetet. Karolinska Institute, Stockholm, Sweden .
    Clock controls angiogenesis2013Inngår i: Cell Cycle, ISSN 1538-4101, E-ISSN 1551-4005, Vol. 12, nr 3, s. 405-408Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Circadian rhythms control multiple physiological and pathological processes, including embryonic development in mammals and development of various human diseases. We have recently, in a developing zebrafish embryonic model, discovered that the circadian oscillation controls developmental angiogenesis. Disruption of crucial circadian regulatory genes, including Bmal1 and Period2, results in marked impairment or enhancement of vascular development in zebrafish. At the molecular level, we show that the circadian regulator Bmal1 directly targets the promoter region of the vegf gene in zebrafish, leading to an elevated expression of VEGF. These findings can reasonably be extended to developmental angiogenesis in mammals and even pathological angiogenesis in humans. Thus, our findings, for the first time, shed new light on mechanisms that underlie circadian clock-regulated angiogenesis.

  • 3.
    Los, Marek Jan
    et al.
    University of Tübingen, Germany .
    Schulze-Osthoff, Klaus
    University of Tübingen, Germany .
    Catching chromatin relaxation in act by flow cytometry2009Inngår i: Cell Cycle, ISSN 1538-4101, E-ISSN 1551-4005, Vol. 8, nr 14, s. 2140-2141Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    Comment on: Cytometric detection of chromatin relaxation, an early reporter of DNA damage response.

  • 4.
    Pron, C. J.
    et al.
    Lund University.
    Attema, J.
    Lund University.
    Rossi, D. J.
    Lund University.
    Sigvardsson, Mikael
    Lund University.
    Bryder, D.
    Lund University.
    Deciphering developmental stages of adult myelopoiesis2008Inngår i: Cell Cycle, ISSN 1538-4101, E-ISSN 1551-4005, Vol. 7, nr 6, s. 706-713Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The ability to subfractionate minor cellular subsets by multiparameter flow cytometry and to evaluate such cells for functional properties has been used to ascertain lineal relationships and detail developmental hierarchies in the hematopoietic system for more than 20 years. However, steady advances in technology combined with the use of novel cell surface markers continues to redefine the developmental landscape as novel subpopulations are purified and characterized. We recently used such an approach to stage progenitor cell hierarchy involved in myeloid development with the use of two markers, Slamf1 and Endoglin that have recently been shown to be associated with hematopoietic stem cells. Here, we provide additional characterization of these cellular subsets to further refine their developmental potential. Little or no alterations in lineage potential were observed in these subsets when evaluated in a BCL2 transgenic setting or in response to various growth factor combinations, although BCL2 significantly enhanced their in vitro readout. Gene expression patterns of functionally opposing transcription factors that are known to play key roles for the appropriate development into separate myeloid lineages were associated with the functional activity of prospectively isolated subsets. Multiple genes traditionally associated with early lymphopoiesis were observed in early candidate granulocyte/monocyte, but not early megakaryocytic and/or erythroid progenitor cells. When functionally evaluated, such early granulocyte/monocyte precursors displayed a latent lymphoid activity, which was pronounced in subsets bearing high expression of the tyrosine kinase receptor FLT3. 

  • 5.
    Rouhi, Pegah
    et al.
    Karolinska Institute, Stockholm, Sweden .
    Lee, Samantha Lin Chiou
    Karolinska Institute, Stockholm, Sweden .
    Cao, Ziquan
    Karolinska Institute, Stockholm, Sweden .
    Hedlund, Eva-Maria
    Karolinska Institute, Stockholm, Sweden .
    Jensen, Lasse Dahl
    Karolinska Institute, Stockholm, Sweden .
    Cao, Yihai
    Karolinska Institute, Stockholm, Sweden .
    Pathological angiogenesis facilitates tumor cell dissemination and metastasis2010Inngår i: Cell Cycle, ISSN 1538-4101, E-ISSN 1551-4005, Vol. 9, nr 5, s. 913-917Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Clinically detectable metastases represent an ultimate consequence of the metastatic cascade that consists of distinct processes including tumor cell invasion, dissemination, metastatic niche formation, and re-growth into a detectable metastatic mass. Although angiogenesis is known to promote tumor growth, its role in facilitating early events of the metastatic cascade remains poorly understood. We have recently developed a zebrafish tumor model that enables us to study involvement of pathological angiogenesis in tumor invasion, dissemination and metastasis. This non-invasive in vivo model allows detection of single malignant cell dissemination under both normoxia and hypoxia. Further, hypoxia-induced VEGF significantly facilitates tumor cell invasion and dissemination. These findings demonstrate that VEGF-induced pathological angiogenesis is essential for tumor dissemination and further corroborates potentially beneficial effects of clinically ongoing anti-VEGF drugs for the treatment of various malignancies.

