05-636

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Histone chaperone CAF-1 mediates repressive histone modifications to protect preimplantation mouse embryos from endogenous retrotransposons.

Yuki Hatanaka et al.

Proceedings of the National Academy of Sciences of the United States of America, 112(47), 14641-14646 (2015-11-08)

Substantial proportions of mammalian genomes comprise repetitive elements including endogenous retrotransposons. Although these play diverse roles during development, their appropriate silencing is critically important in maintaining genomic integrity in the host cells. The major mechanism for retrotransposon silencing is DNA

Combined treatment with PI3K inhibitor BKM120 and PARP inhibitor olaparib is effective in inhibiting the gastric cancer cells with ARID1A deficiency.

Lin Yang et al.

Oncology reports, 40(1), 479-487 (2018-05-17)

Dual blockade of phosphoinositide 3-kinase (PI3K) and poly(ADP-ribose) polymerase (PARP) has been revealed to be an effective treatment strategy for breast, ovarian and prostate cancer. However, the efficacy of this combination for the treatment of gastric cancer, and potential predictive therapeutic biomarkers

Counteracting the activation of pAkt by inhibition of MEK/Erk inhibition reduces actin disruption-mediated apoptosis in PTEN-null PC3M prostate cancer cell lines.

Yong-Tae Ahn et al.

Oncology letters, 6(5), 1383-1389 (2013-11-02)

The actin cytoskeleton is important in the maintenance of cellular homeostasis and in signal transduction pathways leading to cell growth and apoptotic cell death in eukaryotic cells. Disruption of actin dynamics is associated with morphological changes in cancer cells. Deletion

A nuclear lamina-chromatin-Ran GTPase axis modulates nuclear import and DNA damage signaling.

Natalia Dworak et al.

Aging cell, 18(1), e12851-e12851 (2018-12-20)

The Ran GTPase regulates nuclear import and export by controlling the assembly state of transport complexes. This involves the direct action of RanGTP, which is generated in the nucleus by the chromatin-associated nucleotide exchange factor, RCC1. Ran interactions with RCC1

Flavan-3-ols and Proanthocyanidins in Japanese, Bohemian and Giant Knotweed.

Maja Bensa et al.

Plants (Basel, Switzerland), 10(2) (2021-03-07)

Flavan-3-ols and proanthocyanidins of invasive alien plants Japanese knotweed (Fallopia japonica Houtt.), giant knotweed (Fallopia sachalinensis F. Schmidt) and Bohemian knotweed (Fallopia × bohemica (Chrtek & Chrtkova) J.P. Bailey) were investigated using high performance thin-layer chromatography (HPTLC) coupled to densitometry

The ATM substrate KAP1 controls DNA repair in heterochromatin: regulation by HP1 proteins and serine 473/824 phosphorylation.

David White et al.

Molecular cancer research : MCR, 10(3), 401-414 (2011-12-30)

The repair of DNA damage in highly compact, transcriptionally silent heterochromatin requires that repair and chromatin packaging machineries be tightly coupled and regulated. KAP1 is a heterochromatin protein and co-repressor that binds to HP1 during gene silencing but is also

Chk1 inhibition and Wee1 inhibition combine synergistically to impede cellular proliferation.

Kurtis D Davies et al.

Cancer biology & therapy, 12(9), 788-796 (2011-09-06)

Inhibition of the checkpoint kinase Chk1, both as a monotherapy and in combination with DNA damaging cytotoxics, is a promising therapeutic approach for the treatment of a wide array of human cancers. However, much remains to be elucidated in regard

And-1 coordinates with CtIP for efficient homologous recombination and DNA damage checkpoint maintenance.

Yali Chen et al.

Nucleic acids research, 45(5), 2516-2530 (2016-12-13)

To prevent genomic instability, cells respond to DNA lesions by blocking cell cycle progression and initiating DNA repair. Homologous recombination repair of DNA breaks requires CtIP-dependent resection of the DNA ends, which is thought to play a key role in

DNA nicks induce mutational signatures associated with BRCA1 deficiency.

Yi-Li Feng et al.

Nature communications, 13(1), 4285-4285 (2022-07-26)

Analysis of human cancer genome sequences has revealed specific mutational signatures associated with BRCA1-deficient tumors, but the underlying mechanisms remain poorly understood. Here, we show that one-ended DNA double strand breaks (DSBs) converted from CRISPR/Cas9-induced nicks by DNA replication, not

Expression of tert Prevents ALT in Zebrafish Brain Tumors.

Aurora Irene Idilli et al.

