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Showing 1-30 of 533 results for "H8627" within Papers
Stephanie Tirman et al.
Molecular cell, 81(19), 4026-4040 (2021-10-09)
PRIMPOL repriming allows DNA replication to skip DNA lesions, leading to ssDNA gaps. These gaps must be filled to preserve genome stability. Using a DNA fiber approach to directly monitor gap filling, we studied the post-replicative mechanisms that fill the
J Kowshik et al.
PloS one, 9(10), e109114-e109114 (2014-10-09)
Identifying agents that inhibit STAT-3, a cytosolic transcription factor involved in the activation of various genes implicated in tumour progression is a promising strategy for cancer chemoprevention. In the present study, we investigated the effect of dietary astaxanthin on JAK-2/STAT-3
Marco Ruella et al.
Experimental hematology, 41(7), 627-634 (2013-04-02)
The purpose of this study was to investigate telomere length (TL) in Ph-negative chronic myeloproliferative neoplasms (Ph-neg-CMNs), and the possible association of TL with disease progression and hydroxycarbamide (HU) treatment. TL was analyzed in peripheral blood samples from 239 patients
Bente Benedict et al.
Developmental cell, 52(6), 683-698 (2020-02-23)
Premature loss of sister chromatid cohesion at metaphase is a diagnostic marker for different cohesinopathies. Here, we report that metaphase spreads of many cancer cell lines also show premature loss of sister chromatid cohesion. Cohesion loss occurs independently of mutations
Phedias Diamandis et al.
Nature chemical biology, 3(5), 268-273 (2007-04-10)
The identification of self-renewing and multipotent neural stem cells (NSCs) in the mammalian brain holds promise for the treatment of neurological diseases and has yielded new insight into brain cancer. However, the complete repertoire of signaling pathways that governs the
D J Adams et al.
Nature, 627(8002), 130-136 (2024-02-15)
Genomic instability arising from defective responses to DNA damage1 or mitotic chromosomal imbalances2 can lead to the sequestration of DNA in aberrant extranuclear structures called micronuclei (MN). Although MN are a hallmark of ageing and diseases associated with genomic instability
Humberto Itriago et al.
Genes, 14(10) (2023-10-28)
Several sources of DNA damage compromise the integrity and stability of the genome of every organism. Specifically, DNA double-strand breaks (DSBs) can have lethal consequences for the cell. To repair this type of DNA damage, the cells employ homology-directed repair
Mark J Osborn et al.
Human gene therapy, 26(2), 114-126 (2014-12-30)
Genome engineering with designer nucleases is a rapidly progressing field, and the ability to correct human gene mutations in situ is highly desirable. We employed fibroblasts derived from a patient with Fanconi anemia as a model to test the ability
Bingsen Zhou et al.
Cancer research, 73(21), 6484-6493 (2013-09-28)
Ribonucleotide reductase (RNR) is an attractive target for anticancer agents given its central function in DNA synthesis, growth, metastasis, and drug resistance of cancer cells. The current clinically established RNR inhibitors have the shortcomings of short half-life, drug resistance, and
Tania M Zappala et al.
The Australasian journal of dermatology, 53(3), e58-e60 (2012-08-14)
Medication-induced dermatomyositis (DM) is rare, but a recent review highlighted hydroxyurea (HU) as the most common inciting agent. To aid diagnosis, HU-induced DM-like eruption (HU DM-LE) forms a distinct dermopathy where the typical cutaneous features of DM are without systemic
Sara Ovejero et al.
International journal of molecular sciences, 22(14) (2021-07-25)
In order to tackle the study of DNA repair pathways, the physical and chemical agents creating DNA damage, the genotoxins, are frequently employed. Despite their utility, their effects are rarely restricted to DNA, and therefore simultaneously harm other cell biomolecules.
Joao Seco et al.
International journal of molecular sciences, 23(9) (2022-05-15)
We propose a novel mechanism by which cancer cells can modulate the oxygen concentration within the nucleus, potentially creating low nuclear oxygen conditions without the need of an hypoxic micro-environment and suited for allowing cancer cells to resist chemo- and
Remziye Kendirci-Katirci et al.
Journal of assisted reproduction and genetics, 41(9), 2441-2456 (2024-07-28)
Physiological decidual senescence promotes embryo implantation, whereas pathological decidual senescence causes many pregnancy pathologies. The aim of this study was to evaluate the effect of rapamycin on decidual cell subpopulations and endometrial function in physiological and induced senescence and to
G N Zyuz'kov et al.
Bulletin of experimental biology and medicine, 159(1), 58-61 (2015-06-03)
We studied the role of intracellular signaling molecules PI3K, МАРK ERK1/2, and р38 in stimulation of realization of the growth potential of mesenchymal progenitor cells by alkaloid songorine in vitro. Inhibitors of PI3K, ERK1/2 and р38 canceled the increase in
Nunu Huang et al.
