Table 1.

An electrophysiological comparison of a malaria-induced small, linear conductance anion channel with several known chloride channel types (compiled from the review by Jentsch et al. 2002)

	Channel type
	Malaria induced	CFTR	ClC(1–7)	VRAC	Ca2+-activated	Ligand-gated	Maxi
Conductance	12–18 pS	5–9 pS	1–9 pS	40–50 pS(+Vm)	1–10 pS	10–90 pS	200–400 pS
I–V	Linear	Linear	Subtype dependent	Outward rectiflication	[Ca2+]dependent	Ligand-type dependeent	Linear
Permeation	I−>Br−>Cl−	Br−>Cl−>I−	Cl−>Br−>I−	I−>Br−>Cl−	I−>Br−>Cl−	I−>Br−>Cl−	Cl−>acetate
Inhibitors	NPPB niflumate, glibenclamide, tamoxifen, DPC	NPPB, 9-AC, glibenclamide DPC, DIDS*, suramin*	Subtype dependent but including: DPC, 9-AC	NPPB, DIDS, tamoxifen, niflumate, 1,9-dideoxyforskolin	NPPB, DIDS, niflumate	Ligand-type dependent but including: picrotoxin, cyanotriphenylborate	Phalloidin, DIDS, NPPB, pertussis toxin
Modulators	Unknown	Phosphorylation by PKA	Subtype dependent but including: cell swelling hyperpolarisation, internal PH, internal [Ca2+], depolarisation	Cell swelling	Internal[Ca2+]	Specific ligands (e.g.GABA, glycine)	Cell swelling, phorbol esters, PKC

CFTR, cystic fibrosis transmembrane regulator protein; VRAC, volume-regulated anion channel.

^*Intracellular application