| 1999 |
PCAF acetylates p53 in vitro at lysine K320, a residue distinct from that acetylated by p300, and this acetylation increases p53's ability to bind its cognate DNA site. Acetylation at this site is detected in vivo and increases in response to DNA-damaging agents. |
In vitro acetyltransferase assay, site-specific acetylation antibodies, in vivo detection after DNA damage |
Molecular and cellular biology |
High |
9891054
|
| 1997 |
PCAF directly interacts with MyoD and forms a multimeric complex with p300/CBP on promoter elements to drive myogenic differentiation; the histone acetyltransferase activity of PCAF (but not p300) is required for p21 expression and terminal cell-cycle arrest during myogenesis. |
Anti-PCAF antibody microinjection, exogenous expression, reporter assays, HAT-dead mutant analysis |
Molecular cell |
High |
9659901
|
| 1998 |
PCAF directly associates with the DNA-binding domain of nuclear receptors (RXR/RAR heterodimer) in a ligand-dependent manner and independently of p300/CBP, defining a novel cofactor interaction surface on nuclear receptors. |
Ligand-dependent recruitment from mammalian cell extracts, in vitro direct binding assay, transcription reporter assays |
Genes & development |
Medium |
9620851
|
| 1999 |
Adenoviral E1A directly binds PCAF independently of CBP and inhibits PCAF HAT activity in vitro, blocking nucleosomal histone modification by the PCAF complex and p53 acetylation. |
In vitro HAT assay, direct binding assay, in vivo transcription assays |
Cell |
High |
10025405 9687513
|
| 1998 |
PCAF forms a ternary complex with p300 and HIV-1 Tat in cells, and the HAT activity of PCAF (but not p300) is specifically required for Tat transactivation of integrated (but not unintegrated) HIV-1 LTR. |
Co-immunoprecipitation (ternary complex), dominant-negative HAT mutant transfection, integrated vs. unintegrated LTR reporter assays |
The Journal of biological chemistry |
High |
9733796
|
| 2000 |
Mouse Notch1 intracellular region (RAMIC) directly interacts with mouse PCAF (and GCN5) through its ankyrin repeats and transactivation domain, recruiting PCAF to RBP-J and facilitating RBP-J-mediated transactivation; the N-terminal regions of PCAF/GCN5 are required for this interaction. |
Co-immunoprecipitation, domain mapping, transactivation reporter assays, E1A and Twist inhibition |
The Journal of biological chemistry |
Medium |
10747963
|
| 1998 |
Human GCN5 and P/CAF have extended homologous amino-terminal domains enabling acetylation of nucleosomal substrates (not only free histones), unlike the shorter yeast Gcn5p; both interact with CBP/p300 and display similar substrate specificities for histone H3. |
In vitro HAT assay with nucleosomal and free histone substrates, protein interaction assays, immunodetection |
Molecular and cellular biology |
High |
9742083
|
| 2000 |
Kinetic mechanism of human P/CAF follows a fully ordered Bi-Bi mechanism: acetyl-CoA binds first to free enzyme (Kd = 0.64 µM), then histone H3 peptide binds; chemical catalysis (acetyl transfer to Lys-14 of H3) is rate-determining; Glu-570 is the proposed general base catalyst. |
Bi-substrate kinetic analysis, product inhibition, equilibrium dialysis, pre-steady-state quench-flow, pH-dependent activity measurements |
Biochemistry |
High |
11009610
|
| 2003 |
P/CAF auto-acetylates itself intramolecularly at five lysines (416–442) within its nuclear localization signal (NLS) at the C-terminus, and intermolecularly via its N-terminal domain; P/CAF is also acetylated by p300 but not CBP; auto-acetylation increases PCAF HAT activity. |
