| 2000 |
DDX24 was cloned and characterized as a DEAD-box protein containing all conserved DEAD-box motifs; it is ubiquitously expressed across human tissues and localized to human chromosome 14q32. |
cDNA cloning, Northern blot analysis, radiation hybrid mapping, genomic sequence analysis |
Genomics |
Medium |
10936056
|
| 2008 |
DDX24 knockdown inhibits HIV-1 RNA packaging and viral infectivity specifically in the context of Rev/RRE-dependent (but not CTE-dependent) nuclear export of viral RNA, and DDX24 physically interacts with the HIV-1 Rev protein. |
siRNA knockdown, viral infectivity assays, RNA packaging assays, co-immunoprecipitation (DDX24–Rev interaction) |
Virology |
Medium |
18289627
|
| 2013 |
DDX24 negatively regulates RIG-I-like receptor (RLR)-mediated innate immune signaling by associating with adaptor proteins FADD and RIP1, preferentially impeding IRF7 activity; DDX24 preferentially binds RNA over DNA, and its loss augments cytosolic RNA-mediated innate signaling. |
Overexpression and siRNA knockdown assays, co-immunoprecipitation (DDX24–FADD, DDX24–RIP1), IRF7 reporter assays, RNA/DNA binding assays, embryonic lethality phenotype upon DDX24 loss |
PLoS pathogens |
High |
24204270
|
| 2014 |
MDM2 interacts with DDX24 via its central region and mediates non-proteolytic polyubiquitylation of DDX24 both in vitro and in vivo; this polyubiquitylation promotes DDX24 association with pre-ribosomal ribonucleoprotein (pre-rRNP) processing complexes required for early pre-rRNA processing. Depletion of DDX24 impairs pre-rRNA processing, abrogates MDM2 function, and leads to p53 stabilization. |
Co-immunoprecipitation, in vitro and in vivo ubiquitylation assays, siRNA knockdown, pre-rRNA processing assays, p53 stabilization assay |
Molecular and cellular biology |
High |
24980433
|
| 2015 |
DDX24 interacts with p300 and suppresses p300-mediated acetylation of p53, thereby inhibiting p53 transcriptional targets (p21, PUMA). DDX24 knockdown increases p53 acetylation and promotes p53-dependent cell cycle arrest and senescence. |
Co-immunoprecipitation (DDX24–p300), acetylation assays, siRNA knockdown, p53 target gene expression analysis, cell cycle and senescence assays |
Oncogene |
High |
25867071
|
| 2019 |
Point mutations in DDX24 (including ones in the ATP-binding domain) are associated with vascular malformations; DDX24 knockdown in endothelial cells results in elevated migration and tube formation, indicating a role for DDX24 in suppressing endothelial cell function. |
Genetic sequencing, structural modeling, siRNA knockdown, endothelial cell migration and tube formation assays, transcriptomic analysis |
Hepatology |
Medium |
30063812
|
| 2022 |
DDX24 binds the mRNA of LAMB1 (at nucleotides 618–624) and stabilizes it in a manner dependent on interaction between nucleolin and the C-terminal region of DDX24, thereby promoting HCC migration and proliferation. |
RNA immunoprecipitation, mRNA stability assays, co-immunoprecipitation (DDX24–nucleolin), overexpression and knockdown, in vivo xenograft |
Cancer research |
Medium |
35763670
|
| 2022 |
DDX24 interacts with RPL5 and promotes its ubiquitination and degradation, thereby promoting NSCLC metastasis. |
Co-immunoprecipitation followed by mass spectrometry, ubiquitination assays, protein stability assays, Transwell/wound-healing assays, in vivo xenograft |
Cancer medicine |
Medium |
35864588
|
| 2022 |
DDX24 and DDX49 bind predominantly immediate-early and early KSHV mRNAs (identified by RNA immunoprecipitation followed by next-generation sequencing) and their overexpression suppresses KSHV lytic reactivation, reducing viral gene transcription and genome replication. |
RNA immunoprecipitation sequencing (RIP-seq), overexpression studies, KSHV lytic reactivation assays, interferon induction assays |
Viruses |
Medium |
36298642
|
| 2022 |
DDX24 is enriched in planarian muscles; its knockdown disrupts muscle fiber organization, leading to defective pole specification and misregulation of positional control genes during regeneration, and upregulates wound-induced Wnt signaling. Suppressing ectopic Wnt activity rescues the knockdown phenotype. |
RNAi knockdown, immunofluorescence, genetic epistasis (Wnt inhibition rescuing DDX24-KD phenotype), in situ hybridization |
Developmental biology |
Medium |
35523320
|
| 2022 |
LINC02551 acts as a molecular adaptor that blocks the interaction between DDX24 and the E3 ligase TRIM27, thereby preventing ubiquitination and degradation of DDX24. |
Co-immunoprecipitation, ubiquitination assays, RNA pulldown, lincRNA knockdown/overexpression |
Cell death & disease |
Medium |
36335087
|
| 2022 |
DDX24 mutations K11E and E271K represent loss-of-function for cell proliferation; cells expressing these mutants show decreased nucleoli number, slower proliferation, and lower colony formation rates compared to wild-type DDX24. |
Stable cell line construction, immunofluorescence (nucleoli counting), proliferation and colony formation assays, in vivo tumor-bearing mouse model with 18F-FDG PET/CT, transcriptome sequencing |
International journal of medical sciences |
Medium |
35370459
|
| 2023 |
