. Author manuscript; available in PMC: 2009 Apr 13.

Published in final edited form as: Cytokine Growth Factor Rev. 2005 Jul 5;16(6):637–658. doi: 10.1016/j.cytogfr.2005.05.008

Table 5.

Ubiquitination and palmitoylation of intracellular chemokine receptor domains

Mod^a	Receptor	Residues	Cell type	Ligand	Effect	Reference
Ub	CXCR4	K₃₂₇, K₃₃₁, K₃₃₃^b	HEK293^c	CXCL12^d	+ Lysosomal degradation	[69]
					= Endocytosis	[69]
			Monocytes	None		[118]
Palmit	CCR5	C₃₂₁, C₃₂₃, C₃₂₄	CHO-K1^c	None	+ Intracellular diffusion; Surface expression	[126]
					− Intracellular sequestration	[126]
				CCL4-5	+ Duration of response; GTPγS binding	[126]
				CCL4-5; HIV-1	= Binding; endocytosis; Ca; cAMP inhibition; HIVco	[126]
			HEK293T^c	None	+ Surface expression; Half-life	[124]
					− Intracellular sequestration; Early lysosomal degradation	[124]
				CCL4; HIV-1	= Binding; HIVco	[124]
			RBL-2H3^c		= Surface expression	[73]
				CCL5	+ Phosphorylation; Granulosis; Endocytosis	[73]
					− Retarded/prolonged Ca	[73]
					= Binding; P-ERK; Chemotaxis	[73]

Ca: calcium mobilization; HIVco: HIV co-receptor activity; Ub: ubiquitination; Palmit: palmitoylation; Recept: receptor.

Presence of modification is demonstrated after co-transfecting target cells with constructs with tagged moieties (e.g. FLAG-Ub) or after metabolic labeling (e.g. [³H] palmitic acid). These modifications can promote (+), inhibit (−) or not affect the specific effect mentioned.

Not determined yet which of the three residues specifically is ubiquitinated.

Cells transfected with chemokine receptor.

Ligand-dependency = occurrence/increase of modification upon ligand treatment.