| 2008 |
CAP-G (NCAPG) contains two threonine residues (Thr308 and Thr332) that are phosphorylated by cdc2/cyclin B. Mutation of these threonines to alanines results in defects in CAP-G localization with chromosomal DNA during mitosis, establishing phosphorylation as a regulator of condensin chromosomal localization. |
Site-directed mutagenesis (T308A, T332A), in vitro cdc2/cyclin B kinase assay, immunofluorescence localization during mitosis |
Biochemical and biophysical research communications |
High |
18977199
|
| 2004 |
Drosophila condensin subunit Cap-G (ortholog of NCAPG) physically interacts with the centromere-specific histone H3 variant CID (CENP-A homolog), as shown by yeast two-hybrid. Loss-of-function Cap-G mutant embryos show massive sister chromatid segregation defects during mitosis, linking condensin to kinetochore structure and chromatid segregation. |
Genetic modifier screen (rough eye phenotype), yeast two-hybrid interaction assay, analysis of Cap-G mutant embryo mitosis |
Chromosoma |
Medium |
15592865
|
| 2013 |
Drosophila Cap-G associates exclusively with condensin I and not condensin II. In vivo, Cap-G-EGFP shows nuclear enrichment during interphase, but this nuclear localization is dispensable for chromatin association, condensin I complex assembly, and animal viability. Mass spectrometry of condensin II-specific subunit Cap-H2 immunoprecipitates failed to detect Cap-G. |
Immunoprecipitation, in vivo EGFP fusion microscopy, mass spectrometry, in vitro complex formation assays |
PLoS genetics |
High |
23637630
|
| 2016 |
In budding yeast, Ycg1 (Cap-G/NCAPG ortholog) is cell-cycle regulated with protein levels peaking in mitosis and decreasing in G1, controlled by cell-cycle-regulated transcription and constitutive degradation. Ycg1 is limiting for condensin complex formation: overexpression of Ycg1 (but not other condensin subunits) increases intact condensin complex levels and chromatin binding in G1, causing delayed cell-cycle entry and proliferation defects. |
Cell cycle synchronization, Western blotting, chromatin immunoprecipitation (ChIP), overexpression and stabilizing mutation analysis in S. cerevisiae |
PLoS genetics |
High |
27463097
|
| 2019 |
Solution SAXS characterization of the condensin HEAT-repeat subunit Ycg1 (Cap-G/NCAPG ortholog) reveals it is flexible in solution as a free subunit but becomes considerably more rigid upon binding its kleisin partner Brn1. Free Ycg1 tends to oligomerize at higher concentrations in the absence of Brn1. |
Small-angle X-ray scattering (SAXS), dynamic and static multiangle light scattering, normal mode analysis structural modeling |
The Journal of biological chemistry |
High |
31350339
|
| 1995 |
Human macrophage Cap G (CAPG/NCAPG alias) caps but does not sever actin filaments. Gain-of-function mutations converting residues 84LNTLLGE to the gelsolin actin-binding helix sequence (84LDDYLGG) conferred actin-severing activity; adding a second mutation converting 124AFHKTS to 124GFKHV enhanced severing 10-fold. These two regions are critical determinants of the lack of severing activity in wild-type Cap G. |
Site-directed mutagenesis, in vitro actin filament severing assay |
The Journal of biological chemistry |
High |
7814409
|
| 1994 |
The human Cap G gene (CAPG, an alias for NCAPG in the gelsolin-family context) is 16.6 kb, contains 10 exons and 9 introns, and maps to chromosome 2p. Comparison of splice sites with gelsolin and villin indicates CAPG is more closely related to gelsolin. |
Genomic cloning, sequencing, chromosomal mapping, comparative gene structure analysis |
Genomics |
Medium |
7851883
|
| 2003 |
Cap G (gelsolin-family macrophage capping protein) protein and mRNA are upregulated ~2-fold and ~5-fold, respectively, in endothelial cells exposed to atheroprotective (plaque-free) unidirectional shear stress compared to static culture; this increase is absent under plaque-prone flow. The increase occurs in nuclear and cytoskeletal-associated fractions. Overexpression of Cap G in transfection assays increased endothelial cell motility. |
2D gel proteomics, quantitative RT-PCR, subcellular fractionation, transfection overexpression motility assay |
The Journal of biological chemistry |
Medium |
12754261
|
| 2019 |
NCAPG (condensin I subunit) knockdown in HCC cells causes aberrant mitotic division, fragmentation of the mitochondrial network, and increased cell death in vitro; genome-wide CRISPR dropout screens ranked NCAPG as the highest essential gene for HCC growth. Small interfering RNA knockdown reduced cell growth, migration, and downregulated mitochondrial gene expression. |