Cancer biology & therapy, 16(6), 941-948 (2015-05-07)
It has been reported that persistent or excessive autophagy promotes cancer cell death during chemotherapy, either by enhancing the induction of apoptosis or mediating autophagic cell death. Here, we show that miR-15a and miR-16 are potent inducers of autophagy. Rictor
Agnes Miermont et al.
Development (Cambridge, England), 146(12) (2019-04-13)
Embryonic development involves extensive and often rapid cell proliferation. An unavoidable side effect of cell proliferation is DNA damage. The consequences of spontaneous DNA damage during development are not clear. Here, we define an approach to determine the effects of
Dennis J Pelletier et al.
Journal of chemical information and modeling, 47(3), 1196-1205 (2007-04-13)
The identification of phospholipidosis (PPL) during preclinical testing in animals is a recognized problem in the pharmaceutical industry. Depending on the intended indication and dosing regimen, PPL can delay or stop development of a compound in the drug discovery process.
Stephanie Lauer et al.
Cell genomics, 3(11), 100437-100437 (2023-11-29)
Pioneering advances in genome engineering, and specifically in genome writing, have revolutionized the field of synthetic biology, propelling us toward the creation of synthetic genomes. The Sc2.0 project aims to build the first fully synthetic eukaryotic organism by assembling the
Gene transfer using targeted filamentous bacteriophage.
D Larocca et al.
Methods in molecular biology (Clifton, N.J.), 185, 393-401 (2002-01-05)
Matthew P Torres et al.
The Journal of biological chemistry, 286(23), 20208-20216 (2011-04-28)
A diverse array of external stimuli, including most hormones and neurotransmitters, bind to cell surface receptors that activate G proteins. Mating pheromones in yeast Saccharomyces cerevisiae activate G protein-coupled receptors and initiate events leading to cell cycle arrest in G(1)
Jiangbin Wu et al.
Cell communication and signaling : CCS, 12, 66-66 (2014-10-12)
Accelerated cell cycle progression is the common feature of most cancers. MiRNAs can act as oncogenes or tumor suppressors by directly modulating cell cycle machinery. It has been shown that miR-188 is upregulated in UVB-irradiated mouse skin and human nasopharyngeal
John J Strouse et al.
Pediatric blood & cancer, 59(2), 365-371 (2012-04-21)
Hydroxyurea is the only approved medication in the United States for the treatment of sickle cell anemia (HbSS) and is widely used in children despite an indication limited to adults. We review the evidence of efficacy and safety in children
Douglas K Peters et al.
PLoS pathogens, 16(3), e1008403-e1008403 (2020-03-24)
The replication of small DNA viruses requires both host DNA replication and repair factors that are often recruited to subnuclear domains termed viral replication centers (VRCs). Aside from serving as a spatial focus for viral replication, little is known about
Clelia Tiziana Storlazzi et al.
American journal of hematology, 89(4), 438-442 (2014-01-03)
The patient had been diagnosed with polycythemia vera (PV) in 1999, at the age of 61, according to the criteria of the Polycythemia Vera Study Group (PVSG) on the basis of the increased red cell mass by isotope determination, normal
Arik Townsend et al.
Cell reports, 34(4), 108669-108669 (2021-01-28)
Replication stress response ensures impediments to DNA replication do not compromise replication fork stability and genome integrity. In a process termed replication fork protection, newly synthesized DNA at stalled replication forks is stabilized and protected from nuclease-mediated degradation. We report
Karinna Rubio-Peña et al.
RNA (New York, N.Y.), 21(12), 2119-2131 (2015-10-23)
Retinitis pigmentosa (RP) is a rare genetic disease that causes gradual blindness through retinal degeneration. Intriguingly, seven of the 24 genes identified as responsible for the autosomal-dominant form (adRP) are ubiquitous spliceosome components whose impairment causes disease only in the
Carter J Barger et al.
eLife, 10 (2021-04-24)
The FOXM1 transcription factor is an oncoprotein and a top biomarker of poor prognosis in human cancer. Overexpression and activation of FOXM1 is frequent in high-grade serous carcinoma (HGSC), the most common and lethal form of human ovarian cancer, and
Kang Liu et al.
Molecular and cellular biology, 33(23), 4685-4700 (2013-10-02)
Our previous study showed that Akt phosphorylates TopBP1 at the Ser-1159 residue and induces its oligomerization. Oligomerization is required for TopBP1 to bind and repress E2F1 activity. However, the mechanism through which phosphorylation of TopBP1 by Akt leads to its
Yixuan Li et al.
Molecular and cellular biology, 35(20), 3547-3565 (2015-08-05)
Histone deacetylase (HDAC) inhibition leads to cell cycle arrest in G1 and G2, suggesting HDACs as therapeutic targets for cancer and diseases linked to abnormal cell growth and proliferation. Many HDACs are transcriptional repressors. Some may alter cell cycle progression
Liye He et al.
Methods in molecular biology (Clifton, N.J.), 1711, 351-398 (2018-01-19)
Gene products or pathways that are aberrantly activated in cancer but not in normal tissue hold great promises for being effective and safe anticancer therapeutic targets. Many targeted drugs have entered clinical trials but so far showed limited efficacy mostly
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