| 1999 |
LDOC1 encodes a nuclear protein with a leucine zipper-like motif at the N-terminal region and a proline-rich region similar to an SH3-binding domain; EGFP-LDOC1 fusion protein localizes to the nucleus. |
EGFP fusion protein localization assay, Northern blot, chromosomal mapping |
Cancer letters |
Medium |
10403563
|
| 2003 |
LDOC1 inhibits NF-κB transcriptional activity; transient LDOC1 expression blocked NF-κB reporter activity driven by MEKK1, TNF-α, or PMA in a dose-dependent manner, without affecting p53, AP-1, or CRE-dependent reporter expression. |
NF-κB luciferase reporter assay, stable transfection, cell viability assay |
International journal of cancer |
Medium |
12712434
|
| 2005 |
LDOC1 overexpression induces apoptosis via loss of mitochondrial membrane potential, leading to both caspase-3-dependent and -independent pathways; transcription factor MZF-1 physically interacts with LDOC1 and enhances its pro-apoptotic activity. |
Phosphatidylserine externalization assay, mitochondrial membrane potential measurement, caspase-3 activity assay, co-immunoprecipitation (MZF-1/LDOC1 interaction) |
FEBS letters |
Medium |
15670815
|
| 2005 |
LDOC1 binds directly to the verprolin homology (V) domain of WAVE3; WAVE3 expression induces translocation of LDOC1 from the nucleus to the cytoplasm, inhibiting LDOC1-induced apoptosis; LDOC1-induced apoptosis is accompanied by increased p53 protein (not transcription), suggesting LDOC1 inhibits p53 degradation. |
Direct binding assay (pulldown), subcellular localization (fluorescence microscopy), apoptosis assay, p53 protein/mRNA analysis |
Journal of biochemistry |
Medium |
16272576
|
| 2013 |
Restored expression of BEX1 and LDOC1 in OSCC cells suppresses NF-κB signaling, specifically decreasing p50 and p65 expression, and exerts growth inhibitory effects in vitro and in vivo. |
Ectopic expression, NF-κB pathway analysis (western blot for p50/p65), in vivo tumor model |
The Journal of pathology |
Medium |
23362108
|
| 2014 |
Sirh7/Ldoc1 knockout mice show abnormal placental trophoblast giant cell (TGC) differentiation/maturation, leading to overproduction of placental progesterone (P4) and placental lactogen 1 (PL1), and delayed parturition with low pup weaning rate. |
Knockout mouse model, hormonal assays (P4, PL1 measurement), histological analysis of placenta |
Development (Cambridge, England) |
High |
25468940
|
| 2016 |
LDOC1 physically interacts with GNL3L (a nucleolar GTPase); ectopic LDOC1 expression destabilizes endogenous GNL3L and down-modulates GNL3L-induced cell proliferation; GNL3L upregulates NF-κB-dependent transcriptional activity via p65, which is reversed by co-expression of LDOC1. |
Co-immunoprecipitation (protein-protein interaction assays), ectopic expression/knockdown, NF-κB reporter assay, cell proliferation assay |
Cell cycle (Georgetown, Tex.) |
Medium |
27764577
|
| 2015 |
LDOC1 promoter is hypermethylated by cigarette smoke condensate (CSC) exposure via increased nuclear DNMT1 and DNMT3A accumulation; LDOC1 knockdown confers proliferative and clonogenic capacity on untransformed oral cells. |
Quantitative methylation-specific PCR, CSC treatment, DNMT immunofluorescence, loss-of-function knockdown with clonogenicity assay |
Oncotarget |
Medium |
26317789
|
| 2015 |
LDOC1 overexpression in PTC cells suppresses proliferation and induces apoptosis by inhibiting NF-κB activation; LDOC1-overexpressing cells recover responsiveness to TGF-β1 antiproliferative signaling. |
Lentiviral ectopic expression, NF-κB luciferase reporter assay, western blot (p65, IκBα, c-Myc, Bax, Bcl-xL), flow cytometry |
Journal of experimental & clinical cancer research : CR |
Medium |
26637328
|
| 2017 |
LDOC1 expression decreases Wnt5a levels in osteosarcoma cells and suppresses osteosarcoma cell migration and invasion in vitro; in a xenograft model, LDOC1 expression is associated with reduced lung metastasis. |
Lentiviral stable expression, transwell migration/invasion assay, qRT-PCR array for metastasis genes, xenograft model with micro-CT imaging |
Tumour biology |
Medium |
28240050
|
| 2019 |
LDOC1 forms protein complexes with phospho-JAK2 (pJAK2) and E3 ubiquitin ligase LNX1, targeting pJAK2 for ubiquitin-dependent proteasomal degradation; LDOC1 deficiency reduces LNX1-pJAK2 interaction, leading to ineffective pJAK2 ubiquitination and consequent STAT3 activation. |