Genome-wide CRISPR knockout dropout screen, siRNA knockdown, xenograft tumor model, mitochondrial network imaging |
FASEB journal |
High |
31022357
|
| 2017 |
NCAPG knockdown induces mitotic defects and inhibits HCC cell growth, proliferation, and migration in vitro; tetracycline-inducible shRNA knockdown inhibits tumor growth in vivo. NCAPG overexpression is correlated with overexpression of CCNB1 (cyclin B1), a mitotic regulatory protein. |
siRNA and inducible shRNA knockdown, cell proliferation assay, wound-healing migration assay, xenograft tumor model, expression correlation analysis |
Oncology research |
Medium |
29046167
|
| 2019 |
NCAPG overexpression activates the PI3K/AKT/FOXO4 pathway and alters expression of apoptosis-related proteins in HCC cells. The PI3K inhibitor LY294002 abolished NCAPG-mediated promotion of proliferation and reduction of apoptosis, while the PI3K activator 740Y-P had the opposite effect, placing NCAPG upstream of PI3K/AKT/FOXO4 in HCC proliferation signaling. |
siRNA knockdown and plasmid overexpression, EdU proliferation assay, flow cytometry apoptosis, RNA-seq pathway analysis, PI3K inhibitor/activator rescue experiments, Western blotting, xenograft model |
OncoTargets and therapy |
Medium |
31802891
|
| 2020 |
NCAPG overexpression in HER2-positive breast cancer cells promotes trastuzumab resistance by phosphorylating SRC and enhancing nuclear localization and transcriptional activation of STAT3, establishing NCAPG as an upstream activator of the SRC/STAT3 signaling pathway. |
Overexpression and siRNA knockdown, Western blotting for phospho-SRC and nuclear STAT3, cell proliferation/apoptosis assays, in vivo xenograft, immunofluorescence for STAT3 nuclear localization |
Cell death & disease |
Medium |
32683421
|
| 2022 |
NCAPG physically interacts with β-catenin in colorectal cancer cells, activating the Wnt/β-catenin signaling pathway to promote EMT, proliferation, migration, and invasion. |
Co-immunoprecipitation (Co-IP), immunofluorescence, Western blotting, siRNA knockdown and overexpression |
Cancer cell international |
Medium |
35292013
|
| 2022 |
NCAPG promotes HCC proliferation by interacting with CKII (casein kinase II). Their interaction was identified by IP-mass spectrometry and confirmed by Co-IP. NCAPG-CKII interaction promotes PTEN phosphorylation, thereby inhibiting PTEN transcription and function and activating the PI3K/AKT pathway. |
IP-mass spectrometry, Co-immunoprecipitation, transcriptome sequencing, EdU and CCK-8 proliferation assays, FISH, xenograft model |
Journal of translational medicine |
Medium |
35864529
|
| 2020 |
NCAPG silencing in fetal bovine myoblasts prolongs mitosis and impairs differentiation through increased apoptosis. ATAC-seq revealed that NCAPG knockdown alters chromatin accessibility at AP-1 (activating protein 1) binding sites, and knockdown of AP-1 subunits FOSL2 or JUNB partially phenocopied the effect on muscle-specific gene expression. |
siRNA knockdown, ATAC-seq, immunofluorescence, gene expression quantification, AP-1 subunit knockdown |
International journal of molecular sciences |
Medium |
32070024
|
| 2021 |
NCAPG overexpression in lung adenocarcinoma increases phospho-Smad2 and phospho-Smad3 in the TGF-β signaling pathway. Rescue experiments showed that TGF-β pathway inhibitors restored the effect of NCAPG overexpression, placing NCAPG upstream of TGF-β/Smad signaling in LUAD. |
siRNA knockdown and overexpression, Western blotting for p-Smad2/p-Smad3, TGF-β inhibitor rescue, in vitro and in vivo functional assays |
Cancer cell international |
Medium |
34419073
|
| 2022 |
NCAPG promotes NSCLC progression via the NCAPG/CDK1/ERK axis: NCAPG interacts with CDK1, and this interaction promotes phosphorylation of ERK, driving cell growth and metastasis in vitro and in vivo. |
Co-immunoprecipitation, Western blotting for phospho-ERK, siRNA knockdown, xenograft model |
American journal of cancer research |
Low |
39659935
|
| 2023 |
E2F1 transcription factor directly binds the NCAPG promoter and transactivates NCAPG expression in HCC. E2F1 binding was confirmed by ChIP and luciferase reporter assay; HBx transfection co-upregulated both E2F1 and NCAPG. NCAPG knockdown promotes NLRP3 inflammasome-mediated pyroptosis in HCC cells. |