DDX24 is mainly located in the nucleolus; disease-associated mutant DDX24-E271K partitions less into nucleoli in patient tissues and endothelial cells, altering nucleolar morphology. DDX24 physically associates with NPM1 and regulates its liquid-liquid phase separation behavior as a client in the nucleolar granular component. DDX24 mutation or knockdown disrupts ribosome biogenesis and elevates endothelial cell migration and tube formation. |
In vitro condensate assay (LLPS), co-immunoprecipitation (DDX24–NPM1), immunofluorescence in patient tissues and cultured endothelial cells, siRNA knockdown, ribosome biogenesis assay, migration and tube formation assays |
International journal of biological sciences |
High |
37705750
|
| 2023 |
DDX24 binds FANCA mRNA and stabilizes it, promoting VSMC proliferation and cell cycle progression. VSMC-specific Ddx24 knockout mice die before embryonic day 13.5 with vascular defects; FANCA overexpression rescues cell cycle and DNA repair defects caused by DDX24 deficiency. |
Conditional knockout mice (Tagln-Cre), RNA immunoprecipitation with qRT-PCR, RNA pulldown, mRNA stability assays, RNA sequencing, flow cytometry, cell proliferation assays, rescue experiments |
Arteriosclerosis, thrombosis, and vascular biology |
High |
37470182
|
| 2023 |
DDX24 binds HK1 mRNA and positively regulates HK1 expression, promoting glycolysis (glucose uptake and lactate production) in gastric cancer cells. |
RNA immunoprecipitation, glucose uptake and lactate production assays, DDX24 overexpression/knockdown, cell proliferation and migration assays |
Cellular signalling |
Low |
38043669
|
| 2024 |
Endothelium-targeted Ddx24 conditional knockout mice show no developmental abnormality but exhibit vascular hyperpermeability upon ConA challenge, exacerbating immune-mediated hepatitis via upregulation of TNF-α and IFN-γ and downregulation of vascular integrity-associated proteins. |
CRISPR/Cas9-mediated Cre-loxP conditional knockout mice, mass spectrometry of liver proteins, endothelial migration and tube formation assays, in vivo ConA hepatitis model, cytokine measurement |
International immunopharmacology |
Medium |
38354508
|
| 2025 |
DDX24 deficiency in zebrafish enhances VEGFR2 expression by directly binding to its mRNA in non-brain endothelial cells, while suppressing GPR124/RECK-mediated Wnt signaling in brain endothelial cells, causing spatially distinct angiogenesis phenotypes (intersegmental vessel hyperbranching vs. inhibited central artery angiogenesis). |
Zebrafish DDX24 knockout, RNA binding assays (mRNA binding), spatial transcriptomics, pharmacological rescue experiments, in vivo imaging |
PNAS |
High |
40339127
|
| 2025 |
DDX24 binds PPFIA4 mRNA and enhances its stability in cerebral microvascular endothelial cells; PPFIA4 knockdown impairs mitochondrial homeostasis and barrier function. Endothelial-specific Ddx24 knockout mice show increased BBB permeability and learning/memory deficits. DDX24 knockdown causes occludin phosphorylation and mitochondrial dysfunction, reversed by NADPH oxidase inhibition. |
Endothelial-specific Ddx24 conditional knockout mice, RNA immunoprecipitation (DDX24–PPFIA4 mRNA), mRNA stability assay, occludin phosphorylation assay, BBB permeability assay, behavioral tests, pharmacological NADPH oxidase inhibition |
Cell reports |
High |
41105514
|
| 2025 |
DDX24 functions as a splicing factor that directly binds IKBKG pre-mRNA; DDX24 ablation stimulates generation of the long splicing isoform of IKBKG, which promotes autophagy through NF-κB signaling and BECN1 transcription, thereby suppressing lung cancer growth. |
Mass spectrometry, RNA sequencing (alternative splicing analysis), co-immunoprecipitation, luciferase reporter assays, functional rescue experiments, xenograft tumor models |
Theranostics |
Medium |
39897555
|
| 2025 |
DDX24 regulates transcription of heme oxygenase-1 (HO-1) at the promoter/enhancer E1 region level (not by mRNA stability), thereby exerting anti-apoptotic and anti-oxidative effects under oxidative stress conditions. |
RNA sequencing, DDX24 knockdown and overexpression, HO-1 expression and mRNA stability assays, promoter/enhancer reporter assay, cell viability assays |
FASEB journal |
Low |
40847746
|
| 2026 |
DDX24 promotes mRNA decay of CLEC14A and ERG mRNAs in endothelial cells by directly binding these transcripts and promoting their degradation in a CCR4-NOT deadenylase complex-dependent manner, thereby modulating endothelial cell functions critical for angiogenesis. |
Infrared cross-linking immunoprecipitation sequencing (irCLIP-seq), mRNA stability assays, co-immunoprecipitation (DDX24–CCR4-NOT complex), endothelial cell functional assays |
Nucleic acids research |
High |
41728947
|
| 2026 |
SNRPF-mediated splicing controls DDX24 protein abundance: SNRPF depletion induces intron 6 retention in DDX24 pre-mRNA, disrupting the Helicase_C domain and generating premature termination codons that trigger nonsense-mediated decay (NMD), reducing DDX24 protein levels. |
Integrated transcriptomic and proteomic analyses, intron retention analysis, antisense oligonucleotide experiments, NMD pathway validation, xenograft models |
Advanced science |
Medium |
42107058
|