Co-immunoprecipitation, immunofluorescent confocal microscopy, in vivo xenograft with phosphorylation analysis |
Cancers |
Medium |
30634502
|
| 2019 |
AML cell-derived exosomes deliver miR-4532 into hematopoietic stem cells (CD34+), where miR-4532 targets LDOC1 mRNA; loss of LDOC1 activates JAK2/STAT3 phosphorylation and increases DKK1, suppressing normal hematopoiesis; ectopic LDOC1 expression or JAK2 inhibition reverses these effects. |
miRNA target validation (luciferase/binding assay implied), gain- and loss-of-function in CD34+ HSCs, exosome co-culture, colony-forming unit assays, western blot for pJAK2/pSTAT3 |
Stem cell research & therapy |
Medium |
31842997
|
| 2019 |
LDOC1 overexpression in colorectal cancer cells inhibits Wnt/β-catenin signaling, reducing nuclear β-catenin levels and suppressing proliferation, migration, and invasion while promoting apoptosis. |
Lentiviral ectopic expression, western blot, cellular immunofluorescence for β-catenin localization, Transwell and Matrigel assays, flow cytometry |
Oncology reports |
Medium |
31002361
|
| 2020 |
LDOC1 deficiency increases Akt phosphorylation and subsequent inhibitory phosphorylation of GSK-3β (Ser9) upon Candida albicans stimulation, leading to increased IL-1β production; PI3K/Akt inhibitors or constitutively active GSK-3β (S9A mutant) reduce IL-1β in LDOC1-deficient cells, placing LDOC1 upstream of the PI3K/Akt/GSK-3β axis. |
Gain/loss-of-function (ectopic expression and knockdown), western blot for pAkt and pGSK-3β, pharmacological inhibitors (PI3K/Akt), active mutant GSK-3β (S9A) rescue experiment |
Cancers |
Medium |
33120999
|
| 2020 |
LDOC1 is translocated from the nucleus to the cytoplasm in human thyroid cancer; LDOC1 ablation in PTC cells facilitates nuclear p65 expression and NF-κB activity; NF-κB inhibition reverses the effects of LDOC1 ablation on proliferation, apoptosis, migration, and invasion. |
Subcellular fractionation/immunofluorescence, lentiviral KD and OE, NF-κB luciferase reporter, NF-κB inhibitor epistasis experiment |
Cell biology international |
Medium |
31889386
|
| 2024 |
LINC01270 acts as a competing endogenous RNA (ceRNA) for miR-326, maintaining LDOC1 expression; knockdown of LINC01270 downregulates LDOC1 and enhances NF-κB activity; luciferase reporter assay confirmed the LINC01270/miR-326/LDOC1 regulatory axis in NF-κB modulation. |
siRNA knockdown, luciferase reporter assay, RNA immunoprecipitation (RIP), synthetic RNA perturbation experiments |
Cells |
Low |
39682774
|
| 2025 |
LDOC1 loss in PFA1 ependymoma results from H3K27me3-mediated chromatin compaction at the LDOC1 locus; restoration of LDOC1 reduces proliferation, NF-κB signaling, and IL-6 secretion; in vivo competition assay showed LDOC1-transduced tumor cells were outcompeted, indicating loss of LDOC1 is required for PFA tumor growth. |
ChIP (H3K27me3), lentiviral LDOC1 restoration, NF-κB pathway analysis, IL-6 ELISA, in vivo tumor competition model |
Neuro-oncology |
Medium |
39901723
|
| 2026 |
LDOC1 physically interacts with histone H2B, H2Bub1, PSMA1, and THAP12; LDOC1 promotes proteasomal degradation of H2B and H2Bub1 via PSMA1, limiting global H2Bub1 levels; LDOC1 knockdown causes loss of chromatin-bound H2Bub1 and enhanced chromatin compaction partly through THAP12; the LDOC1-H2Bub1 axis regulates metastasis-related genes (cytoskeletal remodeling, cell adhesion, EMT); LDOC1 loss enhances TGF-β-induced epithelial-mesenchymal plasticity and promotes a hybrid E/M phenotype. |
Co-immunoprecipitation, proximity ligation assay, ChIP-seq, ATAC-seq, MNase digestion, transcriptomic profiling, immunofluorescence, flow cytometry, functional migration/adhesion assays |
Cell communication and signaling : CCS |
High |
41484780
|
| 2026 |
LDOC1 regulates STAT1 transcription and phosphorylation in an unexpected bidirectional manner: both gain- and loss-of-function of LDOC1 upregulate STAT1 transcription, revealing a novel role for LDOC1 in modulating STAT1-dependent pro-inflammatory signaling. |
Gain- and loss-of-function (siRNA and overexpression), RT-qPCR, western blot for pSTAT1, downstream target gene analysis |
International journal of molecular sciences |
Low |
41828328
|