Results 61 to 70 of about 25,426 (206)

Sensitizing thermochemotherapy with a PARP1-inhibitor [PDF]

open access: yes, 2017
Cis-diamminedichloroplatinum(II) (cisplatin, cDDP) is an effective chemotherapeutic agent that induces DNA double strand breaks (DSBs), primarily in replicating cells.
Crezee, J.   +23 more
core   +2 more sources

SMAD4 Palmitoylation Drives a Metabolic‐Transcriptional Circuit to Promote Tumorigenesis and Confers Radiosensitivity in Pancreatic Cancer

open access: yesAdvanced Science, EarlyView.
This study identifies palmitoylation as a novel regulatory modification of SMAD4, mediated by ZDHHC22/APT2. It activates fatty acid synthesis, creating a self‐reinforcing SMAD4–FASN–palmitate feedback loop that drives pancreatic cancer growth and enhances radiotherapy sensitivity.
Yang Wang   +16 more
wiley   +1 more source

Synergism between ATM and PARP1 inhibition involves DNA damage and abrogating the G2 DNA damage checkpoint

open access: yes, 2020
PARP inhibitors have emerged as effective chemotherapeutic agents for BRCA1/BRCA2-deficient cancers. Another DNA damage response protein, ATM, is also increasingly being recognized as a target for synthetic lethality with PARP inhibitors.
Mak, Joyce P.Y.   +2 more
core   +1 more source

NAMPT-derived NAD+ fuels PARP1 to promote skin inflammation through parthanatos cell death

open access: yesPLoS Biology, 2021
Several studies have revealed a correlation between chronic inflammation and nicotinamide adenine dinucleotide (NAD+) metabolism, but the precise mechanism involved is unknown.
Francisco J. Martínez-Morcillo   +17 more
doaj  

Discovery of the Oncogenic Parp1, a Target of bcr-abl and a Potential Therapeutic, in mir-181a/PPFIA1 Signaling Pathway

open access: yesMolecular Therapy: Nucleic Acids, 2019
miR-181a is downregulated in leukemia and affects its progression, drug resistance, and prognosis. However, the exact mechanism of its targets in leukemia, particularly in chronic myelogenous leukemia (CML), has not previously been established.
Chunming Gu   +7 more
doaj   +1 more source

Genome-Wide Profiling of PARP1 Reveals an Interplay with Gene Regulatory Regions and DNA Methylation. [PDF]

open access: yesPLoS ONE, 2015
Poly (ADP-ribose) polymerase-1 (PARP1) is a nuclear enzyme involved in DNA repair, chromatin remodeling and gene expression. PARP1 interactions with chromatin architectural multi-protein complexes (i.e. nucleosomes) alter chromatin structure resulting in
Narasimharao Nalabothula   +7 more
doaj   +1 more source

Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

open access: yesAdvanced Science, EarlyView.
Pancreatic neuroendocrine tumors frequently silence MEN1 through epigenetic mechanisms. Here, SIRT7 recruits DNMT1 to the MEN1 promoter, drives hypermethylation, and enhances DNA repair. Inhibiting SIRT7 restores MEN1, reduces MRN complex abundance, impairs double‐strand break repair, and sensitizes PanNET models to radiation, supporting SIRT7 as a ...
Jianyun Jiang   +11 more
wiley   +1 more source

PARP1 in Carcinomas and PARP1 Inhibitors as Antineoplastic Drugs

open access: yes, 2017
Poly (ADP-ribose) polymerase 1 (PARP1), the best-studied isoform of the nuclear enzyme PARP family, plays a pivotal role in cellular biological processes, such as DNA repair, gene transcription, and so on.
Aiping Lu   +7 more
core   +1 more source

Harnessing MDM2‐Mediated Targeted Degradation of Transcriptional and Epigenetic Machinery to Disrupt Oncogenic Addictions in Pediatric Sarcoma

open access: yesAdvanced Science, EarlyView.
MDM2 dependency in pediatric sarcomas is driven by a novel p53‐independent oncogenic cistrome alongside canonical p53 pathway suppression. This study introduces MDM2‐recruiting transcriptional and epigenetic machinery degraders (MDM2‐TEMADs) as a novel precision oncology modality.
Jiawei Zhou   +21 more
wiley   +1 more source

The oncoprotein DEK affects the outcome of PARP1/2 inhibition during mild replication stress

open access: yes, 2019
DNA replication stress is a major source of genomic instability and is closely linked to tumor formation and progression. Poly(ADP-ribose)polymerases1/2 (PARP1/2) enzymes are activated in response to replication stress resulting in poly(ADP-ribose) (PAR)
Kleiner R   +53 more
core   +2 more sources

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