Molecular adapter that acts as a bridge between a variety of multiprotein complexes, and which is involved in embryonic development, immunity, myogenesis and brain development (PubMed:25107474, PubMed:26041538, PubMed:27871306, PubMed:30116001, PubMed:30801883). Plays a key role in nuclear protein degradation by promoting import of proteasomes into the nucleus: directly binds to fully assembled 20S proteasomes at one end and to nuclear import receptor IPO9 at the other end, bridging them together and mediating the import of pre-assembled proteasome complexes through the nuclear pore (By similarity). Involved in innate immunity by regulating the production of interleukin-6 (IL6) downstream of Toll-like receptor (TLR): acts by bridging the NF-kappa-B inhibitor NFKBIZ and the SWI/SNF complex, leading to promote induction of IL6 (PubMed:18066067, PubMed:25107474). Also involved in adaptive immunity by promoting B-cell activation (PubMed:26041538). Involved in brain development: required for the survival and proliferation of cerebral cortical progenitor cells (PubMed:27871306). Involved in myogenesis: required for skeletal muscle formation and skeletal development, possibly by regulating expression of muscle differentiation factors (PubMed:30801883). Also plays a role in facilitating interdigital tissue regression during limb development (PubMed:30116001). Homodimer (By similarity). Interacts with IPO9; the interaction is direct (By similarity). Associates with 20S and 26S proteasomes (By similarity). Interacts with SMARCD1; promoting SWI/SNF complex recruitment (PubMed:25107474). Interacts with NFKBIZ (PubMed:25107474). Interacts with YWHAB (By similarity). Present mainly in the nuclear fraction, and at much lower level in the cytoplasmic and membrane fractions. Expressed throughout cortical development: present throughout the cortical wall at all of these ages, with strong expression in the early ventricular zone and the embryonic preplate/cortical plate (PubMed:27871306). Expressed in the developing limb: expressed in the forelimb bud and somites at 10.5 dpc, as well as in the apical ectodermal ridge (AER) (PubMed:30116001). Ubiquitously expressed throughout the embryonic forelimb at 10.5 dpc: expressed in the dermomyotome and sclerotome divisions of the somite (at protein level) (PubMed:30801883). Mice are embryonic lethal (PubMed:18066067). Null mutant embryos could not be detected even on embryonic day 9.5 (PubMed:18066067). Conditional deletion in macrophages impairs proinflammatory cytokine production in response to Listeria infection and clearance of infecting bacteria (PubMed:25107474). Conditional deletion in B-cells causes a decrease in the splenic B-cell numbers, leading to severe proliferation and activation defects in B-cells (PubMed:26041538). The B-cell viability is also impaired, leading to decreased immune responses to T-dependent and T-independent antigens (PubMed:26041538). Conditional deletion in the cortex leads to severe microcephaly: mice do not survive past birth and exhibit extreme microcephaly, with little dorsal telencephalic tissue and no recognizable cortex (PubMed:27871306). Defects in the cortex are caused to massive cell death of early cortical progenitors (PubMed:27871306). Conditional deletion in somitic muscle precursor cells results in neonatal lethality: mutant embryos show a complete lack of forelimb, intercostal and diaphragm muscles due to extensive apoptosis and loss of myoblasts (PubMed:30801883). Embryos lacking Akirin2 in somitic muscle precursor cells also display severe skeletal defects, including craniofacial abnormalities, disrupted ossification and rib fusions (PubMed:30801883). Conditional deletion in limb bud epithelium leads to soft-tissue syndactyly, characterized by a loss of interdigital cell death and an increase in cell proliferation, resulting in retention of the interdigital web (PubMed:30116001). 'Akiraka ni suru' means 'making things clear' in Japanese. The name is given based on the presence of the clear nuclear localization signal. Belongs to the akirin family.