TRIP13 Control Peptide antibody _CP
- Known as:
- TRIP13 Control Peptide (anti-) _CP
- Catalog number:
- 'AP12502CP-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- TRIP13 Control Peptide antibody _CP
Related genes to: TRIP13 Control Peptide antibody _CP
- Gene:
- TRIP13 NIH gene
- Name:
- thyroid hormone receptor interactor 13
- Previous symbol:
- -
- Synonyms:
- 16E1BP
- Chromosome:
- 5p15.33
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-04
- Date modifiied:
- 2016-10-05
Related products to: TRIP13 Control Peptide antibody _CP
Related articles to: TRIP13 Control Peptide antibody _CP
- - Source: PubMed
Publication date: 2026/07/31
Wu YanyanGuo XuanyanJin LiHuang GuixiangNiu LiangboZhao Yu - Multiple myeloma (MM) is a malignant disorder of plasma cells. Combinations of bortezomib (BTZ) with other therapeutic agents remain the mainstay of MM treatment. However, the rising incidence of drug resistance among patients with MM underscores an urgent need for novel therapeutic strategies. The present study identified triptonide (TN), a small‑molecule monomer extracted from the traditional Chinese herb Hook. f., as a synergistic agent that enhanced the anti‑MM activity of BTZ, following a screening of 198 compounds from a ubiquitination‑focused library. TN effectively inhibited cell proliferation, induced apoptosis, and reduced cell viability in MM cells. Furthermore, the synergistic anti‑MM effect between TN and BTZ was validated across MM cell lines, primary MM cells, and xenograft mouse models of MM. Mechanistic investigations revealed that TN synergizes with BTZ by enhancing DNA damage through the suppression of TRIP13‑mediated DNA repair pathways, including non‑homologous end joining and homologous recombination. Notably, TRIP13 knockdown attenuated TN‑induced DNA damage and apoptosis, and diminished the synergistic effect of TN and BTZ on MM cells. Collectively, TN represents a novel anti‑MM agent, and the combination of TN with BTZ constitutes a promising therapeutic strategy for the treatment of MM. - Source: PubMed
Publication date: 2026/07/17
He FenLi JunjunPeng LijunZhao HongyanLu MaoyouGao RuixinWang SiqiChen YuTang RuihanLi ZhengguoZhang LinlinZhang XinyuLi QianhaoChen WeihuiLiu JiayuLuo CongZeng XiXia Jiliang - Ovarian cancer (OC) is associated with high mortality and frequent resistance to poly (ADP-ribose) polymerase inhibitors, such as Olaparib, particularly in patients with breast cancer gene-proficient tumors. To explore the potential mechanisms underlying Olaparib resistance, Olaparib-resistant OC cell lines were established through stepwise drug induction. Candidate resistance-related genes were screened using bioinformatic analyses and subsequently validated in clinical specimens. Their biological functions and underlying mechanisms were further investigated through gene silencing, coimmunoprecipitation, immunofluorescence, comet assays, and an OVCAR3 xenograft model. Bioinformatic analyses indicated that thyroid hormone receptor interactor 13 (TRIP13) and kinetochore-associated 1 (KNTC1) were highly expressed in Olaparib-resistant cells and were associated with poor prognosis. Their elevated expression was further confirmed by real-time quantitative polymerase chain reaction, Western blotting, and immunohistochemistry. Functional studies showed that silencing either TRIP13 or KNTC1 inhibited cell proliferation and induced apoptosis in Olaparib-resistant OC cells. Mechanistically, coimmunoprecipitation and immunofluorescence analyses confirmed a cytoplasmic interaction between TRIP13 and KNTC1. TRIP13 knockdown impaired nonhomologous end joining (NHEJ)-mediated DNA repair, as evidenced by decreased expression of NHEJ-related proteins, increased γH2AX accumulation, and enhanced comet tail formation. Conversely, TRIP13 overexpression promoted NHEJ repair and reduced Olaparib-induced DNA damage, whereas these effects were partially reversed by the NHEJ inhibitor SCR130. In vivo, TRIP13 overexpression promoted tumor growth and reduced sensitivity to Olaparib, whereas KNTC1 knockdown reversed these effects. Collectively, these findings suggest that TRIP13 and KNTC1 cooperatively promote NHEJ-mediated DNA repair, thereby contributing to Olaparib resistance in breast cancer gene-proficient OC. Targeting the TRIP13/KNTC1 axis may therefore enhance the therapeutic efficacy of Olaparib and provide a promising strategy for overcoming poly (ADP-ribose) polymerase inhibitor resistance. SIGNIFICANCE STATEMENT: Olaparib resistance remains a major obstacle to effective ovarian cancer treatment. This study demonstrates that the thyroid hormone receptor interactor 13/kinetochore-associated 1 axis promotes Olaparib resistance in ovarian cancer by enhancing nonhomologous end joining-mediated DNA damage repair. Targeting this axis restored Olaparib sensitivity in resistant cells, thereby highlighting thyroid hormone receptor interactor 13/kinetochore-associated 1 as a potential therapeutic target for improving the response to poly (ADP-ribose) polymerase inhibitors. - Source: PubMed
