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Showing 1-30 of 56 results for "OP03" within Papers
C J Chiou et al.
Journal of virology, 67(10), 6201-6214 (1993-10-01)
The 80-kDa IE2 nuclear phosphoprotein encoded by the human cytomegalovirus (HCMV) major immediate-early (MIE) gene behaves both as a nonspecific transactivator of heterologous reporter genes and as a specific repressor of its own promoter-enhancer region. To begin to examine the
Yuhei Mizunoe et al.
Autophagy, 13(4), 642-653 (2017-01-26)
Whether obesity accelerates or suppresses autophagy in adipose tissue is still debatable. To clarify dysregulation of autophagy and its role in pathologies of obese adipose tissue, we focused on lysosomal function, protease maturation and activity, both in vivo and in
Avijeet Chopra et al.
PloS one, 11(4), e0153818-e0153818 (2016-04-21)
Mitotic inhibitors are widely utilized chemotherapeutic agents that take advantage of mitotic defects in cancer cells. We have identified a novel class of piperazine-based mitotic inhibitors, of which AK301 is the most potent derivative identified to date (EC50 < 200
Maria Chiara Magnone et al.
Frontiers in neurology, 5, 289-289 (2015-01-30)
Living in the earth's oxygenated environment forced organisms to develop strategies to cope with the damaging effects of molecular oxygen known as reactive oxygen species (ROS). Here, we show that Per2, a molecular component of the mammalian circadian clock, is
Chenghua Lou et al.
Oncology letters, 12(1), 295-300 (2016-06-28)
The present authors have recently demonstrated that hirsutine, one of the major alkaloids in Uncaria species, promotes cell apoptosis by inducing DNA damage and suppresses metastasis of breast cancer cells. Despite its potent anti-cancer activity, certain types of human breast
Thi T Nguyen et al.
Molecular and cellular biology, 25(6), 2147-2157 (2005-03-04)
We performed chromatin immunoprecipitation (ChIP) analyses of developmentally staged solid tissues isolated from wild-type and p53-null mice to determine specific histone N-terminal modifications, histone-modifying proteins, and transcription factor interactions at the developmental repressor region (-850) and core promoter of the
Kai Liu et al.
Molecular cell, 68(2), 281-292 (2017-10-17)
Autophagy is required for benign hepatic tumors to progress into malignant hepatocellular carcinoma. However, the mechanism is unclear. Here, we report that mitophagy, the selective removal of mitochondria by autophagy, positively regulates hepatic cancer stem cells (CSCs) by suppressing the
Terri J Harford et al.
Apoptosis : an international journal on programmed cell death, 22(12), 1532-1542 (2017-09-18)
The muscle regulatory transcription factor MyoD is a master regulator of skeletal myoblast differentiation. We have previously reported that MyoD is also necessary for the elevated expression of the pro-apoptotic Bcl2 family member PUMA, and the ensuing apoptosis, that occurs
Jacob A Gordon et al.
Cancer research, 79(13), 3320-3331 (2019-05-09)
Aberrant cholesterol metabolism is increasingly appreciated to be essential for prostate cancer initiation and progression. Transcript expression of the high-density lipoprotein-cholesterol receptor scavenger receptor B1 (SR-B1) is elevated in primary prostate cancer. Hypothesizing that SR-B1 expression may help facilitate malignant
Subrata K Pore et al.
Journal of cellular biochemistry, 121(1), 804-815 (2019-08-14)
Anticancer drugs exert their effects on cancer cells by deregulating many pathways linked to cell cycle, apoptosis, etc. but cancer cells gradually become resistive against anticancer drugs, thereby necessitating the development of newer generation anticancer molecules. N-end rule pathway has
Angela M Valverde et al.
Molecular biology of the cell, 15(11), 5101-5117 (2004-09-10)
Fetal brown adipocytes are insulin-like growth factor-I (IGF-I) target cells. To assess the importance of the IGF-I receptor (IGF-IR) in brown adipocytes during fetal life, we have generated immortalized brown adipocyte cell lines from the IGF-IR(-/-) mice. Using this experimental
Xun Jin et al.
Experimental & molecular medicine, 42(8), 574-582 (2010-07-16)
Although human telomerase catalytic subunit (TERT) has several cellular functions including telomere homeostasis, genomic stability, cell proliferation, and tumorigenesis, the molecular mechanism underlying anti-apoptosis regulated by TERT remains to be elucidated. Here, we show that ectopic expression of TERT in
R E Shackelford et al.
The Journal of biological chemistry, 276(24), 21951-21959 (2001-04-06)
Ataxia telangiectasia (AT) is an autosomal recessive disorder characterized by neuronal degeneration accompanied by ataxia, telangiectasias, acute cancer predisposition, and sensitivity to ionizing radiation (IR). Cells from individuals with AT show unusual sensitivity to IR, severely attenuated cell cycle checkpoint
Ming Li et al.
Theranostics, 10(19), 8863-8879 (2020-08-06)
Background: As a histone demethylase, JMJD2D can enhance gene expression by specifically demethylating H3K9me2/3 and plays an important role in promoting colorectal cancer progression. However, its role in liver cancer remains unclear. Methods: The expression of JMJD2D was examined in
M Schreiber et al.
