Cell, Journal Year: 2021, Volume and Issue: 184(4), P. 1081 - 1097.e19
Published: Feb. 1, 2021
Language: Английский
Cell, Journal Year: 2021, Volume and Issue: 184(4), P. 1081 - 1097.e19
Published: Feb. 1, 2021
Language: Английский
Nature Cell Biology, Journal Year: 2018, Volume and Issue: 20(8), P. 954 - 965
Published: July 17, 2018
Language: Английский
Citations
365Nature reviews. Cancer, Journal Year: 2018, Volume and Issue: 18(3), P. 168 - 185
Published: Jan. 29, 2018
Language: Английский
Citations
337Nature Reviews Molecular Cell Biology, Journal Year: 2020, Volume and Issue: 21(5), P. 284 - 299
Published: Feb. 24, 2020
Language: Английский
Citations
276Frontiers in Cell and Developmental Biology, Journal Year: 2020, Volume and Issue: 8
Published: Sept. 29, 2020
Genetic mutations and abnormal gene regulation are key mechanisms underlying tumorigenesis. Nucleosomes, which consist of DNA wrapped around histone cores, represent the basic units chromatin. The fifth amino group (Nε) lysine residues is a common site for post-translational modifications (PTMs), these, acetylation second most common. Histone modulated by acetyltransferases (HATs) deacetylases (HDACs), involved in expression. Over past two decades, numerous studies characterizing HDACs HDAC inhibitors (HDACi) have provided novel exciting insights concerning their biological potential anti-cancer treatments. In this review, we detail diverse structures functions, including transcriptional regulation, metabolism, angiogenesis, damage response, cell cycle, apoptosis, protein degradation, immunity other several physiological processes. We also highlight avenues to use HDACi as novel, precision cancer
Language: Английский
Citations
269Cells, Journal Year: 2019, Volume and Issue: 8(9), P. 1105 - 1105
Published: Sept. 18, 2019
Radiotherapy is one of the major cancer treatment strategies. Exposure to penetrating radiation causes cellular stress, directly or indirectly, due generation reactive oxygen species, DNA damage, and subcellular organelle damage autophagy. These radiation-induced responses cooperatively contribute cell death, but paradoxically, radiotherapy also activation damage-repair survival signaling alleviate cytotoxic effects in a small percentage cells, these activations are responsible for tumor radio-resistance. The present study describes molecular mechanisms stress response radioresistance, therapeutic approaches used overcome radioresistance.
Language: Английский
Citations
264The EMBO Journal, Journal Year: 2019, Volume and Issue: 38(18)
Published: Aug. 8, 2019
Language: Английский
Citations
243Molecular Cell, Journal Year: 2020, Volume and Issue: 80(1), P. 21 - 28
Published: Aug. 17, 2020
Language: Английский
Citations
243Neuropharmacology, Journal Year: 2017, Volume and Issue: 134, P. 208 - 217
Published: Nov. 8, 2017
Language: Английский
Citations
236Expert Reviews in Molecular Medicine, Journal Year: 2020, Volume and Issue: 22
Published: Jan. 1, 2020
Abstract DNA damage response (DDR) pathway prevents high level endogenous and environmental being replicated passed on to the next generation of cells via an orchestrated integrated network cell cycle checkpoint signalling repair pathways. Depending type damage, where in it occurs different pathways are involved, with ATM-CHK2-p53 controlling G1 or ATR-CHK1-Wee1 S G2/M checkpoints. Loss control is common cancer through TP53, ATM mutations, Rb loss cyclin E overexpression, providing a stronger rationale for targeting S/G2 This review will focus ATM-CHK2-p53-p21 ATR-CHK1-WEE1 ongoing efforts target these patient benefit.
Language: Английский
Citations
232Cancer Cell, Journal Year: 2019, Volume and Issue: 36(5), P. 545 - 558.e7
Published: Oct. 24, 2019
Language: Английский
Citations
231