CTBP1 Mouse Monoclonal Antibody
- Known as:
- CTBP1 Mouse Monoclonal Antibody
- Catalog number:
- BIN-001487-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CTBP1 Mouse Monoclonal Antibody
Related genes to: CTBP1 Mouse Monoclonal Antibody
- Gene:
- CTBP1 NIH gene
- Name:
- C-terminal binding protein 1
- Previous symbol:
- -
- Synonyms:
- BARS
- Chromosome:
- 4p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2016-10-05
- Gene:
- CTBP1-DT NIH gene
- Name:
- CTBP1 divergent transcript
- Previous symbol:
- C4orf42, CTBP1-AS1, CTBP1-AS2
- Synonyms:
- MGC21675
- Chromosome:
- 4p16.3
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2007-12-19
- Date modifiied:
- 2018-03-22
Related products to: CTBP1 Mouse Monoclonal Antibody
Related articles to: CTBP1 Mouse Monoclonal Antibody
- C-terminal binding protein 1 divergent transcript (CTBP1-DT) is a novel long non-coding RNA (lncRNA) located on human chromosome 4p16.3. Numerous studies have shown that CTBP1-DT plays a critical regulatory role in various human malignancies and non-malignant diseases. In several cancers, the expression of CTBP1-DT is upregulated, closely associated with the risk of 12 types of cancer, and strongly correlated with the clinical pathological features and poor prognosis of 10 of these cancers. Mechanistically, CTBP1-DT is stimulated by the transcription factors ETV5 and Sp1, or methylated by YTHDC1. By competitively inhibiting 12 microRNAs, it activates 3 signaling pathways that influence malignant behaviors of tumor cells, including proliferation, apoptosis, cell cycle arrest, migration, invasion, immune evasion, and chemoresistance. Importantly, it also encodes the microprotein DNA damage up-regulated protein (DDUP), which mediates cisplatin resistance through sustained response to DNA damage signals. Furthermore, CTBP1-DT has been implicated in the progression of non-malignant diseases such as diabetes and related conditions, cardiovascular diseases, and osteoarthritis. This review summarizes the latest research on the RNA and protein functions of CTBP1-DT in human diseases, outlines various molecular regulatory networks centered around CTBP1-DT, and discusses the opportunities and challenges of its clinical applications. - Source: PubMed
Publication date: 2025/02/26
Yang Jingjie - Colorectal cancer, which originates from the human colon or rectum, is one of the leading causes of death worldwide. Timely diagnosis and interventional therapy can significantly improve the prognostic survival of colorectal cancer patients, making regular screening and early detection essential. - Source: PubMed
Publication date: 2024/06/12
Fan RuizhiXu TengKuang Yuting - Recently, mounting evidence has highlighted the essential function of the C-terminal binding protein-1 divergent transcript (CTBP1-DT) in malignancies. However, its role in kidney renal clear cell carcinoma (KIRC) remains largely unknown. Our study aimed to identify the potential function of CTBP1-DT in KIRC. RT-qPCR, Kaplan-Meier survival analysis, Cox regression analysis, and nomogram analysis were utilized to determine the expression and effects of CTBP1-DT on survival. The subcellular localization of CTBP1-DT was determined using RNA fluorescence in situ hybridization (FISH). To investigate the functions of CTBP1-DT in regulating KIRC cell proliferation, migration, invasion, lipid synthesis, and apoptosis, we conducted CCK8, EdU, Transwell, and Oil Red O staining and cell apoptosis staining assays. The relationships between CTBP1-DT and the tumor microenvironment were investigated with multiple bioinformatics analysis algorithms and databases, including CYBERSORT, TIMER2, Spearman correlation test, tumor mutation burden (TMB), microsatellite instability (MSI), and immunophenoscore (IPS). According to our results, CTBP1-DT is a lncRNA located in the nucleus that is significantly upregulated in KIRC and is correlated with better clinical outcomes. Downregulating CTBP1-DT inhibited cell viability, migration, invasion, and lipid synthesis but triggered cell apoptosis. Additionally, we explored the potential effect of CTBP1-DT in regulating immune cell infiltration in KIRC and other malignancies. Furthermore, CTBP1-DT could be used to predict the effectiveness of targeted drugs and immune checkpoint inhibitors. In conclusion, we identified CTBP1-DT as a potential immunological biomarker and discovered the potential role of CTBP1-DT in regulating lipid synthesis and apoptosis resistance. - Source: PubMed
