Stap2, or signal-transducing adaptor protein 2, is an adaptor molecule involved in regulating multiple intracellular signaling pathways [2,3,4]. It contains a pleckstrin homology domain at the N-terminus, an src homology domain in the central part, and a proline-rich region at the C-terminus, with a YXXQ motif potentially binding to STAT3 [4]. It influences pathways such as STAT3 and STAT5 activity, integrin-mediated T cell adhesion, and chemokine-induced T cell migration, playing a crucial role in immune and inflammatory responses [4]. Genetic models, like gene knockout in mice, are valuable for studying its functions.

In in vivo assays, genetic knockout of Stap2 in mice with renal fibrosis remarkably mitigated epithelial-mesenchymal transition, diminished inflammatory cell infiltration, and reduced collagen deposition, indicating that Stap2 promotes the progression of renal fibrosis possibly through modulating the expression level of phosphorylated HSP27 and the PI3K/AKT signaling pathway [1].

In conclusion, Stap2 is essential in regulating immune and inflammatory responses. The gene knockout mouse models have revealed its role in promoting renal fibrosis, providing insights into potential targeted therapies for this disease [1].