TABLE 4.

Lack of effect of most polymorphic variants of human GPR35a on ligand potency

The possible effect of nonsynonomous SNP variation in human GPR35a on ligand potency was assessed for a number of previously reported examples (Abecasis et al., 2010). In each case, the minor allele amino acid (listed second) was introduced into otherwise wild-type human GPR35a and ligand potency was then assessed in PathHunter human GPR35a–β-arrestin-2 interaction assays as in Table 1. Only in the case of Val⁷⁶Met was a significant alteration in potency recorded.

Variant	Expressiona	Lodoxamide EC50	Zaprinast EC50	Cromolyn EC50
		nM	μM	μM
Ala25Thr	0.97 ± 0.13	3.70 ± 1.76	1.84 ± 0.66	2.94 ± 0.48
Val29Ile	1.27 ± 0.15	3.58 ± 1.67	1.70 ± 0.49	3.70 ± 1.72
Val76Met	1.06 ± 0.08	33.38 ± 16.85*	16.37 ± 5.84*	20.26 ± 4.86*
Thr108Met	0.67 ± 0.14	6.49 ± 3.80	3.12 ± 1.07	5.36 ± 1.83
Arg125Ser	1.32 ± 0.16	5.25 ± 2.80	1.55 ± 0.62	3.73 ± 1.43
Thr253Met	0.63 ± 0.18	2.50 ± 0.95	1.60 ± 0.75	1.86 ± 0.74
Ser294Arg	1.48 ± 0.51	3.07 ± 1.46	1.14 ± 0.48	1.95 ± 0.19
Wild type	1.00 ± 0.23	3.97 ± 1.77	2.29 ± 0.79	2.98 ± 1.27

^aExpression as fold relative to wild type.

^*P < 0.05.