Ask about this productRelated genes to: Rag1 Blocking Peptide
- Gene:
- RAG1 NIH gene
- Name:
- recombination activating 1
- Previous symbol:
- -
- Synonyms:
- RNF74, MGC43321
- Chromosome:
- 11p12
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-18
- Date modifiied:
- 2019-04-23
Related products to: Rag1 Blocking Peptide
Related articles to: Rag1 Blocking Peptide
- The metastatic progression of breast cancer involves complex interactions between tumor cells and immune cells, including T cells that exert cytotoxic pressure to limit metastasis. Tumor cells reprogram their metabolism to evade immune surveillance, a critical step to achieving metastatic outgrowth. Using an unbiased CRISPR screen targeting metabolism-related genes and a clinically relevant spontaneous metastasis mouse model, we identified CPT1A, the rate-limiting enzyme in fatty acid β-oxidation, as a suppressor of immune-dependent metastasis. Loss of CPT1A enhances lung metastasis in immunocompetent mice, but not Rag1 KO mice that lack mature lymphocytes. Loss of CPT1A triggers cytosolic mitochondrial DNA (mtDNA) release via the mPTP pore. Cytosolic mtDNA release triggers a STING-dependent inflammatory response, creating an environment that impairs CD8+ T cell function, promoting metastatic outgrowth. Among breast cancer patients, low expression correlates with poor survival when CD8+ T cell infiltration is high. These findings reveal an extrinsic role for CPT1A in immune-tumor dynamics and suggest therapeutic opportunities targeting inflammation in metastatic breast cancer. - Source: PubMed
Publication date: 2026/05/05
Wang XiaoyongChou Shu-TingHwang YoonhaChen JinEdwards Deanna N - Spatial transcriptomics has emerged as a transformative approach for in situ mapping of cellular heterogeneity and interactions, yet existing methods often compromise throughput, cost and tissue coverage. Here we introduce Imaging Reconstruction using Indexed Sequencing (IRISeq): an optics-free, cost-effective platform that leverages spatial interaction mapping by indexed sequencing to profile tissues at adjustable sizes and resolutions (5-50 µm). We applied IRISeq to map gene expression across more than 70 coronal sections from both adult and aged mouse brains, including wild-type and two lymphocyte-deficient models (Rag1 and Prkdc mutants) and generated more than 460,000 spatial transcriptome profiles. Our integrated analysis with 783,264 single-cell transcriptomes revealed region-specific aging signatures that are lymphocyte dependent, notably a downregulation of interferon signaling and inflammation in ventricular regions upon lymphocyte depletion, alongside mutant-specific upregulation of senescence pathways. Furthermore, lymphocyte deficiency was linked to preserved abundance of ependymal cells that line the brain's ventricles and to distinct microglial state dynamics, highlighting a key role for lymphocytes in driving inflammatory processes during brain aging. Overall, IRISeq provides a high-throughput and cost-effective solution for spatially resolved transcriptomic profiling, opening new avenues for elucidating region-specific cellular mechanisms underlying aging and identifying potential therapeutic targets to preserve brain homeostasis. - Source: PubMed
Publication date: 2026/05/12
Abdulraouf AbdulraoufJiang WeirongZhang ZehaoXu ZihanLu ZiyuMerlinsky TiffanyLiao AndrewDoymaz AhmetIsakov SamuelRaihan TanvirZhou WeiCao Junyue - Severe combined immunodeficiency (SCID) is a life-threatening primary immunodeficiency disorder. This study aimed to identify novel recombination activating gene 1 (RAG1) variants in a Chinese pedigree and characterize their impact on protein structure and function, providing a genetic basis for preimplantation genetic testing for monogenic (PGT-M) cycle. - Source: PubMed
Publication date: 2026/05/12
Liu YongxiangShan XiongweiHuang GuilanDuan YuweiLi YunshiHou WenhuiLi ZishuoZhang ShutingWeng ZhiweiZhou ShaohuHuang Xuekun - Hematopoietic stem cell transplantation (HSCT) is a curative treatment for pediatric hematologic and immunologic disorders, with successful immune reconstitution being critical for long-term survival. We report the unique case of persistent hypogammaglobulinemia following fully matched HSCT from a phenotypically normal sibling donor carrying a heterozygous gene mutation. - Source: PubMed
Publication date: 2026/04/22
Wu JingWang HuifangChen WeijieHong Zhiming - Tuberculosis is an infectious disease caused by (), which poses a notable threat to human health. The present review aims to explore the application of humanized mice in the study of infections. Due to differences in immune responses between mice and humans, humanized mice with human immune systems have been developed as models to characterize human immune responses to . The present review searched for research on humanized mice and tuberculosis in Web of Science and PubMed using the keywords 'humanized', 'mice' or 'mouse' and 'tuberculosis', and summarized the findings. Humanized non‑obese diabetic (NOD).Cg‑Rag1Il2rg and NOD.Cg‑PrkdcIl2rg mice have the potential to accelerate the screening of vaccine candidates, therapeutic regimens and the 'bench to bedside' translation process. New therapies, such as IgG1 P1AM25 in humanized Fcγ receptor mice and phage DS6A in humanized NOD.Cg‑Prkdc Il2rg Tg(cytomegalovirus‑interleukin‑3, granulocyte‑macrophage colony‑stimulating factor and KIT ligand)1Eav/MloySzJ mice, may have potential for treating tuberculosis. The humanized bone marrow‑liver‑thymus and human leukocyte antigens transgenic mouse models are effective tools for studying the co‑infection of and human immunodeficiency virus (HIV). The present review highlights the key role of humanized mouse models in advancing the understanding of infection, including host‑pathogen interactions, immune evasion mechanisms, vaccine development, therapeutic interventions and co‑infection with HIV. In conclusion, humanized mice provide a powerful platform for bridging the gap between preclinical research and clinical tuberculosis therapeutics. - Source: PubMed
Publication date: 2026/05/08
Han BinghuaLiu FangLong JinzhaoWang JiongjiongCui YangeYang Haiyan