Genes & development, 13(5), 607-619 (1999-03-11)
The c-jun proto-oncogene encodes a component of the mitogen-inducible immediate-early transcription factor AP-1 and has been implicated as a positive regulator of cell proliferation and G1-to-S-phase progression. Here we report that fibroblasts derived from c-jun-/- mouse fetuses exhibit a severe
Yu-Mi Lim et al.
Nature communications, 5, 4934-4934 (2014-09-27)
Despite growing interest in the relationship between autophagy and systemic metabolism, how global changes in autophagy affect metabolism remains unclear. Here we show that mice with global haploinsufficiency of an essential autophagy gene (Atg7(+/-) mice) do not show metabolic abnormalities
Ariel G Herman et al.
Cancer discovery, 1(4), 312-325 (2012-05-16)
E3 ubiquitin ligases are of interest as drug targets for their ability to regulate protein stability and function. The oncogene Mdm2 is an attractive E3 ligase to target, as it is the key negative regulator of the tumor suppressor p53
Zainab A H Alebady et al.
Cancers, 15(14) (2023-07-29)
The methyltransferase KMT5A has been proposed as an oncogene in prostate cancer and therefore represents a putative therapeutic target. To confirm this hypothesis, we have performed a microarray study on a prostate cancer cell line model of androgen independence following
C Méplan et al.
The Journal of biological chemistry, 274(44), 31663-31670 (1999-10-26)
The p53 tumor suppressor protein is a transcription factor that binds DNA in a sequence-specific manner through a protein domain stabilized by the coordination of zinc within a tetrahedral cluster of three cysteine residues and one histidine residue. We show
Laura Fozzatti et al.
PloS one, 8(6), e67954-e67954 (2013-07-11)
Studies have suggested that the nuclear receptor corepressor 1 (NCOR1) could play an important role in human cancers. However, the detailed molecular mechanisms by which it functions in vivo to affect cancer progression are not clear. The present study elucidated
D Escobar et al.
Cell death & disease, 6, e1816-e1816 (2015-07-17)
The Sall2 transcription factor is deregulated in several cancers; however, little is known about its cellular functions, including its target genes. Recently, we demonstrated that p53 directly regulates Sall2 expression under genotoxic stress. Here, we investigated the role of Sall2
Song Liu et al.
eLife, 6 (2017-08-23)
Standard treatment for metastatic prostate cancer (CaP) prevents ligand-activation of androgen receptor (AR). Despite initial remission, CaP progresses while relying on AR. AR transcriptional output controls CaP behavior and is an alternative therapeutic target, but its molecular regulation is poorly
Eva Calviño et al.
Phytotherapy research : PTR, 25(1), 25-32 (2010-06-23)
Aqueous extracts and a semipurified fraction obtained by methanol extraction and column chromatography were isolated from Ganoderma lucidum [Ganoderma lucidum (Curtis) P. Karst.; Ganodermataceae Donk] and their effects on interleukin 3-dependent lymphoma cells (DA-1) were studied. Cell viability was reduced
Rachel E Rempel et al.
Molecular cancer therapeutics, 13(12), 3219-3229 (2014-10-29)
Human aggressive B-cell non-Hodgkin lymphomas (NHL) encompass the continuum between Burkitt lymphoma and diffuse large B-cell lymphoma (DLBCL), and display considerable clinical and biologic heterogeneity, most notably related to therapy response. We previously showed that lymphomas arising in the Eμ-Myc
Takao Miki et al.
Nature communications, 4, 2444-2444 (2013-09-21)
The mechanistic interconnectivity between circadian regulation and the genotoxic stress response remains poorly understood. Here we show that the expression of Period 2 (Per2), a circadian regulator, is directly regulated by p53 binding to a response element in the Per2
Sun-Young Choi et al.
International journal of oncology, 40(1), 277-286 (2011-09-03)
Proteins involved in the G1 phase of the cell cycle are aberrantly expressed, sometimes in mutated forms, in human cancers including human hepatocellular carcinoma.
Eva Calviño et al.
Cell biochemistry and function, 33(4), 211-219 (2015-04-29)
The relationship between the mitogen-activated protein kinase response, nuclear factor-κB (NFκB) expression and the apoptosis in human acute promyelocytic leukaemia NB4 cells treated with vinblastine was investigated in this work. Cell viability, subdiploid DNA and cell cycle were analysed by
Toshiharu Komori et al.
Genes to cells : devoted to molecular & cellular mechanisms, 14(3), 343-354 (2009-02-13)
DSIF is an evolutionarily conserved, ubiquitously expressed, heterodimeric transcription elongation factor composed of two subunits, Spt4 and Spt5. Previous biochemical studies have shown that DSIF positively and negatively regulates RNA polymerase II elongation in collaboration with other protein factors. While
Sara Gookin et al.
PLoS biology, 15(9), e2003268-e2003268 (2017-09-12)
The cell-cycle field has identified the core regulators that drive the cell cycle, but we do not have a clear map of the dynamics of these regulators during cell-cycle progression versus cell-cycle exit. Here we use single-cell time-lapse microscopy of
Rosanna Beraldi et al.
Human molecular genetics, 24(22), 6473-6484 (2015-09-17)
Ataxia telangiectasia (AT) is a progressive multisystem disorder caused by mutations in the AT-mutated (ATM) gene. AT is a neurodegenerative disease primarily characterized by cerebellar degeneration in children leading to motor impairment. The disease progresses with other clinical manifestations including
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