Dual luciferase reporter assay, chromatin immunoprecipitation (ChIP), Western blotting, scanning electron microscopy for pyroptosis, siRNA knockdown, xenograft model |
Journal of clinical and translational hepatology |
Medium |
38250463
|
| 2023 |
CBX3 transcriptionally regulates NCAPG expression in colorectal cancer, as demonstrated by predicted CBX3 binding sites in the NCAPG promoter and luciferase reporter assay confirming promoter activity. CBX3-mediated NCAPG expression activates Wnt/β-catenin signaling to regulate CRC cell proliferation, cell cycle, and apoptosis. |
Luciferase reporter assay, RT-qPCR, Western blot, CCK-8, flow cytometry, TUNEL assay, caspase activity assay |
Journal of gastrointestinal oncology |
Low |
37201048
|
| 2024 |
CREB1 and MYOD1 bind to the core promoter region (-598/+87) of bovine NCAPG and activate its transcription, as established by deletion reporter assays, site-directed mutagenesis of binding sites, overexpression experiments, and electrophoretic mobility shift assay (EMSA). |
Deletion fragment dual-luciferase reporter assay, site-directed mutagenesis, overexpression, EMSA |
International journal of molecular sciences |
Medium |
38473754
|
| 2025 |
ASPM directly binds NCAPG and promotes its transport from the nucleus to the cytoplasm in gastric cancer cells. ASPM also enhances deubiquitination of NCAPG mediated by BUB3, increasing NCAPG protein levels. Elevated NCAPG then activates the SRC/STAT3 pathway and elevates PD-L1 expression, contributing to immune evasion. |
Co-immunoprecipitation, mass spectrometry, molecular docking, CUT&Tag, transcriptome sequencing, subcellular fractionation/localization, organoid and in vivo experiments |
Journal of translational medicine |
Medium |
40898336
|
| 2025 |
NCAPG promotes EC (endometrial cancer) progression by affecting LEF1 binding to chromatin, thereby activating transcription of SEMA7A. SEMA7A then binds the PI3K regulatory subunit p85 to activate PI3K-AKT signaling, establishing the NCAPG/LEF1/SEMA7A/PI3K-AKT axis. |
ATAC-seq, chromatin immunoprecipitation-qPCR (ChIP-qPCR), Co-immunoprecipitation, functional in vitro and in vivo assays |
Journal of Cancer |
Medium |
39744480
|
| 2025 |
NCAPG promotes ferroptosis resistance in HCC by interacting with NSUN2 at its 446aa–460aa region, inhibiting NSUN2 protein degradation. NSUN2 then promotes m5C modification of GPX4 mRNA at its coding sequence, stabilizing GPX4 mRNA and increasing GPX4 expression to confer ferroptosis resistance. |
Co-immunoprecipitation, domain-mapping of NCAPG-NSUN2 interaction, m5C modification assay, GPX4 mRNA stability assay, NSUN2 knockdown rescue, in vivo and in vitro ferroptosis assays |
Cellular signalling |
Medium |
41260238
|
| 2026 |
Bufalin acts as a molecular glue that specifically degrades NCAPG by coupling it to cathepsin V (CTSV), forming a CTSV-NCAPG complex. This degradation induces G2/M cell cycle arrest and inhibits HCC cell proliferation without triggering apoptosis. Downstream proliferation regulators Cyclin D1 and CDK1 are regulated by bufalin in a CTSV/NCAPG-dependent manner. |
Co-immunoprecipitation, confocal microscopy, siRNA knockdown of CTSV and NCAPG, cell cycle analysis, CCK-8 proliferation assay, Western blotting |
Drug development research |
Medium |
41586569
|
| 2022 |
NCAPG knockdown in bladder cancer cells inhibits proliferation through suppression of the NF-κB signaling pathway, as demonstrated by RNA-seq identifying NF-κB as a downstream pathway and verified by luciferase reporter assay and Western blotting. |
RNA-seq, NF-κB luciferase reporter assay, Western blotting, siRNA knockdown, xenograft model, soft agar assay |
Biochemical and biophysical research communications |
Low |
35843088
|
| 2023 |
NCAPG knockdown in neuroblastoma activates p53-mediated apoptosis and induces G2/S cell cycle arrest, establishing NCAPG as a suppressor of p53-dependent apoptotic signaling. |
siRNA knockdown, flow cytometry cell cycle analysis, apoptosis assay, Western blotting for p53 pathway proteins |
International journal of molecular sciences |
Low |
37834394
|
| 2022 |
NCAPG promotes lung cancer oncogenesis through upregulation of LGALS1 (Galectin-1), and LGALS1 may interact directly with NCAPG. Ncapg+/- mice showed reduced urethane-induced lung tumor formation compared to wild-type, demonstrating an in vivo requirement for NCAPG in lung tumorigenesis. |
Transcriptome sequencing, Ncapg heterozygous mouse model with urethane carcinogenesis, siRNA knockdown, in vivo xenograft, IHC |
Molecular cancer |
Medium |
35180865
|