ArticleDigestive diseases and sciences2026
An Inhibitor of Death-Associated Protein Kinase 3 (DAPK3) Disrupts Hippo Signaling and Intestinal Epithelial Regeneration in Murine DSS-Induced Colitis.
Article in Digestive diseases and sciences, 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
backgroundVarious signaling modules that affect epithelial wound healing are dysregulated in ulcerative colitis. Hippo signaling, acting downstream of cytoskeletal remodeling, is necessary for intestinal epithelial regeneration. Death-associated protein kinase 3 (DAPK3) is a regulator of actin cytoskeleton organization that also controls cellular proliferation and apoptosis responses.
aimRecent genetic linkages between DAPK3 and the Hippo pathway suggest signaling coordination that has not been empirically evaluated.
methodsThe impact of HS38, a DAPK3 inhibitor, on epithelial wound healing was examined using the dextran-sodium-sulphate (DSS) murine model of experimental colitis and Caco-2 human intestinal epithelial cell (IEC) monolayers.
resultsDAPK3 was significantly elevated in IECs isolated from DSS-treated mice, with cytoplasmic staining observed in epithelial crypts. The administration of HS38 to mice receiving DSS impeded the resolution of intestinal injury with attenuated IEC proliferation. HS38 treatment in DSS-colitis was also accompanied with decreased pS127, but not pS397, phosphorylation of Yes-associated protein (YAP). The data suggest that HS38 treatment, and hence DAPK3 inhibition, attenuates Hippo pathway signaling with subsequent nuclear enrichment of YAP. Additional analysis of single-cell RNAseq transcriptomic data from mucosal biopsies of UC patients reveals strong positive correlations between DAPK3 and YAP1 in the epithelial compartment.
conclusionsThis study establishes DAPK3 as a novel factor in intestinal epithelial regeneration and ulcerative colitis progression by way of Hippo/YAP signaling. Nevertheless, the role that DAPK3 plays in different cell types will need further investigation to decipher the full consequence of DAPK3 involvement in epithelial homeostasis.
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