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Vulnerability of HIF1α and HIF2α to damage by proteotoxic stressors

Toxicology and applied pharmacology, 2022-06, Vol.445, p.116041-116041, Article 116041

2022

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Chemical mechanisms of DNA damage by carcinogenic chromium(VI)

Advances in pharmacology (1990), 2023-01, Vol.96, p.25-46

2023

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20S immunoproteasomes remove formaldehyde-damaged cytoplasmic proteins suppressing caspase-independent cell death

Scientific reports, 2017-04, Vol.7 (1), p.654-10, Article 654

2017

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Toxicological Antagonism among Welding Fume Metals: Inactivation of Soluble Cr(VI) by Iron

Chemical research in toxicology, 2018-11, Vol.31 (11), p.1172-1184

2018

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ATR activation by Cr-DNA damage is a major survival response establishing late S and G2 checkpoints after Cr(VI) exposure

Toxicology and applied pharmacology, 2023-10, Vol.477, p.116696-116696, Article 116696

2023

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Sensitive Detection of Histones and γ‑H2AX by Immunoblotting: Problems and Solutions

Chemical research in toxicology, 2024-09, Vol.37 (9), p.1588-1597

2024

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NAD+ metabolism controls growth inhibition by HIF1 in normoxia and determines differential sensitivity of normal and cancer cells

Cell cycle (Georgetown, Tex.), 2021-09, Vol.20 (18), p.1812-1827

2021

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Atypical genotoxicity of carcinogenic nickel(II): Linkage to dNTP biosynthesis, DNA-incorporated rNMPs, and impaired repair of TOP1-DNA crosslinks

The Journal of biological chemistry, 2023-12, Vol.299 (12), p.105385-105385, Article 105385

2023

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p53 Activation by Cr(VI): A Transcriptionally Limited Response Induced by ATR Kinase in S-Phase

Toxicological sciences, 2019-11, Vol.172 (1), p.11-22

2019

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Monoubiquitinated H2B, a Main Chromatin Target of Formaldehyde, Is Important for S-Phase Checkpoint Signaling and Genome Stability

Molecular carcinogenesis, 2024-09

2024

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Vitamin C increases DNA breaks and suppresses DNA damage-independent activation of ATM by bleomycin

Free radical biology & medicine, 2019-05, Vol.136, p.12-21

2019

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Abstract 1220: Carcinogenic nickel(II) is a replication stressor causing genotoxicity via DNA incorporation of rNMPs

Cancer research (Chicago, Ill.), 2023-04, Vol.83 (7_Supplement), p.1220-1220

2023

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Variation in Extracellular Detoxification Is a Link to Different Carcinogenicity among Chromates in Rodent and Human Lungs

Chemical research in toxicology, 2017-09, Vol.30 (9), p.1720-1729

2017

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Vulnerability of HIF1α and HIF2α to damage by proteotoxic stressors

Chemical mechanisms of DNA damage by carcinogenic chromium(VI)

20S immunoproteasomes remove formaldehyde-damaged cytoplasmic proteins suppressing caspase-independent cell death

Toxicological Antagonism among Welding Fume Metals: Inactivation of Soluble Cr(VI) by Iron

ATR activation by Cr-DNA damage is a major survival response establishing late S and G2 checkpoints after Cr(VI) exposure

Sensitive Detection of Histones and γ‑H2AX by Immunoblotting: Problems and Solutions

NAD+ metabolism controls growth inhibition by HIF1 in normoxia and determines differential sensitivity of normal and cancer cells

Atypical genotoxicity of carcinogenic nickel(II): Linkage to dNTP biosynthesis, DNA-incorporated rNMPs, and impaired repair of TOP1-DNA crosslinks

p53 Activation by Cr(VI): A Transcriptionally Limited Response Induced by ATR Kinase in S-Phase

Monoubiquitinated H2B, a Main Chromatin Target of Formaldehyde, Is Important for S-Phase Checkpoint Signaling and Genome Stability

Vitamin C increases DNA breaks and suppresses DNA damage-independent activation of ATM by bleomycin

Abstract 1220: Carcinogenic nickel(II) is a replication stressor causing genotoxicity via DNA incorporation of rNMPs

Variation in Extracellular Detoxification Is a Link to Different Carcinogenicity among Chromates in Rodent and Human Lungs

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