We cloned and functionally characterized the murineBin1gene as a first step to investigate its physiological roles in differentiation, apoptosis, and tumorigenesis. The exon–intron organization of the ≥55-kb gene is similar to that of the human gene. Consistent with a role forBin1in apoptosis, the promoter included a functional consensus motif for activation by NF-κB, an important regulator of cell death. A muscle regulatory module defined in the human promoter that includes a consensus recognition site for myoD family proteins was not conserved in the mouse promoter. However,Bin1is upregulated in embryonic development by E10.5 in myotomes, the progenitors of skeletal muscle, supporting a role in myogenesis and suggesting that the mouse and human genes may be controlled somewhat differently during development. In C2C12 myoblasts antisenseBin1prevents induction of the cell cycle kinase inhibitor p21WAF1, suggesting that it acts at an early time during the muscle differentiation program. Interspecific mouse backcross mapping located theBin1locus betweenMep1bandApcon chromosome 18. Since the human gene was mapped previously to chromosome 2q14, the location ofBin1defines a previously unrecognized region of synteny between human chromosome 2 and mouse chromosome 18.