  • 6.
    Saint-Leger, A.
    et al.
    Institute for Research on Cancer and Aging, Nice (IRCAN), CNRS UMR7284/INSERM U1081, Faculty of Medicine, Nice, France; Laboratoire de Biologie Moléculaire de la Cellule, CNRS UMR5239, Ecole Normale Supérieure de Lyon, Lyon, France.
    Koelblen, M.
    Laboratoire de Biologie Moléculaire de la Cellule, CNRS UMR5239, Ecole Normale Supérieure de Lyon, Lyon, France.
    Civitelli, Livia
    Bah, A.
    Laboratoire de Biologie Moléculaire de la Cellule, CNRS UMR5239, Ecole Normale Supérieure de Lyon, Lyon, France; Institute of Biochemistry (IBC), Eidgenössische Technische Hochschule Zürich (ETHZ), Zürich, Switzerland.
    Djerbi, N.
    Institute for Research on Cancer and Aging, Nice (IRCAN), CNRS UMR7284/INSERM U1081, Faculty of Medicine, Nice, France.
    Giraud-Panis, M.-J.
    Institute for Research on Cancer and Aging, Nice (IRCAN), CNRS UMR7284/INSERM U1081, Faculty of Medicine, Nice, France; Laboratoire de Biologie Moléculaire de la Cellule, CNRS UMR5239, Ecole Normale Supérieure de Lyon, Lyon, France.
    Londono-Vallejo, A.
    Telomeres and Cancer Lab., UMR3244, Institut Curie, Paris, France.
    Ascenzioni, F.
    Istituto Pasteur-Fondazione Cenci Bolognetti, Dipartimento di Biologia e Biotecnologie Charles Darwin, Sapienza Università di Roma, Rome, Italy.
    Gilson, E.
    Institute for Research on Cancer and Aging, Nice (IRCAN), CNRS UMR7284/INSERM U1081, Faculty of Medicine, Nice, France; Laboratoire de Biologie Moléculaire de la Cellule, CNRS UMR5239, Ecole Normale Supérieure de Lyon, Lyon, France; Department of Medical Genetics, Archet 2 Hospital, CHU of Nice, Nice, France.
    The basic N-terminal domain of TRF2 limits recombination endonuclease action at human telomeres2014Inngår i: Cell Cycle, ISSN 1538-4101, E-ISSN 1551-4005, Vol. 13, nr 15, s. 2469-2479Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The stability of mammalian telomeres depends upon TRF2, which prevents inappropriate repair and checkpoint activation. By using a plasmid integration assay in yeasts carrying humanized telomeres, we demonstrated that TRF2 possesses the intrinsic property to both stimulate initial homologous recombination events and to prevent their resolution via its basic N-terminal domain. In human cells, we further showed that this TRF2 domain prevents telomere shortening mediated by the resolvase-associated protein SLX4 as well as GEN1 and MUS81, 2 different types of endonucleases with resolvase activities. We propose that various types of resolvase activities are kept in check by the basic N-terminal domain of TRF2 in order to favor an accurate repair of the stalled forks that occur during telomere replication. © 2014 Landes Bioscience.

  • 7.
    Somasundaram, Rajesh
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten.
    Strid, Tobias
    Lund University, Sweden.
    Sigvardsson, Mikael
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten. Lund University, Sweden.
    Cellular plasticity in B-cell leukemia2017Inngår i: Cell Cycle, ISSN 1538-4101, E-ISSN 1551-4005, Vol. 16, nr 6, s. 495-496Artikkel i tidsskrift (Annet vitenskapelig)
    Abstract [en]

    n/a

  • 8.
    Vilas Jain, Mayur
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
    Jangamreddy, Jaganmohan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten.
    Grabarek, Jerzy
    Pomeranian Medical University, Poland.
    Schweizer, Frank
    University of Manitoba, Canada.
    Klonisch, Thomas
    University of Manitoba, Canada.
    Cieslar-Pobuda, Artur
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten. Silesian Technical University, Poland.
    Los, Marek Jan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten. Pomeranian Medical University, Poland; Medical University of Silesia, Poland.
    Nuclear localized Akt enhances breast cancer stem-like cells through counter-regulation of p21(Waf1/Cip1) and p27(kip1)2015Inngår i: Cell Cycle, ISSN 1538-4101, E-ISSN 1551-4005, Vol. 14, nr 13, s. 2109-2120Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Cancer stem-like cells (CSCs) are a rare subpopulation of cancer cells capable of propagating the disease and causing cancer recurrence. In this study, we found that the cellular localization of PKB/Akt kinase affects the maintenance of CSCs. When Akt tagged with nuclear localization signal (Akt-NLS) was overexpressed in SKBR3 and MDA-MB468 cells, these cells showed a 10-15% increase in the number of cells with CSCs enhanced ALDH activity and demonstrated a CD44(+High)/CD24(-Low) phenotype. This effect was completely reversed in the presence of Akt-specific inhibitor, triciribine. Furthermore, cells overexpressing Akt or Akt-NLS were less likely to be in G0/G1 phase of the cell cycle by inactivating p21(Waf1/Cip1) and exhibited increased clonogenicity and proliferation as assayed by colony-forming assay (mammosphere formation). Thus, our data emphasize the importance the intracellular localization of Akt has on stemness in human breast cancer cells. It also indicates a new robust way for improving the enrichment and culture of CSCs for experimental purposes. Hence, it allows for the development of simpler protocols to study stemness, clonogenic potency, and screening of new chemotherapeutic agents that preferentially target cancer stem cells. Summary: The presented data, (i) shows new, stemness-promoting role of nuclear Akt/PKB kinase, (ii) it underlines the effects of nuclear Akt on cell cycle regulation, and finally (iii) it suggests new ways to study cancer stem-like cells.

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