In 1958, Francis Crick proposed the central dogma of molecular biology: that genomic DNA in the nucleus is transcribed into messenger RNA (mRNA), which is then translated into proteins when it enters the cytoplasm. It is traditionally believed that, at the initial stage of translation, amino acids and their homologous tRNAs undergo aminoacylation through the action of aminoacyl-tRNA synthetase (AARS) to form an aminoacyl-tRNA complex (aa-tRNA). 1,2 Then, aa-tRNA specifically recognizes the codon on the mRNA sequence, binds to the rR-NA-mRNA complex and connects the corresponding amino acid to the polypeptide chain under the action of rRNA so that the polypeptide

βII spectrin, the most common isoform of non-erythrocyte spectrin, is a cytoskeleton protein present in all nucleated cells. Interestingly, βII spectrin is essential for the development of various organs such as nerve, epithelium, inner ear, liver and heart. The functions of βII spectrin include not only establishing and maintaining the cell structure but also regulating a variety of cellular functions, such as cell apoptosis, cell adhesion, cell spreading and cell cycle regulation. Notably, βII spectrin dysfunction is associated with embryonic lethality and the DNA damage response. More recently, the detection of altered βII spectrin expression in tumors indicated that βII spectrin might be involved in the development and progression of cancer. Its mutations and disorders could result in developmental disabilities and various diseases. The versatile roles of βII spectrin in disease have been examined in an increasing number of studies; nonetheless, the exact mechanisms of βII spectrin are still poorly understood. Thus, we summarize the structural features and biological roles of βII spectrin and discuss its molecular mechanisms and functions in development, homeostasis, regeneration and differentiation. This review highlight the potential effects of βII spectrin dysfunction in cancer and other diseases, outstanding questions for the future investigation of therapeutic targets. The investigation of the regulatory mechanism of βII spectrin signal inactivation and recovery may bring hope for future therapy of related diseases.

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