Unraveling the control of inflammatory HSCs and its implications on HSC fate control.
HSCs intrinsically express high levels of ISGs.
Different from the extrinsic inflammatory signal induced ISG expression that drives HSC depletion, the intrinsic ISG program protects HSCs from viral infection and preserves HSC pool.
It remains unclear how HSCs maintain the intrinsic ISGs without compromising function.
These mechanisms will inform strategies to restore stem cell dysfunction associated with inflammatory conditions, such as aging and cancer.
Deciphering the role of novel RBP in HSC fate determination in normal and malignant hematopoiesis.
RBPs act as oncogenes or tumor suppressors in acute myeloid leukemia (AML).
However, our knowledge on how RBPs control stem cell fates in normal and leukemia remain limited.
We aim to identify novel RBPs essential for LSCs and to provide new therapeutic targets for AML treatment.
Functional interrogation of HSC niche on cell fate determination.
HSCs are maintained through their interactions with niche.
These niche cells secret factors and provide extrinsic cues to support HSC function.
Given that the HSC pool is composed of heterogenous clones with distinct self-renewal capacities and lineage bias, it remains unclear what controls HSC clonal heterogeneity.
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We aim at elucidating molecular mechanisms shaping HSC-niche interactions and identify novel extrinsic regulators controlling HSC fate determination, which is critical for improving therapeutic approaches involving HSCs