Reactive Oxygen Species and Mitochondrial Sensitivity to Oxidative Stress Determine Induction of Cancer Cell Death by p21

Induction of p21-Dependent Senescence by an NAE Inhibitor, MLN4924, as a Mechanism of Growth Suppression

(2015) Lijun Jia et al.   NEOPLASIA

Pretreatment Mitochondrial Priming Correlates with Clinical Response to Cytotoxic Chemotherapy

(2011) T. N. Chonghaile et al.   SCIENCE

Genetic modification of primary chronic lymphocytic leukemia cells with a lentivirus expressing CD38

(2010) L. Pearce et al.   HAEMATOLOGICA

Protection of Cells in Physiological Oxygen Tensions against DNA Damage-induced Apoptosis

(2010) Samantha Carrera et al.   JOURNAL OF BIOLOGICAL CHEMISTRY

Decreased expression of Drp1 and Fis1 mediates mitochondrial elongation in senescent cells and enhances resistance to oxidative stress through PINK1

(2010) Sören Mai et al.   JOURNAL OF CELL SCIENCE

Feedback between p21 and reactive oxygen production is necessary for cell senescence

(2010) João F Passos et al.   Molecular Systems Biology

Multiple microRNAs rescue from Ras-induced senescence by inhibiting p21Waf1/Cip1

(2010) V Borgdorff et al.   ONCOGENE

Multiple microRNAs modulate p21Cip1/Waf1 expression by directly targeting its 3′ untranslated region

(2010) S Wu et al.   ONCOGENE

Level of reactive oxygen species induced by p21WAF(1)/CIP(1)is critical for the determination of cell fate

(2009) Takafumi Inoue et al.   CANCER SCIENCE

Gene expression profiling reveals new protective roles for vitamin C in human skin cells

(2008) T DUARTE et al.   FREE RADICAL BIOLOGY AND MEDICINE

Mitochondrial dysfunction is a possible cause of accelerated senescence of mesothelial cells exposed to high glucose

(2007) Krzysztof Ksiazek et al.   BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS