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17A, a non-coding RNA, regulates GABA B alternative splicing and signaling in response to inflammatory stimuli and in Alzheimer disease.
The stable expression of 17A in SHSY5Y neuroblastoma cells induces the synthesis of an
alternative splicing isoform that abolish GABA B2 intracellular signaling (i.e., inhibition of cAMP accumulation and activation of K+ channels).
In RT-PCR experiments, the levels of expression of ncRNA 17A in autoptic brain samples from 16 Alzheimer disease patients were checked.
An averaged 10.0-fold increased level of 17A synthesis was detected.