Ask about this productRelated genes to: RNASEH2A antibody
- Gene:
- RNASEH2A NIH gene
- Name:
- ribonuclease H2 subunit A
- Previous symbol:
- -
- Synonyms:
- RNASEHI, RNHIA, RNHL, AGS4
- Chromosome:
- 19p13.13
- Locus Type:
- gene with protein product
- Date approved:
- 2002-06-05
- Date modifiied:
- 2019-04-23
Related products to: RNASEH2A antibody
Related articles to: RNASEH2A antibody
- Follicular lymphoma (FL) is one of the most common types of indolent non-Hodgkin lymphoma that can undergo rapid progression, which is associated with poor patient outcomes. The homing of B cells into aberrant immunological niches within the germinal center (GC) is a prerequisite for disease development. The C-C chemokine receptor type 7 (CCR7), expressed by circulating B cells, mediates their homing and dissemination to draining lymph nodes (drLNs). Here, we identified activated B cells emerging from adjacent GCs in drLNs as the origin of circulating memory B cells in distant LNs. Transcriptional upregulation of Ccr7 in these memory B cells was found to guide their migration. To model lymphomagenesis, we generated a mouse model with B-cell-specific Myc overexpression, achieved by CRISPR/Cas9-mediated homologous recombination to insert a Myc expression cassette into the Hipp11 locus. Histological signs of aggressive lymphoma were evident in Ccr7 wild-type mice, whereas Ccr7 knockout mice exhibited pre-malignant atypia phenotypes. We in-depth revealed that Ccr7 knockout impeded the differentiation of pre-malignant Rnaseh2a+ memory B cells toward malignant Pax5+ GC B cells. Furthermore, Ccr7 deficiency attenuated the dependency of malignant memory or GC B cells on extensive follicular dendritic cell (FDC) networks and T-cell help. Conversely, IL-1β-induced FDC re-expansion preferentially fostered the proliferation of malignant GC B cells even in the context of Ccr7 knockout. Our findings reveal an unforeseen role for CCR7 in driving the malignant evolution of memory B cells by orchestrating their migratory dynamics and reprogramming the supportive GC niche. - Source: PubMed
Publication date: 2026/05/15
Deng YuweiJia ZhenyuanMu Xiao-QinMao YiyouZhang QingyuanMa Jianli - Triple-negative breast cancer (TNBC) lacks effective targeted therapies and carries a poor prognosis. TNBC cells escape oncogene-induced senescence and adapt to elevated replication stress. Here, we show that cells escaping senescence depend on overexpression of RNase H2, which removes misincorporated ribonucleotides from genomic DNA. RNASEH2A, the catalytic subunit of RNase H2, is overexpressed in TNBC tumors and correlates with poor survival. Genetic silencing or pharmacological inhibition of RNase H2 selectively impairs TNBC viability, spares non-tumorigenic mammary epithelial cells, and suppresses tumor growth in vivo. Mechanistically, RNase H2 inhibition increases replication stress, DNA damage, and cytosolic single-stranded DNA accumulation, triggering innate immune activation and upregulation of T cell-recruiting chemokines. RNase H2 inhibition synergizes with ATR and PARP inhibitors and enhances immune checkpoint blockade efficacy. Together, these findings identify RNase H2 as a therapeutic vulnerability in TNBC and support combined strategies integrating DNA damage modulation and immunotherapy. - Source: PubMed
Publication date: 2026/04/20
Nguyen Thai Quynh AnhZhang JingDai HuiMurat AysegulDu YongMcGrail Daniel JMeric-Bernstam FundaLin Shiaw-Yih - Aicardi-Goutières syndrome (AGS) is a rare, genetically-determined spectrum of neurodegenerative disorders that remains poorly understood. Owing to the paucity of data from Middle-Eastern population, we aimed to delineate the clinical, radiological, and genetic features of AGS in an under-represented Middle-Eastern cohort. - Source: PubMed
Publication date: 2026/03/16
Alwalid OsamahSubhi Marwa AlSerhan Ala Aldeen AlAbdulwahhab Saja BSamran ElhamThabet FarouqBenini RubaAlRayahi Jehan - - Source: PubMed
Publication date: 2025/12/30
Sugawara ShoOkada RyoLoo Tze MunTanaka HisamichiMiyata KenichiChiba MasatomoKawasaki HirokoKatoh KaoruKaji ShizuoMaezawa YoshiroYokote KoutaroNakayama MizuhoOshima MasanobuNagao KojiObuse ChikashiNagayama SatoshiTakubo KeiyoNakanishi AkiraKanemaki Masato THara EijiTakahashi Akiko - Mendelian type I interferonopathies are autoimmune diseases caused by genetic mutations that result in upregulation of interferon signalling. Small molecules that modulate proteins encoded by these genes may drive anti-tumour immunity in cancer patients by increasing interferon levels, but chemical probes and drugs are lacking. Covalent chemoproteomics and structural data were compiled to reveal ligandable cysteines, tyrosines and lysines across diverse proteins associated with interferonopathies. From this analysis, we identified several actionable targets, including ligandable sites on ADAR1, RNASEH2A and SAMHD1, and so our work provides a useful resource for future drug discovery efforts directed towards the development of immunotherapeutics. - Source: PubMed
Publication date: 2025/11/12
Alba Nathan MJones Carys RJones Ffion LJones Lyn H