In vitro acetylation assay, mutational analysis, in vivo acetylation detection |
Nucleic acids research |
Medium |
12888487
|
| 2008 |
P/CAF autoacetylation at the NLS (C-terminal lysines) controls its nuclear localization; HAT-inactive P/CAF accumulates in the cytoplasm; HDAC3 (and to a lesser extent HDAC1/2/4) deacetylates P/CAF leading to cytoplasmic accumulation; P/CAF accumulates in cytoplasm during apoptosis. |
Subcellular fractionation, fluorescence microscopy, HAT-dead mutant, HDAC overexpression/knockdown |
The Journal of biological chemistry |
Medium |
19015268
|
| 2006 |
PCAF interacts physically with PTEN and acetylates PTEN at Lys125 and Lys128 within its catalytic cleft in a growth-factor-dependent manner, reducing PTEN's lipid phosphatase activity and thereby maintaining PI3K/AKT signaling; acetylation-resistant K125R/K128R mutants retain PI3K-suppressing and G1 arrest activities even with PCAF overexpression. |
Co-immunoprecipitation, in vitro acetyltransferase assay, shRNA knockdown, acetylation-resistant mutant analysis, cell cycle assays |
The Journal of biological chemistry |
High |
16829519
|
| 2007 |
PCAF possesses an intrinsic ubiquitin E3 ligase activity (distinct from its acetyltransferase activity) that ubiquitinates Hdm2, promoting its degradation and thereby stabilizing p53; PCAF knockdown stabilizes Hdm2. |
PCAF knockdown in HeLa/U2OS cells, in vitro ubiquitination assay, domain deletion analysis |
Nature cell biology |
High |
17293853
|
| 2002 |
PCAF acetylates HIV-1 Tat at Lys50; acetylated Tat binds the PCAF bromodomain; structural analysis defined critical interaction residues (Y47/R53 in Tat; V763/Y802/Y809 in PCAF bromodomain); mutations at these residues cumulatively inhibit Tat–PCAF interaction and synergistic HIV promoter activation. |
In vitro binding assay, in vivo co-immunoprecipitation, structural analysis of acetyl-peptide–bromodomain complex, site-directed mutagenesis, HIV promoter reporter assay |
The EMBO journal |
High |
12032084
|
| 2000 |
P/CAF directly interacts with Smad3 (via Smad3 MH2 domain and P/CAF N-terminal region) upon TGF-β receptor activation; P/CAF potentiates TGF-β/Smad3-mediated transcription cooperatively with p300 and Smad4. |
In vitro GST pull-down, co-immunoprecipitation in mammalian cells, transcription reporter assays |
Nucleic acids research |
Medium |
11058129
|
| 2000 |
P/CAF-mediated acetylation of TAL1/SCL maps to a lysine-rich motif in the loop region and increases TAL1 DNA binding while selectively inhibiting its interaction with co-repressor mSin3A; an acetylation-defective P/CAF mutant inhibits TAL1 acetylation, DNA binding, transcription, and terminal erythroid differentiation. |
In vitro acetylation assay, domain mapping, DNA-binding EMSA, co-immunoprecipitation, differentiation assay with HAT-dead mutant |
The EMBO journal |
High |
11118214
|
| 2000 |
Mice lacking PCAF are developmentally normal; in PCAF-null mice, PCAF-B/GCN5 protein levels are drastically elevated in tissues where PCAF is normally abundant, indicating functional compensation between PCAF and GCN5. |
Gene knockout mouse model, Western blot quantification of compensatory protein levels |
Proceedings of the National Academy of Sciences of the United States of America |
High |
11027331
|
| 2001 |
Cyclin D1 and the androgen receptor (AR) both bind overlapping domains of P/CAF; cyclin D1 displaces AR binding to P/CAF in vitro; the HAT activity of P/CAF rescues cyclin D1-mediated AR trans-repression. |
In vitro binding/displacement assay, HAT-dead P/CAF rescue experiment, reporter assays |
