Results 61 to 70 of about 77,084 (260)

Loss of E3 Ubiquitin Ligase RINES via CpG Methylation Relieves Suppression of STAT3 and MYC, Facilitating Multiple Tumorigeneses

Advanced Science, EarlyView.
Dysregulated protein modifications drive tumorigenesis. RINES, an E3 ubiquitin ligase, represses tumor cell proliferation and metastasis by facilitating RING domain‐dependent, ubiquitin–proteasome‐mediated degradation of STAT3 and MYC, which consequently restrains cancer stemness and oncogenic progression.
Lili Li, Ka Man Ng, Xingsheng Shu, Xiaoxue Chai, Kai Yau Wong, Gopesh Srivastava, Anthony T.C. Chan, Wai Yee Chan, Qian Tao   +8 more
wiley   +1 more source

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

Advanced 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, Yong Wei, Yongshan Li, Yuxiang Dong, Jiancheng Lv, Mingzhi Yuan, Ao Shen, Fuyang Liu, Yetao Zhang, Youjian Li, Ruixi Yu, Yang Liu, Tong Zhao, Jun Wang, Kai Zhou, Zongyao Fan, Manning Wang, Jun Xu, Mulong Du, Min Gu, Bing Yao, Qingyi Zhu   +21 more
wiley   +1 more source

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

Advanced 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, Shihui Lin, Tianyu Wu, Zhixin Zhang, Hong Zhou, Xue Hong, Youhua Liu   +6 more
wiley   +1 more source

Advances in the use of PARP inhibitor therapy for breast cancer

Drugs in Context, 2018
Poly-ADP-ribose polymerase 1 (PARP-1) and PARP-2 are DNA damage sensors that are most active during S-phase of the cell cycle and that have wider-reaching roles in DNA repair than originally described.
Kelly E McCann, Sara A Hurvitz
doaj   +1 more source

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

Advanced 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, Yonghyeon Kim, Nangyeong Hwang, Gwanho Sung, Sujin Jo, Yeonhu Lee, Ho‐Chul Kang, Jae‐Ho Lee, Yong Won Choi, Hyeseong Cho, Sunwoo Min   +10 more
wiley   +1 more source

Impact of PARP inhibitors on progression-free survival in platinum-sensitive recurrent epithelial ovarian cancer: a retrospective analysis

World Journal of Surgical Oncology
Objective Poly (ADP-ribose) polymerase (PARP) inhibitors such as olaparib and niraparib have shown promise in extending progression-free survival (PFS) in patients with platinum-sensitive recurrent (PSR) epithelial ovarian cancer.
Yumei Zhou, Junfen Xu
doaj   +1 more source

Gut Microbiota‐Isoallolithocholic Acid Crosstalk Promotes Calcium Oxalate Kidney Stone Formation via PARP1‐Mediated Parthanatos

Advanced Science, EarlyView.
ABSTRACT Bile acids have been implicated in calcium oxalate (CaOx) nephrolithiasis. Here, we employ multi‐omics approaches to identify isoallolithocholic acid (isoalloLCA) as the key bile acid elevated in the feces, serum, kidney, and urine of CaOx rats, confirmed by spatial metabolomics.
Zijian Zhou, Ruixi Yu, Xuan Zhou, Feng Shi, Zeyu Lin, Peng Gao, Lujia Wang, Ninghan Feng, Zhong Wu, Dawei Wang   +9 more
wiley   +1 more source

Olaparib modulates DNA repair efficiency, sensitizes cervical cancer cells to cisplatin and exhibits anti-metastatic property

Scientific Reports, 2017
PARP1 trapping at DNA lesion by pharmacological inhibitors has been exploited in several cancers exhibiting defects in DNA repair mechanisms. PARP1 hyperactivation is involved in therapeutic resistance in multiple cancers.
Chandra Bhushan Prasad, Shyam Babu Prasad, Suresh Singh Yadav, Laxmi Kant Pandey, Sunita Singh, Satyajit Pradhan, Gopeshwar Narayan   +6 more
doaj   +1 more source

Loss of CYLD on Chromosome 16q Impairs Homologous Recombination and Genomic Stability Through TIRR Degradation

Advanced Science, EarlyView.
Chromosome 16q loss drives genomic instability through disruption of the CYLD–TIRR–53BP1 axis. CYLD preserves homologous recombination by stabilizing TIRR and limiting 53BP1 accumulation at DNA double‐strand breaks. CYLD deficiency redirects repair toward error‐prone non‐homologous end joining, promotes mutational burden and homologous recombination ...
Mingming Lu, Jialu Kang, Qi Ye, Zixi Wang, Lei Li, Yuzeshi Lei, Leihong Ye, Tianjie Liu, Bin Wang, Tao Liu, Shan Xu, Ke Wang, Yong Zhang, Jian Ma, Lei Li   +14 more
wiley   +1 more source

MOB2 Loss Sensitizes Lung Cancer Cells to PARP Inhibition Through p53-Dependent DNA Damage Signaling

Current Issues in Molecular Biology
Poly(ADP-ribose) polymerase (PARP) inhibitors exploit defects in homologous recombination (HR) but show limited and heterogeneous efficacy in non-small-cell lung cancer (NSCLC), where canonical HR deficiency is uncommon. Identifying alternative molecular
Ramazan Gundogdu
doaj   +1 more source