Guillermina Lozano
University of Texas MD Anderson Cancer Center, TX·Genetics
p53 is one of the body's most important defenses against cancer. It is a tumor suppressor that senses DNA damage and stress.
- Fields
Genetics
Biology
Medicine & Clinical Research
- Topics
p53
tumor suppressor
cancer biology
- Grants
- 1 known grant, through Apr 2027
What they work on
- Determine the roles of Eda2r, a cell-surface receptor that can trigger apoptosis, in p53-dependent cell outcomes and tumor suppression in mouse models.
- Test how important Gtse1, a protein that binds and inhibits p53, is for restraining p53 activity and supporting cell survival in vivo.
- Determine the functional significance of p53 control of Polκ, an error-prone DNA polymerase, in tissue homeostasis, inflammation and cancer.
- Use single-cell analysis of the mouse pancreas after p53 activation by Mdm2 deletion or inflammation to define cell-specific and dynamic p53 responses.
More about the research
It then acts as a transcription factor, switching on many genes that stop damaged cells from multiplying. It can pause the cell cycle, push cells into senescence (permanent retirement from dividing), or trigger apoptosis and other forms of cell death. Still, what this gene program actually does inside living tissues is poorly understood.
Why it matters
Therapies that reactivate p53 are being pursued for cancer. Understanding which genes p53 controls in each tissue, and whether they push cells toward survival or death, is needed to make those therapies work well. Defining the roles of Eda2r, Gtse1 and Polκ, which are altered in breast, colorectal, lung, pancreatic and brain cancers and angiosarcomas, may reveal new therapeutic strategies.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Xinbin Chen
University of California-Davis, CA·Biochemistry
Determine how CDK4/6 enzymes, the RNA-binding protein RBM38 and the protein-synthesis factor eIF4G together boost mutant p53 production, and whether CDK4/6 inhibitors suppress triple-negative breast cancers partly by lowering mutant p53.
Dawn Chandler
Ohio State University, OH·Biochemistry
Identify the RNA sequences and the protein and RNA nuclear factors that regulate MDM2 alternative splicing to produce MDM2-ALT1, a p53-activating isoform, using splice regulation assays and gene editing.
Nimrat Chatterjee
University of Vermont, VT·Biochemistry
Determine how the REV1 polymerase regulates autophagy and cellular metabolism, and how it steers cells toward autophagy or senescence after different types of DNA damage.
The school
University of Texas MD Anderson Cancer Center: 23 labs on PI Pages, $1.4B a year on research.
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