| First Author | Wang X | Year | 2018 |
| Journal | Acta Biochim Biophys Sin (Shanghai) | Volume | 50 |
| Issue | 10 | Pages | 984-995 |
| PubMed ID | 30137205 | Mgi Jnum | J:271697 |
| Mgi Id | MGI:6282943 | Doi | 10.1093/abbs/gmy097 |
| Citation | Wang X, et al. (2018) Tafa-2 plays an essential role in neuronal survival and neurobiological function in mice. Acta Biochim Biophys Sin (Shanghai) 50(10):984-995 |
| abstractText | Tafa is a family of small secreted proteins with conserved cysteine residues and restricted expression in the brain. It is composed of five highly homologous genes referred to as Tafa-1 to -5. Among them, Tafa-2 is identified as one of the potential genes responsible for intellectual deficiency in a patient with mild mental retardation. To investigate the biological function of Tafa-2 in vivo, Tafa-2 knockout mice were generated. The mutant mice grew and developed normally but exhibited impairments in spatial learning and memory in Morris water maze test and impairments in short- and long-term memory in novel object recognition test, accompanied with increased level of anxiety-like behaviors in open-field test and elevated plus maze test, and decreased level of depression-like behaviors in forced-swim test and tail-suspension test. Further examinations revealed that Tafa-2 deficiency causes severe neuronal reduction and increased apoptosis in the brain of Tafa-2-/- mice via downregulation of PI3K/Akt and MAPK/Erk pathways. Conformably, the expression levels of CREB target genes including BDNF, c-fos and NF1, and CBP were found to be reduced in the brain of Tafa-2-/- mice. Taken together, our data indicate that Tafa-2 may function as a neurotrophic factor essential for neuronal survival and neurobiological functions. |
