NFKBIL2 antibody - middle region (P100874_P050)
- Known as:
- NFKBIL2 (anti-) - middle region (P100874_P050)
- Catalog number:
- p100874_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NFKBIL2 antibody - middle region (P100874_P050)
Related genes to: NFKBIL2 antibody - middle region (P100874_P050)
- Gene:
- TONSL NIH gene
- Name:
- tonsoku like, DNA repair protein
- Previous symbol:
- NFKBIL2
- Synonyms:
- IKBR
- Chromosome:
- 8q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-09-12
- Date modifiied:
- 2017-02-21
Related products to: NFKBIL2 antibody - middle region (P100874_P050)
Related articles to: NFKBIL2 antibody - middle region (P100874_P050)
- Copy number variation (CNV) plays a fundamental role in modulating plant agronomic traits and tumorigenesis in animals. While frequently linked to replication stress, the mechanisms giving rise to CNVs are not fully elucidated. Here we characterize the mutational consequences associated with losing the conserved TONSOKU (TSK/TONSL) pathway (CAF-1-H3.1-TSK), which is required to resolve impaired DNA replication forks. Using Arabidopsis thaliana, we demonstrate that tsk mutants rapidly accumulate large, heritable tandem duplications within their genomes that are consistent with DNA Polymerase θ (Pol θ) activity. These duplications are associated with late replicating heterochromatin enriched in sources of replication stress. We also show that stochastic developmental phenotypes in tsk plants are the result of the DNA Damage Response (DDR), with phenotype suppression occurring when ATR-WEE1 checkpoint signaling is removed. We thus describe a previously uncharacterized source of large tandem duplications that are relevant to understanding genome stability in diverse eukaryotes, and in disease contexts. - Source: PubMed
Publication date: 2026/03/27
Thomson GeoffreyPoulet AxelHuang Yi-ChunLiao Hong-ShengLeBlanc ChantalJacob Yannick - Tandem duplications (TDs) are a common form of genomic rearrangements with both adaptive and pathogenic consequences. While prevalent in genomically unstable cancer genomes, TDs are rarely detected in normal tissues, suggesting the existence of robust protective mechanisms. Here, we identify the histone chaperone TONSL/TONSOKU (tnsl-1 in C. elegans) as a critical suppressor of TD formation. Loss of tnsl-1 results in the accumulation of TDs in two distinct size classes (~25 kb and ~300 kb), arising from different developmental contexts: small TDs emerge in rapidly dividing embryonic cells, whereas large TDs form in slower-dividing germline progenitors. Both classes depend on polymerase theta-mediated end joining (TMEJ), implicating DNA double-strand breaks in their genesis. Inhibition of break-induced replication (BIR) via Pif1 helicase loss reduces TD size, revealing a role for BIR in TD expansion. Remarkably, TONSL-deficient Arabidopsis thaliana exhibit an identical TD signature, highlighting the evolutionary conservation of this genome surveillance mechanism. These findings position TONSL as a cross-kingdom guardian of genome integrity through suppression of TD formation. - Source: PubMed
Publication date: 2026/03/27
van Schendel RobinRomeijn RonKralemann Lejon E MHooykaas Paul J JTijsterman Marcel - - Source: PubMed
Publication date: 2026/03/12
Luo Min-RuiLiao Jia-LinFang Shu-JieZhang Dong-YanLei Ling - Several long non-coding RNAs (lncRNAs) have been identified as oncogenic factors in hepatocellular carcinoma (HCC). This study aims to investigate the biological function and prognostic value of lncRNA RHPN1-AS1 in HCC. - Source: PubMed
Publication date: 2025/12/23
Li XiaoxuanLi YujingLuan XinchiLeng ChuanyuLi XinSun XueyingTian JingwenSong JialinGuo JingQiu Wensheng - Homologous recombination (HR) deficiency upon Breast Cancer Gene 2 (BRCA2) loss arises from defects in the formation of RAD51 nucleoprotein filaments. We demonstrate that loss of the anti-recombinase Fidgetin Like 1 (FIGNL1) retains RAD51 loading at DNA double-stranded breaks (DSBs) in BRCA2-deficient cells, leading to genome stability, HR proficiency, and viability of BRCA2-deficient mouse embryonic stem cells. Mechanistically, we demonstrate that strand invasion and subsequent HR defects upon BRCA2 loss primarily arise from the unrestricted removal of RAD51 from DSB sites by FIGNL1, rather than from defective RAD51 loading. Furthermore, we identify that the MMS22L-TONSL complex interacts with FIGNL1 and is critical for HR in BRCA2/FIGNL1 double-deficient cells. These findings identify a pathway for tightly regulating RAD51 activity to promote efficient HR, offering insights into mechanisms of chemoresistance in BRCA2-deficient tumors. - Source: PubMed
Publication date: 2025/10/30
Kuthethur RaviprasadVz Safa NasrinSengodan Satheesh KumarFonseca CarmenBraunshier StefanNagar NupurAcharya AnanyaWang XingdeTheil Arjan FIbini OluwakemiManolika Eleni-Mariade Koning KellyDessapt JulienFradet-Turcotte AmélieLebbink Joyce H GKanaar RolandPoluri Krishna MohanSharan Shyam KCejka PetrRay Chaudhuri Arnab