| 2010 |
ASF1B expression is proliferation-dependent: both mRNA and protein decrease upon cell cycle exit in cultured cells. Depletion of ASF1B severely compromises proliferation and leads to aberrant nuclear structures, indicating a specific requirement for ASF1B (not ASF1a) in cell proliferation. |
siRNA depletion, cell cycle exit experiments, Western blot, immunofluorescence, transcriptional profiling |
The EMBO journal |
High |
21179005
|
| 2010 |
HCF-1 directly and simultaneously interacts with both HSV DNA replication proteins and ASF1B. ASF1B co-localizes with HCF-1 at viral replication foci late in HSV infection, and depletion of ASF1B results in significantly reduced viral DNA accumulation, indicating ASF1B functions in viral DNA replication via chromatin reorganization downstream of HCF-1 recruitment. |
Co-immunoprecipitation, co-localization (immunofluorescence), siRNA depletion with viral DNA quantification |
Proceedings of the National Academy of Sciences of the United States of America |
High |
20133788
|
| 2013 |
ASF1a and ASF1b, which arose by gene duplication at the ancestor of jawed vertebrates, have distinct preferential interactions with different H3-H4 chaperones; regions outside the primary interaction surface (in the N- and C-terminal regions) are key determinants of these preferential interactions, as demonstrated by biochemical and structural analyses. |
Biochemical binding assays, structural analysis, evolutionary/comparative genomics, positive selection analysis |
Molecular biology and evolution |
Medium |
23645555
|
| 2016 |
ASF1B promotes human β-cell proliferation in a histone-binding-dependent manner; the histone-binding-deficient mutant V94R fails to induce proliferation. Co-expression of histone H3.3 (but not H3.1 or H3.2) synergistically augments ASF1B-mediated β-cell proliferation, and suppression of endogenous H3.3 attenuates the stimulatory effect of ASF1B, establishing that ASF1B requires histone H3.3 binding for its proliferative function. |
Overexpression, dominant-negative (V94R) mutant, siRNA knockdown of H3.3, multiple proliferation assays (BrdU, Ki67, mitotic markers) |
Cell cycle (Georgetown, Tex.) |
High |
27753532
|
| 2016 |
Loss of ASF1B in mice reduces female reproductive capacity; ASF1B is specifically expressed in germ cells with peak expression correlating with meiosis, and Asf1b-null female mice show altered timing of meiotic entry and defective gonad development, indicating ASF1B plays a role in chromatin modifications at meiotic entry. |
Asf1b gene-trap knockout mouse, β-galactosidase reporter assay, histological analysis, reproductive phenotyping |
Reproduction (Cambridge, England) |
Medium |
26850882
|
| 2020 |
ASF1B forms stable complexes with CDK9 and positively regulates CDK9 stabilization in cervical cancer cells; ASF1B knockdown reduces CDK9 protein levels. |
Co-immunoprecipitation, Western blot, siRNA knockdown, in vivo tumor xenograft model |
Cell death & disease |
Medium |
32848135
|
| 2021 |
Asf1a, but not Asf1b, is required for histone H3.3 assembly in the paternal pronucleus after fertilization. Knockdown of Asf1b (but not Asf1a) nearly eliminates nuclear accumulation of PCNA in morula-stage embryos, indicating ASF1B specifically safeguards pre-implantation embryo development by regulating cell proliferation, while Asf1a regulates H3K56ac levels and Oct4 expression. |
Morpholino-mediated knockdown, immunofluorescence with specific antibodies, confocal microscopy in mouse embryos |
Epigenetics & chromatin |
Medium |
34906203
|
| 2022 |
ASF1B knockdown in HCC cells reduces expression of PCNA, cyclinB1, cyclinE2, and CDK9, and ASF1B interacts with CDK9 in HCC cells, consistent with a role for ASF1B-CDK9 complex in cell cycle regulation. |
Co-immunoprecipitation, Western blot, siRNA knockdown |