Molecular endocrinology (Baltimore, Md.) |
Medium |
11328859
|
| 1999 |
Cyclin D1 interacts with the histone acetyltransferase P/CAF, facilitating P/CAF–estrogen receptor (ER) association; P/CAF potentiates cyclin D1-stimulated ER transcriptional activity in a dose-dependent, HAT-activity-dependent manner. |
Co-immunoprecipitation, reporter assay, HAT-dead mutant analysis |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
10318892
|
| 2003 |
P/CAF acetylates the ETS transcription factor ER81 at K116 (and p300 additionally at K33); acetylation enhances ER81 transactivation, DNA binding activity, and in vivo half-life; oncogenic HER2/Neu stimulates p300-mediated ER81 acetylation via the Ras→Raf→MAPK pathway. |
In vitro and in vivo acetylation assay, acetylation-deficient mutant analysis, DNA binding assay, protein stability measurement |
Molecular and cellular biology |
Medium |
12917345
|
| 1998 |
NF-Y complex associates with human GCN5 and P/CAF in vivo and possesses HAT activity through these interactions; the NF-YB:YC histone-fold motif is sufficient for stable interaction with GCN5 in vitro; deletion of N- or C-terminal regions of GCN5 disrupts NF-Y interaction. |
In vivo co-immunoprecipitation, in vitro interaction assay, deletion mutant analysis, transient transfection reporter assay |
The Journal of biological chemistry |
Medium |
9430679
|
| 2002 |
The adenovirus E1B 55-kDa oncoprotein specifically inhibits PCAF-mediated acetylation of p53 at K320 in vivo and in vitro (without affecting histone acetylation or PCAF autoacetylation) by physically binding PCAF and interfering with the PCAF–p53 interaction. |
In vitro acetylation assay, co-immunoprecipitation, competition assay, in vivo acetylation measurement |
Molecular and cellular biology |
Medium |
10891493
|
| 2002 |
MDM2 interacts with PCAF in vitro and in cells and inhibits PCAF-mediated acetylation of p53 at K320 in vitro and in overexpression experiments, repressing PCAF-dependent p53 transcriptional activation without affecting p53 levels. |
GST pull-down, co-immunoprecipitation, in vitro acetylation assay, reporter assay, chromatin immunoprecipitation |
The Journal of biological chemistry |
Medium |
12068014
|
| 2008 |
PCAF associates with actin and hnRNP U in nuclear extracts via affinity chromatography and protein-protein interaction assays; PCAF-associated HAT activity is released by disruption of the actin–hnRNP U complex; PCAF, actin, and hnRNP U co-occupy promoters and coding regions of pol II genes and associate with nascent ribonucleoprotein complexes, supporting a role for PCAF in pol II transcription elongation. |
Affinity chromatography, co-immunoprecipitation, biochemical fractionation, chromatin immunoprecipitation, RNA immunoprecipitation, bromouridine incorporation assay |
Molecular and cellular biology |
Medium |
18710935
|
| 2008 |
PCAF and HDAC4 associate with cardiac sarcomeres (Z-disc and I/A bands) in cardiomyocytes; PCAF acetylates the Z-disc protein MLP (muscle LIM protein); increased acetylation via HDAC inhibition enhances myofilament calcium sensitivity in wild-type but not MLP-knockout mice. |
Immunohistochemistry, electron microscopy, co-immunoprecipitation, in vitro acetylation assay, calcium sensitivity measurement, knockout comparison |
The Journal of biological chemistry |
Medium |
18250163
|
| 2008 |
PCAF acetylates β-catenin, inhibiting its ubiquitination and increasing its stability; the key ubiquitination sites K19 and K49 of β-catenin are the critical residues for PCAF-induced acetylation and stabilization; PCAF knockdown reduces β-catenin protein level, transcriptional activity, promotes differentiation, and inhibits migration. |
