A5015664805- Cancer-related Molecular Pathways
- Ubiquitin and proteasome pathways
- Epigenetics and DNA Methylation
- Ferroptosis and cancer prognosis
- RNA modifications and cancer
- Sirtuins and Resveratrol in Medicine
- Cancer, Hypoxia, and Metabolism
- Autophagy in Disease and Therapy
- Histone Deacetylase Inhibitors Research
- DNA Repair Mechanisms
- Genetics and Neurodevelopmental Disorders
- Cancer, Lipids, and Metabolism
- Adipose Tissue and Metabolism
- Protein Degradation and Inhibitors
- Cancer-related molecular mechanisms research
- Chromatin Remodeling and Cancer
- Biochemical effects in animals
- Cancer Research and Treatments
- PARP inhibition in cancer therapy
- Cell death mechanisms and regulation
- Mitochondrial Function and Pathology
- Immune cells in cancer
- Microtubule and mitosis dynamics
- Diet and metabolism studies
- Immune Cell Function and Interaction
Cancer Genetics (United States)
2016-2025
Columbia University
2016-2025
Anhui Agricultural University
2022-2025
Huizhou University
2025
Guangzhou University of Chinese Medicine
2024-2025
Anhui Medical University
2025
Royal College of Physicians
2014-2024
Columbia University Irving Medical Center
2007-2024
Jiangsu Province Hospital
2022-2024
Nanjing Medical University
2014-2024
Significance Nonapoptotic cell death-induced tissue damage has been implicated in a variety of diseases, including neurodegenerative disorder, inflammation, and stroke. In this study, we demonstrate that ferroptosis, newly defined iron-dependent death, mediates both chemotherapy- ischemia/reperfusion-induced cardiomyopathy. RNA-sequencing analysis revealed up-regulation heme oxygenase 1 by doxorubicin as major mechanism ferroptotic As result, degrades releases free iron cardiomyocytes, which...
Ferroptosis is a form of cell death that results from the catastrophic accumulation lipid reactive oxygen species (ROS). Oncogenic signaling elevates ROS production in many tumor types and counteracted by metabolites are derived amino acid cysteine. In this work, we show import oxidized cysteine (cystine) via system xC- critical dependency pancreatic ductal adenocarcinoma (PDAC), which leading cause cancer mortality. PDAC cells used to synthesize glutathione coenzyme A, which, together,...
Although Mdm2-mediated ubiquitination is essential for both degradation and nuclear export of p53, the molecular basis differential effects Mdm2 remains unknown. Here we show that low levels activity induce monoubiquitination whereas high promote p53's polyubiquitination degradation. A p53-ubiquitin fusion protein mimics monoubiquitinated p53 was found to accumulate in cytoplasm an Mdm2-independent manner, indicating critical trafficking. These results clarify nature ubiquitination-mediated...
We generated mice that overexpress the sirtuin, SIRT1. Transgenic have been by knocking in SIRT1 cDNA into beta-actin locus. Mice are hemizygous for this transgene express normal levels of and higher protein several tissues. display some phenotypes similar to on a calorie-restricted diet: they leaner than littermate controls; more metabolically active; reductions blood cholesterol, adipokines, insulin fasted glucose; glucose tolerant. Furthermore, transgenic perform better rotarod challenge...
The positively charged lysine residue plays an important role in protein folding and functions. Neutralization of the charge often has a profound impact on substrate proteins. Accordingly all known post-translational modifications at have pivotal roles cell physiology pathology. Here we report discovery two novel, vivo histones, propionylation butyrylation. We confirmed, by vitro labeling peptide mapping mass spectrometry, that previously acetyltransferases, p300 CREB-binding protein, could...
Significance Although it is commonly accepted that p53-mediated cell-cycle arrest, apoptosis, and senescence all serve as major mechanisms of tumor suppression, accumulating evidence indicates other activities p53, such ferroptosis, are also critical for suppression. However, the molecular by which ferroptosis operates not completely understood. In this study, we discovered p53 can execute ferroptotic cell-death responses directly activating its target gene SAT1 , coded spermidine/spermine N...