Personal profile

Research Interests

Historically, reactive oxygen species (ROS) have been thought to be cellular damaging agents, lacking a physiological function. Accumulation of ROS and oxidative damage have been linked to multiple pathologies, including neurodegenerative diseases, diabetes, cancer, and premature aging. This guilt by association relationship left a picture of ROS as a necessary evil of oxidative metabolism, a product of an imperfect system. Yet few biological systems possess such flagrant imperfections, thanks to the persistent optimization of evolution, and it appears that oxidative metabolism is no different. More and more evidence suggests that low levels of ROS are critical for healthy cellular function. We are testing whether mitochondrial release of H2O2 has evolved as a method of communication between mitochondrial function and other cellular processes to maintain homeostasis (e.g. stem cell function and immune responses) and promote adaptation to stress (e.g. hypoxia).

Keywords

  • Cancer: Lung/Chest
  • Immune System
  • Lung Cancer / Chest Cancer

Fingerprint Fingerprint is based on mining the text of the person's scientific documents to create an index of weighted terms, which defines the key subjects of each individual researcher.

  • 31 Similar Profiles
Reactive Oxygen Species Medicine & Life Sciences
Hypoxia Medicine & Life Sciences
Mitochondria Medicine & Life Sciences
Neoplasms Medicine & Life Sciences
Cell Death Medicine & Life Sciences
Oxygen Medicine & Life Sciences
Apoptosis Medicine & Life Sciences
Lung Medicine & Life Sciences

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Research Output 1993 2017

A CRISPR screen identifies a pathway required for paraquat-induced cell death

Reczek, C. R., Birsoy, K., Kong, H., Martínez-Reyes, I., Wang, T., Gao, P., Sabatini, D. M. & Chandel, N. S. Dec 1 2017 In : Nature Chemical Biology. 13, 12, p. 1274-1279 6 p.

Research output: Research - peer-reviewArticle

Clustered Regularly Interspaced Short Palindromic Repeats
Paraquat
Cell Death
Reactive Oxygen Species
Cytochrome P-450 Enzyme System
3 Citations

Beneficial Effects of Myo-Inositol Oxygenase Deficiency in Cisplatin-Induced AKI

Dutta, R. K., Kondeti, V. K., Sharma, I., Chandel, N. S., Quaggin, S. E. & Kanwar, Y. S. May 1 2017 In : Journal of the American Society of Nephrology : JASN. 28, 5, p. 1421-1436 16 p.

Research output: Research - peer-reviewArticle

Inositol Oxygenase
Cisplatin
Reactive Oxygen Species
In Vitro Techniques
Small Interfering RNA
1 Citations

Cancer-Associated IDH1 Promotes Growth and Resistance to Targeted Therapies in the Absence of Mutation

Calvert, A. E. , Chalastanis, A. , Wu, Y. , Hurley, L. A. , Kouri, F. M. , Bi, Y. , Kachman, M. , May, J. L. , Bartom, E. , Hua, Y. , Mishra, R. K. , Schiltz, G. E. , Dubrovskyi, O. , Mazar, A. P. , Peter, M. E. , Zheng, H. , James, C. D. , Burant, C. F. , Chandel, N. S. , Davuluri, R. V. & 2 others Horbinski, C. & Stegh, A. H. May 30 2017 In : Cell Reports. 19, 9, p. 1858-1873 16 p.

Research output: Research - peer-reviewArticle

Bearings (structural)
Isocitrate Dehydrogenase
Gene encoding
Methylation
Differentiation Antigens

Metabolism and skeletal muscle homeostasis in lung disease

Ceco, E., Weinberg, S. E., Chandel, N. S. & Sznajder, J. I. Jul 1 2017 In : American Journal of Respiratory Cell and Molecular Biology. 57, 1, p. 28-34 7 p.

Research output: Research - peer-reviewReview article

Lung Diseases
Skeletal Muscle
Homeostasis
Pulmonary diseases
Metabolism

Mitochondria control acute and chronic responses to hypoxia

McElroy, G. S. & Chandel, N. S. Jul 15 2017 In : Experimental Cell Research. 356, 2, p. 217-222 6 p.

Research output: Research - peer-reviewArticle

Mitochondria
Hypoxia
Carotid Body
Muscle Contraction
Erythropoietin