Results 81 to 90 of about 25,426 (206)

NAD+ Metabolism Licenses Zygotic Genome Activation via PARP7‐Mediated ADP‐Ribosylation of UHRF1 in Mouse Early Embryos

open access: yesAdvanced Science, EarlyView.
This study uncovers a metabolic‐epigenetic axis licensing zygotic genome activation (ZGA) in mouse embryos. A developmental decline in NAD+ levels activates PARP7, which mono‐ADP‐ribosylates and stabilizes UHRF1. This modification promotes the establishment of permissive histone acetylation marks, thereby facilitating timely ZGA.
Guangyi Cao   +13 more
wiley   +1 more source

Abstract A20: Synthetic lethality induced by pharmacological inhibition of ATM and PARP1

open access: yes, 2017
DNA double-stranded breaks (DSBs) are highly deleterious and need to be repaired for maintaining genomic stability and viability. Cells resolve DSBs via non-homologous end-joining or homologous recombination repair (HRR).
Randy Yat Choi Poon   +2 more
core   +1 more source

Penfluridol Triggers GSDME‐Mediated Immunogenic Pyroptosis to Potentiate Antitumor Immunotherapy

open access: yesAdvanced Science, EarlyView.
A high‐throughput screen of FDA‐approved antipsychotics identifies penfluridol as a potent pyroptosis inducer acting via direct TTI1 inhibition. This triggers TNFA‐NFKB signaling and caspase‐8/‐3‐dependent GSDME cleavage. The compound stimulates antitumor immunity alone and synergizes with anti‐PD‐1 therapy, while low TTI1 expression emerges as a ...
Linfeng Li   +11 more
wiley   +1 more source

Investigation about non-canonical G-quadruplex stabilization as an alternative approach to PARP1 inhibition

open access: yes, 2022
PARP1 is a nuclear enzyme involved in DNA repair processes. Since its inhibition causes sensitization to DNA damaging chemotherapy (the so-called “synthetic lethality”), several inhibitors have been recently developed and exploited for clinical use ...
Artali, R.   +8 more
core  

Tumor suppressive effect of PARP1 and FOXO3A in gastric cancers and its clinical implications. [PDF]

open access: yes, 2015
Poly (ADP-ribose) polymerase1 (PARP1) has been reported as a possible target for chemotherapy in many cancer types. However, its action mechanisms and clinical implications for gastric cancer survival are not yet fully understood.
Kim, KM   +9 more
core   +1 more source

The MYC Paralog-PARP1 Axis as a Potential Therapeutic Target in MYC Paralog-Activated Small Cell Lung Cancer

open access: yesFrontiers in Oncology, 2020
Poly (ADP-ribose) polymerase 1 (PARP1) is highly expressed in small cell lung cancer (SCLC) and has emerged as an attractive target for treatment of SCLC. However, the clinical significance of PARP1 expression in SCLC remains elusive.
Xing Bian   +23 more
doaj   +1 more source

Vacancy defect‐induced electron homing breaks phosphodiester bonds for RNA depletion‐driven cancer therapy

open access: yesBMEMat, EarlyView.
Illustration of 5% S‐vacancy Bi2S3 mediated phosphodiester bonds cleavage in RNA of hepatocellular carcinoma cells, which suppressing ERI3 expression, inhibiting cell proliferation and promoting apoptosis. Abstract Genome‐wide hypertranscription is a hallmark of malignant progression.
Chuncheng Yang   +12 more
wiley   +1 more source

Glycosylated dendrimer nanoamplifiers hijack DNA damage‐immune crosstalk for enhanced dual‐track therapy of orthotopic glioblastoma

open access: yesBMEMat, EarlyView.
A glycosylated dendrimer nanoamplifier hijacks DNA damage‐immune crosstalk for enhanced radio‐immunotherapy of glioblastoma. The responsive release of demethylcantharidin simultaneously blocks repair‐mediated resistance by inhibiting DNA repair and overcomes adaptive immune resistance.
Cong Song   +10 more
wiley   +1 more source

Imaging poly(ADP-ribose) polymerase-1 (PARP1) in vivo with 18F-labeled brain penetrant positron emission tomography (PET) ligand

open access: yes
Poly(ADP-ribose) polymerase 1 (PARP1) is a multifunctional protein involved in diverse cellular functions, notably DNA damage repair. Pharmacological inhibition of PARP1 holds potential therapeutic benefits for various pathologies.
Richard S. , Van   +23 more
core   +1 more source

Targeting EGFR Induced Oxidative Stress by PARP1 Inhibition in Glioblastoma Therapy

open access: yesPLoS ONE, 2010
Despite the critical role of Epidermal Growth Factor Receptor (EGFR) in glioblastoma pathogenesis [1], [2], EGFR targeted therapies have achieved limited clinical efficacy [3]. Here we propose an alternate therapeutic strategy based on the conceptual framework of non-oncogene addiction [4], [5].
Masayuki Nitta   +16 more
openaire   +6 more sources

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