Toxic component of an atypical type II toxin-antitoxin (TA) system. Upon overexpression in the absence of its cognate antitoxin SocA, leads to inhibition of colony formation, cellular filamentation, incomplete DNA replication and induction of the SOS response. Exercises toxicity by binding the beta sliding clamp (dnaN), blocking DNA replication and leading to premature replication fork collapse and incomplete cell division. Unlike most type II TA systems, the SocB toxin is unstable and targeted by its cognate antitoxin SocA for degradation by ClpXP. Not toxic upon expression in E.coli. Interacts with cognate antitoxin SocA and with beta sliding clamp (dnaN). A tagged overexpressed form of SocB forms a discrete locus during DNA replication which co-localizes with beta sliding clamps (dnaN), but the locus disperses early. Loci formation depends on DnaA, the replication initiator protein (PubMed:24239291). Induced by DNA damaging agent mitomycin C, part of the socA-socB operon. Degraded by ClpXP, recognition of SocB by ClpX requires SocA. Deletion of this gene allows growth of cells disrupted for clpP or clpX, deletions which are otherwise lethal.