Pseudokinases lacking protein kinase activity and unable to bind ATP-analogs (PubMed:24556575). Negative regulator of pathogen-associated molecular patterns- (PAMP-) triggered immunity by limiting BAK1-receptor complex formation in the absence of ligands (PubMed:24388849). Interacts constitutively with BAK1, when phosphorylated, thereby preventing interaction with the ligand-binding LRR-RLK FLS2. Upon infection, pathogen-associated molecular patterns (PAMP) perception leads to BIR2 release from the BAK1 complex and enables the recruitment of BAK1 into the FLS2 complex. Induced by nonpathogenic bacteria or pathogen-associated molecular patterns (PAMP) treatments. The protein kinase domain is predicted to be catalytically inactive. Phosphorylated by BAK1, this interacts promotes interaction with BAK1. Increased cell death spreading after Alternaria brassicicola infection, and enhanced salicylic acid (SA) responses and resistance to the biotrophic bacterial pathogen Pseudomonas syringae pv. tomato DC3000. Impact on several BAK1-regulated processes, such as hyperresponsiveness to pathogen-associated molecular patterns (PAMP), enhanced cell death, and resistance to bacterial pathogens, but normal brassinosteroid-(BR-)regulated growth. Belongs to the protein kinase superfamily. Ser/Thr protein kinase family. Nucleotide binding site is not accessible for binding to ATP-analogs.