Angela Alexander
First author of the study showing that the DNA-damage kinase ATM also works in the cytoplasm, where it switches on TSC2 in response to reactive oxygen species and so turns mTORC1 down
Morgan Welch Inflammatory Breast Cancer Research Program, MD Anderson Cancer Center · postdoctoral work in Experimental Radiation Oncology (Khandan Keyomarsi) · Department of Carcinogenesis, MD Anderson, Smithville (Cheryl Walker lab, about 2010)
Angela Alexander is first author of ALE2010, done in Cheryl Lyn Walker's group in the Department of Carcinogenesis at MD Anderson's Smithville campus. The paper found that, when reactive oxygen species rise, ATM activates TSC2 in the cytoplasm through the LKB1–AMPK route. This represses mTORC1 and induces autophagy. ATM-deficient cells had high ROS and poorly controlled mTORC1, and rapamycin delayed lymphoma in Atm-deficient mice. The same year she was also an author on a related Autophagy paper on ATM, TSC2 and mTORC1.
She later did postdoctoral work in Khandan Keyomarsi's group in Experimental Radiation Oncology at MD Anderson, moving toward inflammatory breast cancer. Her more recent papers (2022, 2025) list her in the Department of Breast Medical Oncology and the Morgan Welch Inflammatory Breast Cancer Research Program at MD Anderson in Houston. Her exact current title was not found in the sources checked.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2010 | M | ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS ALE2010 First author: ATM activates TSC2 in the cytoplasm through LKB1 and AMPK in response to ROS, repressing mTORC1 and inducing autophagy. |
Co-authors in the Atlas
People with a profile here who share at least one study with Angela Alexander.
- Cheryl Lyn Walker Cancer biologist and toxicologist who studies how environmental exposures reprogram the epigenome and target tumour suppressor genes; senior author of the study linking ATM to TSC2 and mTORC1 in the response to oxidative stress
- Ken Inoki Showed as a postdoc in Kun-Liang Guan's lab that Akt switches off TSC2, that TSC2 is the off-switch (GAP) for the small GTPase Rheb, and that AMPK and GSK3 feed energy and Wnt signals into the same brake. His Michigan lab studies mTOR signalling in metabolism and kidney disease
- Kun-Liang Guan Showed how growth-factor and energy signals reach mTORC1 through TSC2 and Rheb, and, in parallel with the Sabatini lab, that the Rag GTPases carry the amino-acid signal. His lab also found that AMPK and mTORC1 control autophagy by phosphorylating the kinase ULK1 at different sites
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