| 2013 |
CHAF1A, as a subunit of chromatin assembly factor 1 (CAF-1), regulates H3K9 trimethylation at target gene loci controlling proliferation, survival, and differentiation; loss-of-function of CHAF1A drives neuronal differentiation in vitro and in vivo in neuroblastoma models. |
Loss-of-function experiments (knockdown/knockout) with transcriptome analysis and epigenetic readouts in neuroblastoma cell lines and in vivo models |
Cancer research |
Medium |
24335960
|
| 2021 |
CHAF1A gain-of-function upregulates polyamine metabolism, which blocks neuronal differentiation and promotes cell cycle progression in neuroblastoma; targeting polyamine synthesis enhances retinoic acid-induced differentiation. |
Gain-of-function experiments in zebrafish neural crest, human neural crest, and human neuroblastoma models; metabolic pathway analysis and pharmacological rescue |
Advanced science (Weinheim, Baden-Wurttemberg, Germany) |
Medium |
34365742
|
| 2022 |
CHAF1A and CHAF1B are required for silencing of unintegrated HIV-1 DNAs early in infection; KD of CHAF1A reduced H3K9me3 levels on viral DNA without major changes in histone loading, and KD of the H3K9me3-binding protein HP1γ also accelerated HIV-1 expression, placing CHAF1A upstream of H3K9me3/HP1γ-mediated silencing. The silencing function of CHAF1A was independent of its interaction with RBBP4 and did not extend to murine leukemia virus. |
RNAi-mediated knockdown of CHAF1A/CHAF1B and HP1γ; chromatin immunoprecipitation (ChIP) for histone marks on viral DNA; viral gene expression assays |
Proceedings of the National Academy of Sciences of the United States of America |
High |
35074917
|
| 2025 |
CHAF1A stability is regulated by antagonistic post-translational modifications: O-GlcNAcylation stabilizes CHAF1A and promotes HIV-1 latency, while ubiquitination drives its proteasomal degradation. The drug trifluridine disrupts O-GlcNAcylation, triggering CHAF1A ubiquitination and degradation, thereby reactivating latent HIV-1. |
In vivo ubiquitination and O-GlcNAcylation assays; pharmacological disruption with trifluridine; proteasome inhibition; latency reactivation assays in primary CD4+ T cells |
Journal of virology |
Medium |
41334912
|
| 2018 |
CHAF1A directly interacts with TCF4 and co-occupies the promoters of c-MYC and CCND1, acting as a co-activator in the Wnt signaling pathway to promote gastric cancer cell proliferation. CHAF1A expression itself is transcriptionally upregulated by Sp1, including in response to Helicobacter pylori infection. |
Co-immunoprecipitation (Co-IP) of CHAF1A with TCF4; chromatin immunoprecipitation (ChIP) at c-MYC and CCND1 promoters; CHAF1A knockdown/overexpression functional assays; luciferase reporter assays for Sp1-dependent transcription |
EBioMedicine |
Medium |
30449701
|
| 2022 |
The E3 ubiquitin ligase SPOP binds to a consensus SPOP-binding motif in CHAF1A and induces its degradative ubiquitination; loss of SPOP in DLBCL leads to CHAF1A accumulation, which then directly binds TFEB promoters (as shown by ChIP-qPCR) to activate TFEB transcription and downstream lysosomal biogenesis and autophagy. |
In vivo ubiquitination assays; ChIP-qPCR at TFEB promoter; SPOP knockdown/mutation studies; xenograft tumor models |
Journal of translational medicine |
Medium |
35773729
|
| 2007 |
CAF-1b (CHAF1A ortholog) is required for S-phase progression and differentiation in vivo in zebrafish; loss of caf-1b causes S-phase arrest and p53-mediated apoptosis in retinal precursor cells. p53 deficiency rescues apoptosis but not differentiation, demonstrating that CAF-1 activity is independently essential for differentiation. |
Zebrafish forward genetic mutant characterization; epistasis with p53 loss-of-function; BrdU/cell cycle analysis; histological differentiation markers |
Cell cycle (Georgetown, Tex.) |
High |
18156805
|
| 2019 |
CHAF1A knockdown reduces thymidylate synthetase (TS) expression in gastric cancer cells and sensitizes them to 5-FU, suggesting CHAF1A regulates TS expression as a downstream mechanism affecting fluoropyrimidine chemosensitivity. |
siRNA knockdown of CHAF1A; TS protein expression by Western blot; IC50 determination for 5-FU; bioinformatics correlation of RNA-seq and proteome data |
Gene |
Low |
31377317
|
| 2015 |
CHAF1A knockout in glioblastoma cells causes G1 phase arrest and apoptosis, and inhibition of CHAF1A reduces phosphorylation of the AKT/FOXO3a/Bim signaling axis, placing CHAF1A upstream of this survival pathway. |
CRISPR/Cas9 knockout of CHAF1A; cell cycle analysis by flow cytometry; Western blot for AKT/FOXO3a/Bim phosphorylation |
Biochemical and biophysical research communications |
Low |
26740175
|
| 2021 |
CHAF1A knockdown in cervical cancer cells suppresses invasion and EMT, and overexpression of CHAF1A upregulates ZEB1 (an EMT-related transcription factor), placing CHAF1A upstream of ZEB1 in a pro-invasive pathway. |
CHAF1A shRNA knockdown and overexpression; Transwell invasion assay; Western blot for EMT markers and ZEB1; luciferase reporter assay confirming miR-1179 targeting of CHAF1A 3'UTR |
Acta biochimica Polonica |
Low |
33740340
|
| 2023 |
CHAF1A promotes proliferation and growth of epithelial ovarian cancer cells via the JAK2/STAT3 phosphorylation pathway; inhibition of JAK2/STAT3 with peficitinib abolishes the proliferative effect of CHAF1A overexpression. |
CHAF1A siRNA knockdown and overexpression in EOC cell lines; Western blot for p-JAK2 and p-STAT3; pharmacological rescue with JAK2/STAT3 inhibitor peficitinib; cell proliferation and apoptosis assays |
Biochemistry and biophysics reports |
Low |
37575547
|
| 2024 |
Heterozygous loss-of-function variants in CHAF1A cause oculo-auriculo-vertebral spectrum (OAVS) in humans, establishing CHAF1A's role as a histone H3-H4 deposition factor during DNA replication as essential for normal craniofacial and branchial arch development. |
Human genetic analysis (identification of heterozygous LoF variants in 8 individuals including a 3-member family); phenotypic characterization of OAVS features |
European journal of human genetics : EJHG |
Medium |
39333427
|