Response regulator member of the two-component regulatory system CpxA/CpxR which responds to envelope stress response by activating expression of downstream genes including cpxP, degP, dsbA and ppiA (PubMed:7883164, PubMed:9401031). Required for efficient binding of stationary phase cells to hydrophobic surfaces, part of the process of biofilm formation (PubMed:11830644). Induced upon cell surface binding, subsequently induces genes it controls (cpxP, dsbA and spy, degP is only partially induced) (PubMed:11830644). Binds and activates transcription from the degP promoter (PubMed:7883164); binding is enhanced by phosphorylation (PubMed:9401031). This system combats a variety of extracytoplasmic protein-mediated toxicities by increasing the transcription of the periplasmic protease, DegP in concert with sigma factor E (PubMed:7883164), as well as that of CpxP protein. Other downstream effectors may include SrkA (PubMed:23416055). The two-component system is activated by envelope stress such as overexpression of some (misfolded) periplasmic proteins (PubMed:7883164, PubMed:9351822). Activated by spheroplasting (which removes the periplasm) in an autoregulatory cpxA-cpxR-dependent fashion (PubMed:10972835). Cpx two-component system is activated at pH 8.0; in a degP deletion mutant activation is halved (PubMed:9473036, PubMed:16166523). The CpxA kinase activity is inhibited by periplasmic accessory protein CpxP; proteolysis of CpxP relieves inhibition (PubMed:16166523, PubMed:17259177, PubMed:25207645). Interacts with cognate sensor kinase CpxA. Induced about 3-fold when stationary phase cells bind to hydrophobic surfaces; requires direct contact with hydrophobic surfaces for up-regulation of Cpx activity (PubMed:11830644). Phosphorylated by CpxA. Loss of the Cpx envelope stress response (PubMed:10972835). A double cpxR-cpxA mutant decreases transcription of degP (PubMed:7883164). Cells are less sensitive to killing by nalidixic acid; double cpxR-srkA disruption mutants are as sensitive to killing as single srkA mutants, suggesting the SrkA protein kinase is partially regulated by CpxR. Hypersensitive to alkaline pH (greater than pH 8.8) (PubMed:9473036). Decreased numbers of stationary phase cells bind to hydrophobic surfaces, cellular adhesion has altered dynamic properties; no induction of cpxR when cells bind to hydrophobic surfaces (PubMed:11830644).