Tnks 2 Antibody (C-term)
- Known as:
- Tnks 2 Antibody (C-terminus)
- Catalog number:
- AP5313b
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- Tnks 2 Antibody (C-term)
Related genes to: Tnks 2 Antibody (C-term)
- Gene:
- TNKS NIH gene
- Name:
- tankyrase
- Previous symbol:
- -
- Synonyms:
- TIN1, TINF1, TNKS1, PARP-5a, PARP5A, pART5
- Chromosome:
- 8p23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-08
- Date modifiied:
- 2016-03-01
Related products to: Tnks 2 Antibody (C-term)
Related articles to: Tnks 2 Antibody (C-term)
- Endometrial cancer (EC) incidence continues to rise, underscoring the need for effective therapies beyond BRCA-mutant disease. Although PTEN loss, a frequent alteration in EC, has been implicated in impaired homologous recombination and increased sensitivity to PARP inhibitors, responses to PARP inhibitor monotherapy remain variable and are often limited by resistance mechanisms in PTEN-deficient tumours. Here, we show that the dual PARP/tankyrase (TNKS) inhibitor JPI-547 exerts potent antitumor activity, particularly in PTEN-deficient Ishikawa tumours. In vitro, JPI-547 and olaparib more effectively reduced cell survival in PTEN-deficient cells, and combined treatment with olaparib and the TNKS inhibitor XAV-939 induced synergistic cytotoxicity with elevated DNA double-strand breaks. Dual PARP/TNKS inhibition did not further suppress RAD51 but modulated non-homologous end joining and attenuated Wnt/β-catenin signalling in a PTEN-dependent manner. PTEN knockdown further showed enhanced vulnerability to combined targeting. These findings show that JPI-547 enhances antitumor efficacy in PTEN-deficient EC by disrupting DNA repair pathways and Wnt signalling, supporting dual PARP/TNKS inhibition as a potential therapeutic strategy and providing a rationale for further clinical evaluation. - Source: PubMed
Kang Sung WanEum HyerimLee Ji-YoungLee Min-SeoKim Yong-ManKim Tae WonLee Shin-Wha - SNAREs participate in tumor progression; however, existing studies on SNAREs remain fragmented. The discovery of suitable SNARE targets and delineation of their application limits are critical. - Source: PubMed
Publication date: 2026/06/08
Zhang YinghaoWang HaoranWang JinhaiSui YufangZhang WanhongLin XuhongZhang Pengpai - The human genome reference established a shared coordinate system for genome function, but it is incomplete and not fully representative of human diversity. Here, we benchmark how genome representation and corresponding analytical frameworks for each representation shape functional genomics using chromatin accessibility sequencing (ATAC-seq), RNA sequencing, whole-genome bisulfite sequencing, and chromosome conformation capture (Hi-C) data from lymphoblastoid cell lines derived from five individuals with fully phased genome assemblies. We compare results across hg38, CHM13, the draft human pangenome, and each individual's maternal and paternal assemblies. Because current pipelines and quality control conventions are tuned to hg38, several of these comparisons reflect genome representation in the context of available methods, rather than sequence alone. Individual identity accounts for 57.52-78.47% of total variance in functional estimates, whereas genome choice contributes 0.002-7.85% and sample-by-genome interactions contribute 0.63-5.43%. About 2% of biological signals are detectable only with personal assemblies. Although these effects are modest overall, some biologically important features remain inaccessible to linear references. Consistent with this, graph-based DNA methylation analysis in the human pangenome reveals a non-reference AluY5a insertion within a putative TNKS enhancer at chromosome 8p23.1 that becomes visible and hypermethylated only in the pangenome. - Source: PubMed
Publication date: 2026/05/26
Macias-Velasco Juan FZhuo XiaoyuTomlinson ChadBelter Eddie AKremitzki MilinnAlbracht DerekLindsay TinaXing XiaoyunTekkey NinaZhang WenjinGarza John EXu ZhengXin ZilanFu QichenLawson Heather AStitziel Nathan OFulton Robert SLi Daofeng Wang Ting - Tankyrases (TNKS1 and TNKS2) are multifunctional enzymes of the poly(ADP-ribose) polymerase (PARP) family that regulate cellular homeostasis by catalyzing poly(ADP-ribosyl)ation and stabilizing protein-protein interactions through their ankyrin repeat clusters. By engaging with diverse sets of proteins, TNKSs act as central hubs that coordinate signaling and metabolic pathways. In this review, we discuss how TNKS -protein interactions underpin their roles across multiple biological pathways, including Wnt/β-catenin, YAP and SRC signaling, mTORC1 signaling, DNA damage repair (via PARP crosstalk and recruitment of repair factors), telomere maintenance, cell-cycle regulation, glucose metabolism, cytoskeleton rearrangement, autophagy, proteasomal degradation, and apoptosis. We highlight the structural basis of these interactions, emphasizing ankyrin repeat domain recognition motifs and the consequences of TNKS-mediated PARylation on protein stability and localization. By integrating findings from oncology, virology, and metabolism, we illustrate how TNKS functions as a nodal regulator linking genome stability, signaling fidelity, and metabolic control. The interplay between TNKS and these varied pathways is essential for the well-being of the organism, with its dysregulation having severe biological and clinical consequences, which are discussed here. Finally, we consider therapeutic implications of disrupting TNKS-protein interactions, with particular attention paid to selective small-molecule inhibitors and their translational potential in cancer, viral infections, and degenerative diseases. - Source: PubMed
Publication date: 2026/02/14
Chalabi Hagkarim NafisehGrand Roger J - Colorectal cancer (CRC) is a multifactorial malignancy frequently driven by aberrant activation of the Wnt/β-catenin cascade, which promotes uncontrolled cell proliferation and tumor progression. Tankyrases (TNKS1/TNKS2), members of the PARP family, regulate this pathway by mediating AXIN degradation, thereby stabilizing β-catenin. Inhibition of TNKS can restore AXIN levels and attenuate Wnt signalling, positioning TNKS as a promising therapeutic target. Leveraging the structural diversity, biochemical specificity, and evolutionary refinement of natural microbial compounds, this study screened 36,588 microbial and fungal natural products obtained from the NPATLAS database. High-throughput screening was carried out using Python and the RDKit package, applying stringent physicochemical, structural, and drug-likeliness filters. Exhaustive virtual screening, molecular docking, and 300 ns molecular dynamics (MD) simulations identified two promising candidates, namely Malassezione (NPA018503) and Xenocockiamide B (NPA033189), which exhibited the most favourable and stable binding interactions with TNKS-1, with binding affinities of - 11.45 kcal/mol and - 12.48 kcal/mol, respectively. Further validation through MM-PBSA calculations, Principal component analysis (PCA), DCCM, and free energy landscape (FEL) analyses revealed robust conformational stability and distinct clustering mechanisms of these top hits within the TNKS-1 active site. Density functional theory (DFT) calculations additionally confirmed favourable electronic characteristics for both compounds, including optimal HOMO-LUMO energy gaps and chemical reactivity parameters. Pharmacokinetic profiling indicated high GI absorption, metabolic resilience, and minimal toxicity risk. Although XAV939 is a known TNKS-1 inhibitor, it demonstrated comparatively reduced efficacy across binding and stability metrics. In conclusion, this integrative computational evidence supports microbial-derived compounds as promising natural candidates for TNKS-1 inhibition, offering a new avenue for validation and structure-guided discovery of next-generation microbe-based therapeutics for colorectal cancer. - Source: PubMed
Publication date: 2026/02/19
Sharma DivyaSamreen AdeebaNair AkshadaArumugam Sivakumar