The premise of a direct "DAT to STING" pathway is not supported by the supplied evidence. DAT (dopamine transporter) appears in a Drosophila PIGA-CDG screen as a dopamine-signaling modifier of seizure phenotypes , while STING regulation is documented via ALK-EGFR-AKT, SPOP, and CK1Ξ± axes . No record connects them. The map below therefore presents both pathways honestly, with the unverified link marked as a hypothesis, not evidence.
Quantitatively, the two arms are anchored by different effect measures. In the PIGA-CDG fly model, DAT heterozygosity rescued bang sensitivity to 91.7% (females) and 83.1% (males) versus 15% in PIGA heterozygous-null flies alone . In the STING arm, ALK inhibition with LDK378 lifted CLP sepsis survival from 41.2% to 88.2% in STING+/+ mice (n=17/group) .
Known STING modulators in the evidence base are ALK/EGFR/AKT , SPOP (with CK1Ξ³1-primed degron) , and CK1Ξ± as a bimodal rheostat . Dopamine signaling is not among them in these records.
What is missing: any experiment testing dopamine/DAT manipulation on cGAMP-stimulated IFN-Ξ², p-TBK1, or STING trafficking; any shared model organism; any reported value linking the two arms. If such a crossover were demonstrated, the dashed edge above would need solid evidence; until then, treating DAT as a STING regulator would be an unsupported inference. Additional context shows STING activation varies by age/sex in diabetic kidney disease , which any future DATβSTING hypothesis would need to account for.
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