|
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 differentiationb
|
n.d.
|
[56]
|
|
Myc
|
n.d.
|
[77]
|
|
p53
|
Upregulationa
|
[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