Frontiers in cell and developmental biology, 8, 65-65 (2020-03-03)

The activation of a telomere maintenance mechanism (TMM) is an essential step in cancer progression to escape replicative senescence and apoptosis. Alternative lengthening of telomeres (ALT) is found in a subset of malignant brain tumors with poor outcomes. Here, we

A Class of Environmental and Endogenous Toxins Induces BRCA2 Haploinsufficiency and Genome Instability.

Shawn Lu Wen Tan et al.

Cell, 169(6), 1105-1118 (2017-06-03)

Mutations truncating a single copy of the tumor suppressor, BRCA2, cause cancer susceptibility. In cells bearing such heterozygous mutations, we find that a cellular metabolite and ubiquitous environmental toxin, formaldehyde, stalls and destabilizes DNA replication forks, engendering structural chromosomal aberrations. Formaldehyde

Mrg15 null and heterozygous mouse embryonic fibroblasts exhibit DNA-repair defects post exposure to gamma ionizing radiation.

Sandra N Garcia et al.

FEBS letters, 581(27), 5275-5281 (2007-10-27)

MORF4-related gene on chromosome 15 (MRG15) is a core component of the NuA4/Tip60 histone acetyltransferase complex that modifies chromatin structure. We here demonstrate that Mrg15 null and heterozygous mouse embryonic fibroblasts exhibit an impaired DNA-damage response post gamma irradiation, when

Nuclear Countermeasure Activity of TP508 Linked to Restoration of Endothelial Function and Acceleration of DNA Repair.

Barbara Olszewska-Pazdrak et al.

Radiation research, 186(2), 162-174 (2016-07-09)

There is increasing evidence that radiation-induced damage to endothelial cells and loss of endothelial function may contribute to both acute radiation syndromes and long-term effects of whole-body nuclear irradiation. Therefore, several drugs are being developed to mitigate the effects of

Localization of Double-Strand Break Repair Proteins to Viral Replication Compartments following Lytic Reactivation of Kaposi's Sarcoma-Associated Herpesvirus.

Robert Hollingworth et al.

Journal of virology, 91(22) (2017-09-01)

Double-strand breaks (DSBs) in DNA are recognized by the Ku70/80 heterodimer and the MRE11-RAD50-NBS1 (MRN) complex and result in activation of the DNA-PK and ATM kinases, which play key roles in regulating the cellular DNA damage response (DDR). DNA tumor

Reducing oxidative protein folding alleviates senescence by minimizing ER-to-nucleus H2 O2 release.

Fang Cheng et al.

EMBO reports, 24(8), e56439-e56439 (2023-06-12)

Oxidative protein folding occurs in the endoplasmic reticulum (ER) to generate disulfide bonds, and the by-product is hydrogen peroxide (H2 O2 ). However, the relationship between oxidative protein folding and senescence remains uncharacterized. Here, we find that the protein disulfide

Synthetic lethal targeting of DNA double-strand break repair deficient cells by human apurinic/apyrimidinic endonuclease inhibitors.

Rebeka Sultana et al.

International journal of cancer, 131(10), 2433-2444 (2012-03-02)

An apurinic/apyrimidinic (AP) site is an obligatory cytotoxic intermediate in DNA Base Excision Repair (BER) that is processed by human AP endonuclease 1 (APE1). APE1 is essential for BER and an emerging drug target in cancer. We have isolated novel

Transcription Factor RFX2 Is a Key Regulator of Mouse Spermiogenesis.

Yujian Wu et al.

Scientific reports, 6, 20435-20435 (2016-02-09)

The regulatory factor X (RFX) family of transcription factors is crucial for ciliogenesis throughout evolution. In mice, Rfx1-4 are highly expressed in the testis where flagellated sperm are produced, but the functions of these factors in spermatogenesis remain unknown. Here

Tissue-infiltrating macrophages mediate an exosome-based metabolic reprogramming upon DNA damage.

Evi Goulielmaki et al.

Nature communications, 11(1), 42-42 (2020-01-04)

DNA damage and metabolic disorders are intimately linked with premature disease onset but the underlying mechanisms remain poorly understood. Here, we show that persistent DNA damage accumulation in tissue-infiltrating macrophages carrying an ERCC1-XPF DNA repair defect (Er1F/-) triggers Golgi dispersal

Poly(ADP-ribose) polymerase 1 is a novel target to promote axonal regeneration.

Camille Brochier et al.

Proceedings of the National Academy of Sciences of the United States of America, 112(49), 15220-15225 (2015-11-26)

Therapeutic options for the restoration of neurological functions after acute axonal injury are severely limited. In addition to limiting neuronal loss, effective treatments face the challenge of restoring axonal growth within an injury environment where inhibitory molecules from damaged myelin

Telomere crisis in kidney epithelial cells promotes the acquisition of a microRNA signature retrieved in aggressive renal cell carcinomas.