Publication date: 2024/03/21
Li HaolinFei MintianZhang YiXu QiliFeng RuiCao JingQu YanXiao Haibing - Sustained activation of DNA damage response (DDR) signaling has been demonstrated to play vital role in chemotherapy failure in cancer. However, the mechanism underlying DDR sustaining in cancer cells remains unclear. In the current study, we found that the expression of the DDUP microprotein, encoded by the CTBP1-DT lncRNA, drastically increased in cisplatin-resistant ovarian cancer cells and was inversely correlated to cisplatin-based therapy response. Using a patient-derived human cancer cell model, we observed that DNA damage-induced DDUP foci sustained the RAD18/RAD51C and RAD18/PCNA complexes at the sites of DNA damage, consequently resulting in cisplatin resistance through dual RAD51C-mediated homologous recombination (HR) and proliferating cell nuclear antigen (PCNA)-mediated post-replication repair (PRR) mechanisms. Notably, treatment with an ATR inhibitor disrupted the DDUP/RAD18 interaction and abolished the effect of DDUP on prolonged DNA damage signaling, which resulted in the hypersensitivity of ovarian cancer cells to cisplatin-based therapy in vivo. Altogether, our study provides insights into DDUP-mediated aberrant DDR signaling in cisplatin resistance and describes a potential novel therapeutic approach for the management of platinum-resistant ovarian cancer. - Source: PubMed
Publication date: 2023/08/26
Ren LiangliangQing XingrongWei JihongMo HaixinLiu YuanjiZhi YaofengLu WenjieZheng MingzhuZhang WeijianChen YuanZhang YuejiaoPan TaijinZhong QianLi RonggangZhang XinRuan XiaohongYu RuyuanLi Jun - Esophageal carcinoma (ESCA) is one of the most prevalent malignant tumors in the world. The prognosis of patients has significantly improved with the development of surgery, targeted therapy and immunotherapy. But the 5-year survival rate of ESCA patients is still incredibly low. Cuproptosis is a type of mitochondrial cell death induced by copper. It is unclear how cuproptosis-related lncRNAs (CRLs) affect ESCA prognosis. In this study, we obtained the clinical data of ESCA patients, the transcriptome data from TCGA and identified CRLs by co-expression analysis, lasso regression, and cox regression analysis, to build a prognostic model. Then we validated the prognostic model using the Kaplan-Meier curve, cox regression analysis, and ROC, to create a nomogram based on risk score to forecast the prognosis of ESCA. Next, the immune escape of the CRLs was examined using the TIDE algorithm to assess its sensitivity to possible ESCA medications. To predict the prognosis of ESCA patients, we created a predictive model using 6 CRLs (AC034199.1, AC125437.1, AC107032.2, CTBP1-DT, AL024508.1, and AC008610.1), validated by the Kaplan-Meier and ROC curves. The model has a higher diagnostic value compared to other clinical features. The 6 CRLs expressed high in TCGA and ESCA specimens. Enrichment analysis revealed CRLs largely contributed to the interaction between cytokines and their receptors as well as complement coagulation cascades. The immunity escape analysis demonstrated that immunotherapy had a worse effect in the low-risk group than in the high-risk group. Additionally, we screened out potential antineoplastic drugs according to the results of the immunoassay and obtained 5 drugs, including CP-466722, crizotinib, MS-275, KIN001-135, and CP-466722. The prognosis of patients with ESCA can be correctly predicted by the 6 CRLs chosen from this investigation. It lays the groundwork for more investigation into the ESCA mechanism and the identification of novel therapeutic targets. - Source: PubMed
Publication date: 2023/04/13
Zhang LimingZong LingLi WenhuiNing LuZhao YajunWang ShaoqiangWang Lina