Frontiers in oncology |
Low |
35087760
|
| 2022 |
ASF1B knockdown increases S-phase cell cycle arrest and activates checkpoint kinases Chk1 and Chk2, indicating ASF1B normally suppresses replication checkpoint activation in pancreatic cancer cells. |
siRNA knockdown, flow cytometry cell cycle analysis, Western blot for Chk1/Chk2 phosphorylation |
Cancer biomarkers : section A of Disease markers |
Low |
35599471
|
| 2023 |
ASF1B interacts with and occupies the TLK1 gene locus (ChIP assay), and the interaction between ASF1B and TLK1 promotes proliferation, cell cycle progression, and metastasis of low-grade glioma cells; overexpression of TLK1 rescues the effects of ASF1B interference. |
ChIP assay, co-expression rescue experiments, siRNA knockdown, cell functional assays |
Annals of medicine |
Low |
36947060
|
| 2024 |
Transcription factor FOXM1 directly binds the ASF1B promoter region and regulates ASF1B transcription. In turn, ASF1B regulates PRDX3 transcription in a FOXM1-dependent manner, forming a FOXM1-ASF1B-PRDX3 axis that controls GC cell proliferation and oxidative stress balance. |
ChIP assay, FOXM1 inhibitor (thiostrepton) treatment, knockdown/overexpression experiments, in vitro and in vivo tumor models |
Cancer letters |
Medium |
38537775
|
| 2024 |
CDAN1 dimerizes and assembles into cytosolic complexes with CDIN1 and multiple copies of ASF1A/B. Cryo-EM structures reveal that CDAN1 engages ASF1B via two B-domains (found in other ASF1-binding partners) and two helices that mimic histone H3 binding. CDAN1 can recruit two ASF1 molecules simultaneously and sequesters/inhibits ASF1 chaperone function; ASF1A and ASF1B have different requirements for CDAN1 engagement. |
Single-particle cryo-EM, biochemical reconstitution, structural analysis |
bioRxiv (preprint)preprint |
High |
bio_10.1101_2024.08.08.607204
|
| 2025 |
ASF1B promotes gastric cancer progression by downregulating histone H2AC20, which activates the PI3K/AKT and ERK1/2 signaling pathways; identified by IP-MS and TMT proteomics to define the ASF1B-interacting protein network. |
Immunoprecipitation-Mass Spectrometry (IP-MS), TMT proteomics, ASF1B knockout/overexpression, in vitro and in vivo tumor models, organoids |
Frontiers in pharmacology |
Medium |
40041497
|
| 2026 |
ASF1B recruits the transcription factor HOXB3, promoting ZDHHC9 transcription. ZDHHC9 then palmitoylates PCBP1 at residue C109, inhibiting PCBP1 ubiquitination and suppressing SLC7A11-mediated ferroptosis, thus promoting gastric cancer liver metastasis. Identified by immunoprecipitation and LC-MS analyses. |
Immunoprecipitation/LC-MS, transcriptome sequencing, label-free proteomics, spleen-injection liver metastasis model, IHC, immunofluorescence |
NPJ precision oncology |
Medium |
41535416
|
| 2026 |
ASF1B occupies >70% of H3.3 nucleosomes in mouse fetal liver erythroid cells and determines H3.3 enrichment at erythroid gene promoters and enhancers. ASF1B predominantly regulates H3.3-encoding genes and erythroid genes (with ASF1A serving a compensatory function). Loss of ASF1B de-represses embryonic/fetal globin genes by altering H3.3 enrichment, erythroid transcription factor binding, and chromatin accessibility. The regulatory pathway involves recruitment of chromatin remodeler BRG1 and accumulation of H3K27ac at active chromatin. |
ChIP-seq, ATAC-seq, ASF1B knockout in mouse fetal liver cells, transcriptome sequencing, co-immunoprecipitation for BRG1 interaction |
Nucleic acids research |
High |
42100853
|
| 2026 |
ASF1B recruits the lactyltransferase p300, thereby promoting histone H3K18 lactylation (H3K18la) in hepatocellular carcinoma cells, forming a positive feedback loop with H3K18la. |
Co-immunoprecipitation, ChIP sequencing, Cut&Run, dual-luciferase reporter assay |
Cells |
Medium |
42193960
|