Charles Lowenstein
Johns Hopkins University, MD·Medicine & Clinical Research
Venous thromboembolism (VTE), in which abnormal blood clots form in the veins and can travel to the lungs, is a major cause of illness and death. Inherited genes raise the risk, but many of these genes remain unknown.
- Fields
Medicine & Clinical Research
Genetics
Biochemistry
- Topics
venous thromboembolism
blood clots
thrombosis
- Grants
- 1 known grant, through Jul 2028
What they work on
- Test whether BCOR, a gene-silencing protein, suppresses Factor VII production in liver cells by controlling the epigenetic complexes PRC1.1 and ATAC, which regulate how DNA is packaged and read.
- Determine whether the human BCOR genetic variant linked to venous thromboembolism lowers BCOR levels by altering binding of the protein TEAD1 to a BCOR enhancer, a DNA region that boosts gene activity.
- Test in mice whether reducing BCOR in the liver raises Factor VII levels and increases blood coagulation and thrombosis.
More about the research
Clotting depends on coagulation factors, proteins made by liver cells called hepatocytes. How the liver controls how much of these proteins it makes is not well understood. The lab uses human genome-wide association studies (GWAS), which scan many people's DNA for variants linked to a disease, to find new genes that affect VTE risk.
Why it matters
Abnormal blood clots in the legs and lungs are a leading vascular cause of death and disease. Showing how BCOR and its partner complexes control Factor VII in the liver could improve prediction of who is at inherited risk of venous thromboembolism. It could also point to epigenetic pathways that might be targeted by new treatments to prevent or treat clots.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Anthony Sochet
Johns Hopkins University, MD·Medicine & Clinical Research·Early-career
Determine how the intensity of invasive mechanical ventilation affects functional fibrinolysis, the body's ability to break down clots, in critically ill children.
Congqing Wu
University of Kentucky, KY·Medicine & Clinical Research
Determine how NINJ1 in myeloid immune cells such as macrophages contributes to thrombosis. NINJ1 is the protein that actively ruptures the cell membrane during pyroptosis, an inflammatory form of cell death.
Julie Jaffray
University of California-San Diego, CA·Medicine & Clinical Research·Early-career
Prospectively validate a pediatric hospital-acquired venous thromboembolism (VTE) risk assessment model from the CHAT Consortium, using a case-control design and electronic medical record review.
The school
Johns Hopkins University: 100 labs on PI Pages, $4.1B a year on research, 622 research doctorates a year.
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