Beck Lab
Principal Investigator: David Beck
Institution: New York University (New York, NY)
Primary Subfield: Molecular & Cell Bio
Recruitment Status: ✅ Accepting PhD Students ✅ Hiring Postdocs
Research Focus
ABSTRACT The expansion of somatically mutated clones is prevalent in hematopoiesis with profound implications for physiological aging and across a myriad of pathologies. This has been recently highlighted by the discovery of the inflammatory disorder – vacuoles E1 enzyme X-linked autoinflammatory somatic (VEXAS) syndrome. VEXAS is caused by somatic mutation in the ubiquitin-activating enzyme E1 (UBA1) gene that arises in hematopoietic stem cells (HSCs). Mutated UBA1 leads to accumulation of misfolded proteins, activation of the unfolded protein response and ultimately systemic inflammation accompanied by severe clinical manifestations. However, we currently lack the ability to target disease-initiating mutant HSCs, as the mechanisms that lead to HSC inflammation, differentiation bias and survival are unknown. This limitation stems in part from the fact that somatic clones are admixed with wild-type HSCs, limiting the ability to define mutant-specific phenotypes with either bulk or single-cell techniques. To overcome this gap, we have developed genotype-aware single-cell multi- omics techniques that are specifically designed to map somatic genotypes to phenotypes. These tools turn t…
Active NIH Awards
- 5R01HL175155-02: Defining targetable vulnerabilities in UBA1-mutated VEXAS HSCs for clonal eradication (2026)
- 5R01AR083407-03: Regulation of inflammation by the ubiquitin proteasome pathway (2026)
- 1R01AR087136-01A1: Defining Flares in VEXAS Syndrome (2026)
- 5R01AR083407-02: Regulation of inflammation by the ubiquitin proteasome pathway (2025)
- 1R01HL175155-01A1: Defining targetable vulnerabilities in UBA1-mutated VEXAS HSCs for clonal eradication (2025)
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