Results 91 to 100 of about 693,900 (279)

Poly(ADP-ribose) polymerase (PARP) and PARP inhibitors

open access: yes
PARP-1 protects cells from endogenous and therapeutically inflicted DNA damage. PARP inhibitors have been under development since 1980 and first entered clinical trial in 2003.
Curtin NJ
core   +5 more sources

Clinical approaches to overcome PARP inhibitor resistance

open access: yesMolecular Cancer
PARP inhibitors have profoundly changed treatment options for cancers with homologous recombination repair defects, especially those carrying BRCA1/2 mutations.
Yutian Zou   +8 more
doaj   +1 more source

Combinations of PARP Inhibitors with Temozolomide Drive PARP1 Trapping and Apoptosis in Ewing's Sarcoma.

open access: yesPLoS ONE, 2015
Ewing's sarcoma is a malignant pediatric bone tumor with a poor prognosis for patients with metastatic or recurrent disease. Ewing's sarcoma cells are acutely hypersensitive to poly (ADP-ribose) polymerase (PARP) inhibition and this is being evaluated in
Sonja J Gill   +11 more
doaj   +1 more source

Nanoparticle‐Mediated TIPE1 mRNA Delivery Enhances Paclitaxel Sensitivity in Triple‐Negative Breast Cancer by Modulating RAB7A Ubiquitination‐Associated Stability and Autophagy

open access: yesAdvanced Science, EarlyView.
TIPE1m NPs nanoparticles restore TIPE1 expression, promote RAB7A ubiquitination and degradation, suppress autophagic flux, and resensitize paclitaxel‐resistant triple‐negative breast cancer to therapy. ABSTRACT Acquired paclitaxel (PTX) resistance remains a major obstacle in triple‐negative breast cancer (TNBC) treatment.
Wei Hu   +9 more
wiley   +1 more source

Poly (ADP-Ribose) Polymerase-1 (PARP-1) Inhibitors in Diabetic Retinopathy: An Attractive but Elusive Choice for Drug Development

open access: yesPharmaceutics
Owing to its promiscuous roles, poly (ADP-ribose) polymerase-1 (PARP-1) is involved in various neurological disorders including several retinal pathologies.
Etelka Pöstyéni   +2 more
doaj   +1 more source

EP300‐Mediated MTF1‐K218 Lactylation Buffers AR‐Driven Copper Overload to Suppress Cuproptosis in Castration‐Resistant Prostate Cancer

open access: yesAdvanced Science, EarlyView.
Androgen receptor (AR) drives copper accumulation in prostate cancer while inducing MTF1 to buffer copper toxicity. EP300‐mediated lactylation of MTF1 at K218 promotes its nuclear translocation and metallothionein expression, sequestering cytosolic copper and preventing mitochondrial cuproptosis.
Kai Li   +21 more
wiley   +1 more source

Klotho‐Derived Peptide 1 Protects against Acute Kidney Injury by Directly Targeting Mitochondrial ATAD3A

open access: yesAdvanced Science, EarlyView.
This study uncovers that KP1, a Klotho‐derived peptide, protects the kidney against acute kidney injury, a clinical syndrome with high morbidity and mortality. KP1 enters tubular epithelial cells via endocytosis, directly interacts with the mitochondrial ATAD3A/HIGD2A complex, thereby preventing cytochrome c release, and caspases activation, and ...
Xiaoyao Zhang   +6 more
wiley   +1 more source

Metabolic Memory in Cardiovascular Disease: Encoding, Propagation, and Therapeutic Targeting

open access: yesAdvanced Science, EarlyView.
Cardiovascular risk often persists after metabolic abnormalities are corrected. This conceptual Review frames such persistence as metabolic memory, encoded through a narrowing therapeutic window from reversible marks to irreversible damage, with continuous input from peripheral organs.
Cheng Cheng   +12 more
wiley   +1 more source

Theranostic Potential of an NAD(P)H‐Activatable Fluorophore: Assessing Cancer Aggressiveness and Triggering Apoptosis

open access: yesAngewandte Chemie, EarlyView.
DE‐CQ, an NAD(P)H‐activatable theranostic probe, enables the quantification of cancer aggressiveness via glucose‐stimulated fluorescence imaging and selectively induces apoptosis. Its multifaceted efficacy is demonstrated across 2D cells, 3D spheroids, and in vivo models.
Yujin Cha   +11 more
wiley   +2 more sources

RSF1‐Dependent PAR Turnover Promotes 53BP1 Liquid Condensate Formation at DNA Damage Sites

open access: yesAdvanced Science, EarlyView.
At sites of DNA damage, RSF1 recruits PARG to accelerate PAR turnover, triggering a switch from PAR‐driven condensates to 53BP1 condensates. This condensate transition enables p53‐dependent gene transcription and coordinates the DNA damage response.
Yungyeong Heo   +10 more
wiley   +1 more source

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