Co-immunoprecipitation, in vitro acetylation assay, site-directed mutagenesis, ubiquitination assay, shRNA knockdown, cell migration and differentiation assays |
Molecular biology of the cell |
High |
18987336
|
| 2013 |
PCAF/KAT2B interacts with GLI1 (downstream effector of Hedgehog signaling) and is required for H3K9 acetylation on Hh target gene promoters; PCAF depletion impairs Hh target gene expression, reduces medulloblastoma/glioblastoma cell proliferation, and reduces tumor-forming potential of neural stem cells in vivo. |
Co-immunoprecipitation, siRNA knockdown, ChIP for H3K9ac, proliferation assay, apoptosis assay, in vivo neural stem cell tumor assay |
Cancer research |
Medium |
23943798
|
| 2013 |
PCAF acts as a novel E3 ubiquitin ligase for GLI1; in response to genotoxic stress, p53-elevated PCAF promotes GLI1 ubiquitination and proteasome-dependent degradation (requires the ubiquitination domain of PCAF, not a deletion mutant lacking it), thereby inhibiting Hedgehog signaling. |
In vitro ubiquitination assay, deletion mutant of PCAF ubiquitination domain, shRNA knockdown of p53/PCAF, GLI1 rescue experiment, in vivo medulloblastoma model |
Cell death and differentiation |
High |
24013724
|
| 2013 |
KAT2B (PCAF) is recruited by dephosphorylated CRTC2 to gluconeogenic gene promoters, where it acetylates H3K9 (H3K9Ac); KAT2B cooperates with WDR5 to stimulate the gluconeogenic program; depletion of KAT2B or WDR5 decreases gluconeogenic gene expression and a KAT2B antagonist lowers blood glucose in insulin-resistant mice. |
Mouse knockout/knockdown models, in vitro acetylation assays, ChIP, small-molecule KAT2B inhibitor in vivo |
The Journal of clinical investigation |
High |
24051374
|
| 2016 |
KAT2A and KAT2B (PCAF) acetylate PLK4 kinase domain at K45 and K46; K45/K46 acetylation impairs PLK4 kinase activity in vitro (molecular dynamics suggests shift to inactive conformation); the PLK4 K45R/K46R mutant does not cause centrosome overamplification when overexpressed; impairing KAT2A/2B acetyltransferase activity results in excess centrosome numbers in cells. |
Shotgun proteomics acetylome, in vitro kinase assay after acetylation, molecular dynamics modelling, mutant overexpression centrosome assay |
Nature communications |
High |
27796307
|
| 2014 |
PCAF acetylates PGC-1α at K328 and K450, triggering its proteasomal degradation and suppressing gluconeogenic transcriptional activity; adenoviral PCAF expression in obese mouse liver represses gluconeogenic enzyme activation and improves glucose homeostasis; liver-specific PCAF knockdown increases blood glucose. |
In vitro acetylation assay, site-directed mutagenesis, adenoviral overexpression in vivo, liver-specific knockdown, glucose tolerance tests |
Cell reports |
High |
25497092
|
| 2015 |
PCAF acetylates EZH2 primarily at K348; K348 acetylation decreases EZH2 phosphorylation at T345 and T487, increases EZH2 stability without disrupting PRC2 formation, and enhances EZH2's capacity to suppress target genes; SIRT1 deacetylates EZH2. |
Co-immunoprecipitation, in vitro acetylation assay, site-directed mutagenesis, protein stability assay, PRC2 complex immunoprecipitation |
Nucleic acids research |
Medium |
25800736
|
| 2003 |
PCAF directly interacts with cdk2; PCAF inhibits cyclin/cdk2 activity by two mechanisms: (i) disrupting cyclin–cdk2 interaction and (ii) acetylating cdk2 at K33 (within the ATP-binding pocket), thereby inhibiting cdk2 kinase activity; PCAF overexpression arrests cells at S and G2/M in a cdk2-dependent manner. |
