Multifunctional protein that is involved in the regulation of many processes including cell proliferation, apoptosis, cell cycle progression or transcription (PubMed:21636789). Regulates the proliferation of neuronal stem cells, differentiation of leukemic cells and progression from G1 to S phase of the cell cycle. As negative regulator of caspase-3-dependent apoptosis, may act as an antagonist of ANP32A in regulating tissue homeostasis (By similarity). Exhibits histone chaperone properties, able to recruit histones to certain promoters, thus regulating the transcription of specific genes (By similarity). Also plays an essential role in the nucleocytoplasmic transport of specific mRNAs via the uncommon nuclear mRNA export receptor XPO1/CRM1 (By similarity). Participates in the regulation of adequate adaptive immune responses by acting on mRNA expression and cell proliferation (PubMed:30890743). Interacts with histones H3 and H4. Interacts with KLF5; this interaction induces promoter region-specific histone incorporation and inhibition of histone acetylation by ANP32B. Accumulates in the nuclei at the S phase. Histone binding is mediated by the concave surface of the LRR region. Some glutamate residues are glycylated by TTLL8. This modification occurs exclusively on glutamate residues and results in a glycine chain on the gamma-carboxyl group. Directly cleaved by caspase-3/CASP3. Deficient mice display an highly penetrant perinatal lethality in a mixed genetic background and a fully penetrant lethality in a pure C57BL/6 background (PubMed:21636789). Mutants also show enhanced clinical symptoms correlated with depletion of naive effector T-cells, exhaustion of lymphocytes and enhanced prevalence of follicular T-helper cells (PubMed:30890743). In addition, mice show significantly reduced H3N2 or H5N1 influenza viral loads, inflammatory cytokine response and reduced pathogenicity compared to WT (PubMed:32231671). Belongs to the ANP32 family.