MALAT1 and retinitis pigmentosa: In murine models of retinitis pigmentosa, a degeneration-dependent increase in expression of ATP-gated purinergic (P2X) receptors [22] has been proposed as the mechanism of entry of DENAQ into RGCs enabling this cationic photoswitch to bind to hyperpolarization-activated cyclic-nucleotide gated channels (HCN) and control sodium influx [13].