Co-immunoprecipitation, in vitro kinase assay, in vitro acetylation with K33 mutagenesis, cell cycle analysis, cdk2 rescue overexpression |
Nucleic acids research |
Medium |
19773423
|
| 2010 |
During keratinocyte differentiation, PCAF acetylates Rb at sites within its nuclear localization sequence; PCAF HAT activity is required for normal differentiation; acetylation-deficient Rb is mislocalized to the cytoplasm during differentiation, and SIRT1 overexpression or PCAF reduction causes the same Rb mislocalization. |
shRNA depletion, HAT-dead PCAF, acetylation-site Rb mutants, subcellular fractionation/immunofluorescence, differentiation assays |
Journal of cell science |
Medium |
20940255
|
| 2008 |
PCAF is an HIF-1α cofactor that acetylates HIF-1α under hypoxia-mimicking conditions; PCAF-mediated acetylation of p53 at K320 is preferentially reduced under hypoxia compared to K382 acetylation (by p300), redirecting acetylated p53 to p21 promoters while preventing recruitment to pro-apoptotic BID promoter. |
Co-immunoprecipitation, chromatin immunoprecipitation, acetylation site-specific analysis under hypoxia |
Oncogene |
Medium |
18574470
|
| 2012 |
PCAF HAT activity is required for stress-induced H3K9 and H3K14 acetylation at the p21 promoter and for p53-dependent p21 transcription in response to multiple stresses (nutlin-3, DNA damage, p14ARF); this role is independent of p53 K320 acetylation; PCAF loss prevents cell cycle arrest. |
siRNA knockdown, HAT-dead PCAF mutant, chromatin immunoprecipitation for H3K9ac/H3K14ac, p53 promoter occupancy assay, cell cycle analysis |
Cell cycle (Georgetown, Tex.) |
Medium |
22713239
|
| 2017 |
PCAF/GCN5 PCAF-deficient macrophages exhibit markedly reduced cytokine production upon LPS stimulation; chemical inhibition of PCAF/GCN5 bromodomains alone is insufficient to recapitulate this immune phenotype, but PCAF/GCN5 PROTAC-mediated degradation potently modulates inflammatory mediator expression. |
PCAF-deficient macrophage functional assay, bromodomain inhibitor comparison, PROTAC-mediated degradation, cytokine expression assay |
ACS chemical biology |
Medium |
30200762
|
| 2017 |
PCAF acetylates RPA1 at K163; DNA-PK phosphorylates and activates PCAF upon UV damage to promote K163 acetylation; K163 acetylation of RPA1 is critical for accumulation of XPA at damaged DNA and activation of nucleotide excision repair (NER) specifically; HDAC6 and SIRT1 deacetylate RPA1. |
In vitro acetylation assay, co-immunoprecipitation, site-directed mutagenesis, NER assay, XPA recruitment to damage sites, HDAC identification |
Cell reports |
High |
28854354
|
| 2020 |
PCAF is a fork-associated protein at stalled replication forks; PCAF acetylates H4K8 at stalled forks, recruiting MRE11 and EXO1 (via an H4K8ac-binding domain) to promote fork degradation in BRCA-deficient cells; ATR phosphorylates PCAF at S264 to limit its fork association and activity; low PCAF levels stabilize stalled forks and cause PARPi resistance in BRCA-deficient cells. |
Chromatin fractionation at forks, in vitro H4K8 acetylation assay, S264 phospho-site mapping, MRE11/EXO1 H4K8ac binding domain analysis, PARPi resistance assay, ATR inhibition |
Molecular cell |
High |
32966758
|
| 2009 |
hSIRT1 deacetylates PCAF in vitro and modulates PCAF acetylation in vivo; hSIRT1 represses E2F1-dependent p73 promoter activity by forming a hSIRT1–PCAF–E2F1 complex on the P1p73 promoter; upon apoptotic DNA damage, decreased nuclear NAD+ inactivates hSIRT1's deacetylase activity (without disrupting SIRT1–PCAF interaction), releasing PCAF to form active PCAF/E2F1 complexes on the P1p73 promoter. |