Luis Jaime Castro-Vega et al.

Carcinogenesis, 34(5), 1173-1180 (2013-01-30)

Telomere shortening is a major source of chromosome instability (CIN) at early stages during carcinogenesis. However, the mechanisms through which telomere-driven CIN (T-CIN) contributes to the acquisition of tumor phenotypes remain uncharacterized. We discovered that human epithelial kidney cells undergoing

Human papillomavirus E7 induces rereplication in response to DNA damage.

Fan, X; Liu, Y; Heilman, SA; Chen, JJ

Journal of virology null

Inhibition of Estrogen Signaling Reduces the Incidence of BRCA1-associated Mammary Tumor Formation.

Hye Jung Baek et al.

International journal of biological sciences, 14(12), 1755-1768 (2018-11-13)

BRCA1-deficient breast cancer is a very well-known hereditary cancer. However, except for resection of normal mammary glands and ovaries, there is no acceptable measure for proactively preventing tumor development. Importantly, inherited BRCA1 mutations are closely associated with tumors in hormone-responsive

The Alkylating Agent Methyl Methanesulfonate Triggers Lipid Alterations at the Inner Nuclear Membrane That Are Independent from Its DNA-Damaging Ability.

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.

Loss of Tumor Suppressor STAG2 Promotes Telomere Recombination and Extends the Replicative Lifespan of Normal Human Cells.

Zharko Daniloski et al.

Cancer research, 77(20), 5530-5542 (2017-08-19)

Sister chromatids are held together by cohesin, a tripartite ring with a peripheral SA1/2 subunit, where SA1 is required for telomere cohesion and SA2 for centromere cohesion. The STAG2 gene encoding SA2 is often inactivated in human cancer, but not

Targeting telomerase reverse transcriptase with the covalent inhibitor NU-1 confers immunogenic radiation sensitization.

Yue Liu et al.

Cell chemical biology, 29(10), 1517-1531 (2022-10-08)

Beyond synthesizing telomere repeats, the telomerase reverse transcriptase (TERT) also serves multiple other roles supporting cancer growth. Blocking telomerase to drive telomere erosion appears impractical, but TERT's non-canonical activities have yet to be fully explored as cancer targets. Here, we

hnRNP H/F drive RNA G-quadruplex-mediated translation linked to genomic instability and therapy resistance in glioblastoma.

Pauline Herviou et al.

Nature communications, 11(1), 2661-2661 (2020-05-29)

RNA G-quadruplexes (RG4s) are four-stranded structures known to control mRNA translation of cancer relevant genes. RG4 formation is pervasive in vitro but not in cellulo, indicating the existence of poorly characterized molecular machinery that remodels RG4s and maintains them unfolded.

HDAC1 dysregulation induces aberrant cell cycle and DNA damage in progress of TDP-43 proteinopathies.

Cheng-Chun Wu et al.

EMBO molecular medicine, 12(6), e10622-e10622 (2020-05-26)

TAR DNA-binding protein 43 (TDP-43) has been implicated in frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-TDP) and amyotrophic lateral sclerosis. Histone deacetylase 1 (HDAC1) is involved in DNA repair and neuroprotection in numerous neurodegenerative diseases. However, the pathological mechanisms of

BRCA1 degradation in response to mitochondrial damage in breast cancer cells.

Kana Miyahara et al.

Scientific reports, 11(1), 8735-8735 (2021-04-24)

BRCA1 is a well-studied tumor suppressor involved in the homologous repair of DNA damage, whereas PINK1, a mitochondrial serine/threonine kinase, is known to be involved in mitochondrial quality control. Genetic mutations of PINK1 and Parkin cause autosomal recessive early-onset Parkinson's

The canonical NF-κB pathway differentially protects normal and human tumor cells from ROS-induced DNA damage.

Alexandros Sfikas et al.

Cellular signalling, 24(11), 2007-2023 (2012-07-04)

DNA damage responses (DDR) invoke senescence or apoptosis depending on stimulus intensity and the degree of activation of the p53-p21(Cip1/Waf1) axis; but the functional impact of NF-κB signaling on these different outcomes in normal vs. human cancer cells remains poorly

DNA Damage In Situ Ligation Followed by Proximity Ligation Assay (DI-PLA).

Alessandro Galbiati et al.

Methods in molecular biology (Clifton, N.J.), 1896, 11-20 (2018-11-27)

Cells have evolved DNA repair mechanisms to maintain their genetic information unaltered and a DNA damage response pathway that coordinates DNA repair with several cellular events. Despite a clear role for DNA damage in the form of DNA double-strand breaks

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