. Author manuscript; available in PMC: 2009 Jul 1.

Published in final edited form as: Mol Pharmacol. 2008 Apr 18;74(1):203–212. doi: 10.1124/mol.108.044891

Table 3.

Second-order rate constants for MTSEA-Biotin derivatization of mutant receptors in the absence and presence of FLZM, Ro15-1788, βCCM, GABA and PENTO.

A.	FLZM P
	Control		FLZM		Ro15-1788		BCCM		GABA		PENTO
Receptor	k₂ (M ⁻¹ s⁻¹)	n	k₂ (M⁻¹ s⁻¹)	n	k₂ (M ⁻¹ s⁻¹)	n	k₂ (M⁻¹ s⁻¹)	n	k₂ (M⁻¹ s⁻¹)	n	k₂ (M ⁻¹ s⁻¹)
α₁H101C β₂ γ₂	2194.6 ± 354.1	6	678.3 ± 145.8^*	4	59.0 ± 18.2^*	3	ND		9047.5 ± 1494.0^*	4	2299.0 ± 457.6
α₁N102C β₂ γ₂	46.7 ± 5.5	7	30.9 ± 3.0	3	^#		16.9 ± 3.7^*	3	91.2 ± 24.7^*	3	54.5 ± 14.9
α₁ S106C β₂ γ₂	28.9 ± 8.2	6	45.6 ± 7.5^*	3	11.9 ± 3.1^*	3	ND		20.0 ± 5.4	3	ND

B.	I-GABA
	Control		FLZM		Ro15-1788		BCCM		GABA		PENTO
Receptor	k ₂ (M⁻¹ s⁻¹)	n	k ₂ (M⁻¹ s⁻¹ )	n	k ₂ (M ⁻¹s⁻¹)	n	k ₂ (M⁻¹ s⁻¹ )	n	k ₂ (M⁻¹ s⁻¹ )	n	k ₂ (M ⁻¹s⁻¹)
α₁D97C β₂ γ₂	20.5 ± 5.7	6	9.2 ± 3.3^*	3	^#		Block		20.6 ± 5.2	3	ND
α₁H101C β₂ γ⁻;₂	122.3 ± 10.8	5	117.2 ± 5.0	4	289.8 ± 136.8^*	5	ND		154.4 ± 42.6	5	ND
α₁N102C β₂ γ₂	52.9 ± 22.1	8	32.1 ± 11.7	3	^#		11.7 ± 1.0^*	3	81.2 ± 9.2	3	124.2 ± 47.7^*
α₁ S106C β₂ γ₂	11.3 ± 3.9	7	12.0 ± 4.0	3	7.0 ± 1.0	4	ND		9.7 ± 5.3	3	ND
α₁ H101C β₂	121.4 ± 40.4	5	101.4 ± 27.7	3	145.8 ± 19.3	3	ND		166.5 ± 34.4	4	ND

A. The rates of decrease in FLZM potentiation resulting from MTSEA-Biotin application. B. The rates of change in I-GABA resulting from MTSEA-Biotin application. Data represent mean ±SD.

indicates significant differences from control rates (p < 0.05) for each receptor.

rates were not measured because Ro15-1788 potentiated I-GABA. “Block” indicates that BCCM slowed the rate of modification of α₁D97C to the extent that a rate could not be accurately determined using the available MTSEA-Biotin concentrations. ND = data not determined.