In vitro deacetylation assay, co-immunoprecipitation, chromatin immunoprecipitation, NAD+ manipulation, reporter assay |
Molecular and cellular biology |
Medium |
19188449
|
| 2010 |
PTH treatment increases PCAF acetylation at the MMP-13 promoter in a p300-dependent manner; p300-dependent PCAF acetylation and mutual p300–PCAF promoter recruitment is required for PTH-induced MMP-13 transcription; HAT activities of both PCAF and p300 are additively required. |
ChIP, siRNA knockdown of PCAF/p300/Runx2, reporter assay with HAT-dead mutants |
The Journal of biological chemistry |
Medium |
20870727
|
| 2013 |
PCAF directly acetylates cytoplasmic GLI1 at K518, preventing its nuclear translocation and promoter occupancy, suppressing Hedgehog signaling in hepatocellular carcinoma; PCAF-mediated GLI1 acetylation reduces BCL2 expression and upregulates BAX. |
In vitro acetylation assay, site-directed mutagenesis, subcellular fractionation, ChIP, in vivo xenograft model |
Cell death & disease |
Medium |
25855960
|
| 2008 |
GCN5L (KAT2B) stably associates with Mediator containing the cdk8 subcomplex (T/G-Mediator) together with TRRAP; cdk8 phosphorylates H3 serine-10, which then stimulates H3K14 acetylation by GCN5L within the complex, producing tandem H3 phosphoacetylation that correlates with transcriptional activation. |
Reconstituted human transcription system, co-immunoprecipitation, in vitro histone modification assay, cdk8 knockdown, ChIP |
The EMBO journal |
High |
18418385
|
| 2014 |
PCAF (Kat2b) and Gcn5 negatively regulate IFN-β production through a HAT-independent, non-transcriptional mechanism by inhibiting the innate immune kinase TBK1 in the cytoplasm; Gcn5/PCAF-mediated H3K9ac is dispensable for IFNB expression and the vast majority of active genes in fibroblasts. |
HAT-dead mutant analysis, cytoplasmic TBK1 inhibition assay, genetic knockout of Gcn5/PCAF, IFN-β production assay |
EMBO reports |
Medium |
25269644
|
| 2013 |
PCAF acetylates HOXA10 at K338 and K339, inhibiting HOXA10-mediated ITGB3 (β3-integrin) transcription and thereby impairing endometrial receptivity and embryo adhesion. |
Co-immunoprecipitation, in vitro acetylation assay with site mapping, luciferase reporter assay, ChIP, BeWo spheroid attachment assay, PCAF overexpression/knockdown |
The Journal of clinical endocrinology and metabolism |
Medium |
24037888
|
| 2012 |
PCAF directly interacts with p27Kip1 (via aa 91–120 of p27; PCAF catalytic domain required) and acetylates p27 at K100; PCAF overexpression induces proteasomal degradation of p27 (Skp2-independent); K100R mutant p27 is resistant to PCAF-induced degradation and remains stable through the cell cycle. |
Co-immunoprecipitation, in vitro acetylation assay, K100R mutagenesis, protein half-life measurement, proteasome inhibitor assay, ubiquitylation assay |
Nucleic acids research |
Medium |
22547391
|
| 2020 |
PCAF-dependent acetylation of ISX at K69 promotes ISX interaction with BRD4 (acetylated at K332) and nuclear translocation of the ISX–BRD4 complex; in the nucleus, the complex binds EMT gene promoters with H3K9/K14/K18 acetylation, activating EMT transcription and cancer metastasis. |
Co-immunoprecipitation, site-directed mutagenesis, subcellular fractionation, ChIP, histone acetylation analysis |
EMBO reports |
Medium |
31908141
|
| 2020 |
SIRT7 directly interacts with PCAF and deacetylates PCAF at K720 upon glucose deprivation; deacetylated PCAF binds MDM2 more strongly, promoting MDM2 ubiquitination/degradation, elevating p53, and inducing p21/cell-cycle arrest. |
