CBX8
- Known as:
- CBX8
- Catalog number:
- Y214058
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CBX8
Related genes to: CBX8
- Gene:
- CBX8 NIH gene
- Name:
- chromobox 8
- Previous symbol:
- -
- Synonyms:
- RC1, HPC3, PC3
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-25
- Date modifiied:
- 2015-11-24
Related products to: CBX8
Related articles to: CBX8
- Colorectal cancer (CRC) is among the most common cancers worldwide. Cellular senescence, characterized by an irreversible state of growth arrest, has been recognized as a promising therapeutic strategy for combating cancer. Here, the oncogenic role of Chromobox homolog 8 (CBX8) in CRC and its regulatory mechanisms in cell senescence and transcriptional regulation were systematically investigated. We demonstrated that CBX8 deficiency suppresses colorectal tumorigenesis and promotes tumor cell senescence in both and models. Mechanistically, CBX8 inhibits autophagy-dependent senescence in CRC by modulating the mTOR signaling pathway through transcriptional repression of DDIT4, a known negative regulator of mTOR. CBX8 achieves this by recruiting TRIM28 to bind the promoter region of DDIT4, thereby maintaining the H3K27me3 modification status and repressing expression of DDIT4. Furthermore, our findings highlight the therapeutic potential of CBX8 inhibitors in combination with senescence-targeting agents, which significantly enhances antitumor effects in CRC xenograft models. These results provide novel insights into the molecular mechanisms underlying CRC progression and underscore the potential of CBX8 as a therapeutic target for developing targeted therapies and senolytic-based anticancer strategies. This study advances our understanding of CRC pathogenesis and offers promising directions for precision medicine in CRC treatment. - Source: PubMed
Publication date: 2026/02/26
Li TiankangZhang EnjianLiu XinZhou HuiZhang PengboZhang ChongZhang XiuzhongWu NaiGong ShuaiRen ZeqiangDing JieZhang Yi - Targeted covalent inhibitors (TCIs) are increasingly popular as drug candidates and chemical probes. Among current TCIs, the chemistry is largely limited to cysteine and lysine side chain reactivity. Here, we investigated the utility of cyclic imine Mannich electrophiles as covalent warheads to target protein tyrosine and tryptophan side chains. We characterized the intrinsic reaction rates of several cyclic imines to tyrosine and other amino acid side chains and validated reactivity using protein affinity labeling of a cyclic imine-modified trimethoprim with tyrosine and tryptophan mutants of E. coli dihydrofolate reductase. To validate the utility of the approach, we appended cyclic imine warheads to a CBX8 chromodomain inhibitor to label a non-conserved tyrosine, which improved both the potency and selectivity of the inhibitor for CBX8 in vitro and in cells. These findings indicate that Mannich electrophiles are promising and robust chemical warheads for tyrosine and tryptophan bioconjugation and development of covalent inhibitors. - Source: PubMed
Publication date: 2026/01/28
Wang SijieWang LeiHadisurya MarcoNia Siavash ShahbaziTao W AndyDykhuizen Emily CKrusemark Casey J - Direct reprogramming of fibroblasts into cardiomyocytes by overexpressing cardiac transcription factors Gata4, Mef2c, and Tbx5 (GMT) is a promising way for cardiac repair, however, the low reprogramming efficiency remains a significant challenge. Cellular senescence, an irreversible cell-cycle arrest occurring in mitotic cells, has been reported to influence the efficiency of induced pluripotent stem cell (iPSC) reprogramming. - Source: PubMed
Publication date: 2025/12/29
Fang JuntaoYang QiangbingMaas Renée G CVader PieterMokry Michalvan den Dungen Noortje A MQian LiXiao JunjieSchiffelers RaymondLei ZhiyongSluijter Joost P G - To assess the efficacy and safety of azacitidine combined with lenalidomide in MDS patients and explore potential mechanisms of therapeutic response. Sixteen MDS patients with TP53 mutations received azacitidine plus lenalidomide at ZhongDa Hospital, Southeast University (January 2021-June 2025). Efficacy and safety were assessed, and TP53 mutation status was correlated with treatment response. Whole-transcriptome sequencing and bioinformatics were used to explore molecular biomarkers associated with therapeutic efficacy. Sixteen patients (median age 69.5 years, range 52-82; 8 males, 8 females) were enrolled. According to the Molecular International Prognostic Scoring System (IPSS-M), 1, 2, and 13 patients were classified as median low, high, and very high risk, respectively. Among 16 TP53-mutated patients, 11 had biallelic mutations and 5 had monoallelic mutations. Overall response rate was 56.3% (9/16), composite complete remission rate (CRc) was 31.3% (5/16), and hematology improvement rate was 25% (4/16). Among TP53-mutated patients, the response rate was 56.3% (9/16), with variant allele frequency dropping from 65.6% to 16.5% in responders (=0.017). In patients with TP53 mutations and complex karyotype, response rate was 53.8% (7/13), with 57.1% (4/7) showing disappearance of CK post-treatment. The most common grade 3-4 nonhematologic adverse events were infections (9/16, 56.3% ), including pneumonia (4/16, 25.0% ), gastrointestinal infections (3/16, 18.8% ), perianal infections (1/16, 6.3% ) and sepsis (1/16, 6.3% ). High CBX8 expression may be linked to treatment response. Azacitidine plus lenalidomide is an effective and safe therapy for MDS, including patients with TP53 mutations and complex karyotypes. Treatment markedly reduces TP53 variant allele frequency in responders, and high CBX8 expression may predict therapeutic response. - Source: PubMed
Yan XGuo C HYang CLin C QSong D DCai Z MWang YWang LGe Z - The Polycomb group (PcG) protein chromobox 8 (CBX8) is the subunit of Polycomb repressive complex 1 (PRC1) and recognizes the trimethylation of histone H3 on Lysine 27 (H3K27me3), and coordinates with PRC2 complex to function as an epigenetic gene silencer. CBX8 plays a key role in cell proliferation, stem cell biology, cell senescence, and cancer development. However, the post-translational modifications of CBX8 remain poorly understood. Here, we report that protein kinase D1 (PKD1) interacts and phosphorylates CBX8 at Thr234 and Ser256 /311 residues. PKD1-mediated CBX8 phosphorylation at Thr234 reduced its expression level by promoting its ubiquitination-mediated degradation, whereas Ser256/311 phosphorylation decreased CBX8 binding to other PRC1 components BMI1 and RING1A. Overall, CBX8 phosphorylation by PKD1 impaired PRC1 complex integrity and activity, mitigated H2AK119ub1 level, caused the upregulation of multiple target genes repressed by CBX8, and decreased CBX8, H2AK119ub1, and H3K27me3 enrichment at INK4A/ARF locus, thereby derepressing p16 and facilitating cellular senescence. Collectively, these results suggest that PKD1-mediated CBX8 phosphorylation at T234 and S256/311 is a key mechanism governing CBX8 function, including cell senescence. - Source: PubMed
Publication date: 2025/12/15
Fang ZhiqiangLiu DoudouSu YuanyuanHao FengxinQin RuodongLi GuodongChen Jun