ArticleMolecular medicine (Cambridge, Mass.)2026
WHAMM deficiency alters splenic B-cell populations, BCR signaling, and actin remodeling.
Article in Molecular medicine (Cambridge, Mass.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Members of the Wiskott-Aldrich syndrome protein (WASP) family orchestrate cytoskeletal reorganization that modulates B-cell receptor (BCR) signaling and B-cell fate decisions. WHAMM, a WASP-family nucleation-promoting factor member that associates with actin, membranes and microtubules, has not been functionally characterized in B cells. To investigate the role of WHAMM in B-cell development and function, we analyzed a conditional mouse model in which Whamm was deleted in the B-cell lineage. WHAMM-deficient mice exhibited altered splenic B-cell composition, characterized by an accumulation of splenic transitional B cells and a reduction of follicular B cells. Meanwhile, WHAMM deficiency altered the spatial organization and kinetics of proximal BCR signaling, and modified the dynamics of BCR-induced actin remodeling. However, WHAMM-deficient B cells showed largely preserved BCR internalization, antigen presentation, PI3K-AKT-mTOR signaling, ROS production, and mitochondrial membrane potential. Together, this work indicates that WHAMM helps shape splenic B-cell populations and regulates proximal BCR signaling and actin dynamics, while several downstream functional responses remain largely preserved in this study.
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