Co-immunoprecipitation, in vitro deacetylation assay, K720 site mapping, MDM2 ubiquitination assay, cell cycle analysis |
Oncogene |
Medium |
32404984
|
| 2013 |
PCAF interacts with GLI1 and ubiquitinates it (E3 ubiquitin ligase activity), inhibiting HCC cell metastasis and EMT; PCAF-mediated GLI1 targeting suppresses Gli1-driven EMT in hepatocellular carcinoma. |
Co-immunoprecipitation, in vitro ubiquitination assay, siRNA knockdown, migration/invasion assay |
Cancer letters |
Medium |
26945969
|
| 2017 |
PCAF acetylates MKL1 in response to pro-inflammatory stimuli (TNF-α, LPS); acetylation promotes MKL1 nuclear enrichment, enhances MKL1–NF-κB interaction, and stabilizes MKL1 binding to NF-κB target promoters, activating pro-inflammatory transcription. |
Co-immunoprecipitation, in vivo acetylation analysis, MKL1 lysine mutant functional assay, nuclear fractionation, ChIP |
Biochimica et biophysica acta. Gene regulatory mechanisms |
Medium |
28571745
|
| 2013 |
PCAF regulates the EB1–TIP150 interaction at kinetochore microtubule plus ends by acetylating EB1; persistent EB1 acetylation by PCAF perturbs the EB1–TIP150 interaction, leading to metaphase alignment defects, spindle checkpoint activation, and chromosome aneuploidy. |
siRNA knockdown, co-immunoprecipitation, acetylation assay, live cell imaging of chromosome alignment, spindle checkpoint assay |
The Journal of biological chemistry |
Medium |
23595990
|
| 2018 |
PCAF (and GCN5) acetylate influenza A virus nucleoprotein (NP) in vitro; PCAF acetylates NP at Lys-31 while GCN5 targets Lys-90; PCAF silencing increases viral polymerase activity, indicating that PCAF-mediated NP acetylation at K31 negatively regulates influenza replication. |
In vitro acetyltransferase assay, LC-MS site identification, RNAi silencing, viral polymerase activity assay |
The Journal of biological chemistry |
Medium |
29555684
|
| 2003 |
PCAF binds p73; the N-terminal transactivation domain and OD of p73 and the HAT domain of PCAF are required for interaction; PCAF HAT activity is required for stimulating p73-mediated transactivation of p21 and induction of apoptosis. |
Co-immunoprecipitation, domain mapping, reporter assay, PCAF-specific siRNA, colony formation assay |
Oncogene |
Medium |
14614455
|
| 2010 |
PCAF and CBP/p300 are repressed by inhibitory (myelin, CSPG) substrates in neurons; HDAC inhibition restores PCAF/CBP/p300 expression; PCAF and CBP/p300 acetylate histone H3 at K9–14 and p53, initiating a pro-neuronal outgrowth transcriptional program that promotes axon growth and counteracts growth cone collapse. |
Gene silencing, gain-of-function, chromatin acetylation analysis, neurite outgrowth quantification |
Cell death and differentiation |
Medium |
20094059
|
| 2014 |
Gcn5 and PCAF double knockout blocks PPARγ expression (preventing adipocyte differentiation) and is essential for Prdm16 expression (required for brown adipogenesis); Gcn5/PCAF facilitate PPARγ RNA pol II recruitment and Prdm16 transcript elongation. |
Double-knockout cell lines, PPARγ rescue expression, ChIP for pol II, nascent RNA analysis |
Molecular and cellular biology |
Medium |
25071153
|
| 2010 |
HIPK2 cooperates with PCAF to induce PCAF-mediated p53 acetylation after nonapoptotic DNA damage; HIPK2 depletion abolishes PCAF-dependent p53 acetylation and reduces p53 binding to the p21Waf1 promoter, inhibiting p21 transactivation and allowing cell proliferation. |
RNAi knockdown of HIPK2, ChIP, acetylation analysis, cell cycle assay |
Oncogene |
Medium |
15897882
|