Publication date: 2026/06/16
Guo XingziTang JieLi HeMao SaipingTang Yan-XiangTang Zhen-ZiGong Lianghui - BackgroundOvarian cancer remains one of the most lethal gynecological malignancies, largely due to delayed diagnosis and limited effectiveness of current biomarkers. Identifying candidate biomarkers through integrated gene expression analysis may enhance understanding of OC biology and support future diagnostic and prognostic investigations.MethodsFour microarray datasets were retrieved from the Gene Expression Omnibus and analyzed using the limma package in R to identify differentially expressed genes (DEGs) through a bidirectional filter (|logFC| ≥ 1.2). Overlapping DEGs across all four datasets were subjected to Gene Ontology and KEGG pathway enrichment analyses. Protein-protein interaction networks were constructed using the STRING database, and hub genes were identified by consensus across three centrality algorithms in Cytoscape. Prognostic significance was evaluated using Kaplan-Meier survival analysis via GEPIA2; diagnostic performance was assessed using Youden Index-based ROC analysis; and external validation was performed using an independent dataset.ResultsA total of 209 overlapping DEGs were identified, yielding 35 hub genes. Functional enrichment analysis implicated cell cycle dysregulation, metabolic reprogramming, and extracellular matrix remodeling as central biological processes. TRIP13, FGF13, and LYVE1 were significantly associated with overall survival, while ALDH1A1, GATA6, and WNT5A were associated with disease-free survival. KDR demonstrated the highest diagnostic accuracy, and external validation confirmed the generalizability of the diagnostic findings.ConclusionThis study identifies a panel of candidate diagnostic and prognostic biomarkers in ovarian cancer, providing a molecular framework for future experimental validation and translational investigation. - Source: PubMed
Publication date: 2026/07/14
Woode MichaelAppah Mark AkuamoahAlhassan Emmanuel KpalakusoMakwo TimothyAsante Du-BoisAgyirifo Daniel Sakyi - Early and accurate diagnosis remains a major challenge in cervical cancer management. This study aimed to identify reliable diagnostic biomarkers for cervical cancer by integrating bioinformatics and machine learning approaches and to further validate their biological relevance experimentally. Transcriptomic data from the Gene Expression Omnibus and The Cancer Genome Atlas were analyzed using differential expression analysis, weighted gene co-expression network analysis, and three machine learning algorithms to identify core genes. Diagnostic performance was evaluated using receiver operating characteristic curves and a nomogram model. Functional relevance was explored by drug sensitivity analysis, ssGSEA, immune infiltration analysis, and single-cell RNA sequencing. RT-qPCR validation was performed in 10 paired cervical cancer and adjacent normal tissues, while Western blotting was performed in three paired tissue samples. In vitro validation was conducted using SiHa and HeLa cells. Four genes, CCND1, TRIP13, MYBL2, and GNB4, were identified as potential diagnostic biomarkers, and the combined model showed superior diagnostic performance compared with any single gene (AUC = 0.989). Treatment with 3-methyladenine altered the expression of these genes, suggesting their potential association with PI3K/AKT-related pathway activity. Moreover, siRNA-mediated GNB4 knockdown suppressed cervical cancer cell proliferation and reduced PI3K and AKT phosphorylation, providing preliminary evidence for the functional involvement of GNB4 in PI3K/AKT pathway activation. CCND1, TRIP13, MYBL2, and GNB4 may serve as promising diagnostic biomarkers for cervical cancer. Their dysregulation was associated with PI3K/AKT pathway activity and may reflect molecular alterations involved in cervical cancer progression. In particular, GNB4 showed potential diagnostic relevance and preliminary functional significance, suggesting that it may represent a candidate biomarker and molecular target for further investigation. - Source: PubMed
Publication date: 2026/06/23
Zhang HailongXie LuhongLiu YamengYang HanlinMin ShaojuZhu YurongRen JieLi XuehuiTan Yujie