Also published as: Jin He, M. He, Juan He, Z. He, Yuan He, Geng‐Jun He, Jinxuan He, Weijiang He, BJ He, J. He, Q He, Q. He, Weiling He, Clifford Jiajun He, Andrew He, Fajian He, Ya-Mei He, N He, Luxin He, Y He, Jianping He, C. He, Xiangdong He, X He, Jianfeng He, Fang He, Zhen-Dan He, Jun He, Y. He, X.M. He, L He, F. He, S. He, Y.F. He, Xiao-Peng He, W. He, Bo He, D He, Z He, Xin He, S He, F He, Yuting He, G He, W.J. He, K He, JZ He, JX He, Xiaolin He, Yao He, Bridgewater HE, Q.-Y. He, Yihui He, Li-Xin He, Shu-Fen He, C He, R. He, Badr HE, H He, B He, J He, Miaoling He, Chuanxin He, Miao He, Liang He, Geng-Jun He, X. He, QL He
Mitochondrial Ca 2+ uptake plays a pivotal role both in cell energy balance and in cell fate determination. Studies on the role of mitochondrial Ca 2+ signaling in pathophysiology have been favored Show more
Mitochondrial Ca 2+ uptake plays a pivotal role both in cell energy balance and in cell fate determination. Studies on the role of mitochondrial Ca 2+ signaling in pathophysiology have been favored by the identification of the genes encoding the mitochondrial calcium uniporter (MCU) and its regulatory subunits. Thus, research carried on in the last years on one hand has determined the structure of the MCU complex and its regulation, on the other has uncovered the consequences of dysregulated mitochondrial Ca 2+ signaling in cell and tissue homeostasis. Whether mitochondrial Ca 2+ uptake can be exploited as a weapon to counteract cancer progression is debated. In this review, we summarize recent research on the molecular structure of the MCU, the regulatory mechanisms that control its activity and its relevance in pathophysiology, focusing in particular on its role in cancer progression. Show less
Li-Bin Wu, Wen-Yi Su, Ya-Mei He+3 more · 2015 · Synthesis and Reactivity in Inorganic, Metal-Organic, and Nano-Metal Chemistry · Taylor & Francis · added 2026-05-01
AbstractFormation and repair of platinum (Pt)‐induced DNA adducts is a critical step in Pt drug‐mediated cytotoxicity. Measurement of Pt–DNA adduct kinetics in tumors may be useful for better understa Show more
AbstractFormation and repair of platinum (Pt)‐induced DNA adducts is a critical step in Pt drug‐mediated cytotoxicity. Measurement of Pt–DNA adduct kinetics in tumors may be useful for better understanding chemoresistance and therapeutic response. However, this concept has yet to be rigorously tested because of technical challenges in measuring the adducts at low concentrations and consistent access to sufficient tumor biopsy material. Ultrasensitive accelerator mass spectrometry was used to detect [14C]carboplatin–DNA monoadducts at the attomole level, which are the precursors to Pt–DNA crosslink formation, in six cancer cell lines as a proof‐of‐concept. The most resistant cells had the lowest monoadduct levels at all time points over 24 hr. [14C]Carboplatin “microdoses” (1/100th the pharmacologically effective concentration) had nearly identical adduct formation and repair kinetics compared to therapeutically relevant doses, suggesting that the microdosing approach can potentially be used to determine the pharmacological effects of therapeutic treatment. Some of the possible chemoresistance mechanisms were also studied, such as drug uptake/efflux, intracellular inactivation and DNA repair in selected cell lines. Intracellular inactivation and efficient DNA repair each contributed significantly to the suppression of DNA monoadduct formation in the most resistant cell line compared to the most sensitive cell line studied (p < 0.001). Nucleotide excision repair (NER)‐deficient and ‐proficient cells showed substantial differences in carboplatin monoadduct concentrations over 24 hr that likely contributed to chemoresistance. The data support the utility of carboplatin microdosing as a translatable approach for defining carboplatin–DNA monoadduct formation and repair, possibly by NER, which may be useful for characterizing chemoresistance in vivo. Show less