The histone variant H2A.Z in gene regulation

Table 4 Histone variant H2A.Z at enhancers

TFs	Effects of H2A.Z depletion	References
AhR	Reduced induction upon treatment	[88]
AP-1	Upregulation	[72]
AR	Reduced induction upon treatment	[51, 52, 59, 119]
ER	Lack of induction upon treatment	[50, 54, 87, 118]
FoxA2	n.d.	[237]
GR	n.d.	[69, 86]
ISGF3	Increased induction upon treatment	[73]
Muscle differentiation^b	n.d.	[56]
Myc	n.d.	[77]
p53	Upregulation^a	[49, 134, 217]
PU.1	n.d.	[120]
∆Np63α	Upregulation	[134, 217]
RARγ	n.d.	[71]
RBPJ	Upregulation	[57]
SMAD3	Downregulation	[161]

^aVariable based on the cell type; ^bthe TFs have not been investigated; however, H2A.Z localizes at enhancers
The table lists only the cases described in mouse and human. Enhancers are defined as those sites that are bound by signal-specific transcription factors (TFs). AhR aryl hydrocarbon receptor (also known as dioxin receptor), AP-1 activator protein-1, AR androgen receptor, ER estrogen receptor, FoxA2 forkhead box protein A2, GR glucocorticoid receptor, ISGF3 interferon-stimulated gene factor complex 3 (IRF9 and phosphorylated STAT1 and STAT2), RARγ retinoic acid receptor γ, n.d. not determined

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