Ask about this productRelated genes to: NHEJ1 antibody
- Gene:
- NHEJ1 NIH gene
- Name:
- non-homologous end joining factor 1
- Previous symbol:
- -
- Synonyms:
- Cernunnos, XLF, FLJ12610
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 2006-03-30
- Date modifiied:
- 2019-04-23
Related products to: NHEJ1 antibody
Related articles to: NHEJ1 antibody
- - Source: PubMed
Publication date: 2026/05/15
Alhaider AlanoudAlmutairi MansourAlomari AbdulazizAltuwaijri AlwaleedAlmarshoud GhaidaAlakrash Lamia - The DNA damage response (DDR) is a complex network of cellular pathways that ensures the faithful maintenance of our genomes upon a wide array of genomic insults. To elucidate the functional architecture of this network, we conducted unbiased genetic interaction screens using the Cas12a genome editor to disrupt 233 DDR genes frequently mutated in cancer and other genetic diseases, either individually or in pairwise combinations. This approach enabled us to assess the phenotypic effects induced by the disruption of >27,000 DDR gene pair combinations under unperturbed cell growth conditions. From this analysis, we identified over 750 high-confidence positive (buffering) or negative (synthetic lethal/sick) gene-gene interactions, along with multiple connections between previously unlinked DDR pathways and modules, allowing us to define novel aspects of the cellular response to spontaneous, DNA replication-associated DNA damage. Among the identified genetic interactions, we uncovered profound synthetic lethal interactions between genes encoding 1) the translesion polymerase REV1-Pol ζ complex and the MCM8-MCM9-HROB DNA helicase complex; 2) Fanconi Anemia (FA) proteins and the mitotic DNA repair factors GEN1, CIP2A, and RHINO; and 3) the DNA translocase SMARCAL1 and components of the FANCM complex, suggesting novel opportunities for targeted therapies in tumors carrying mutations in these genes. Additionally, we identified robust suppressor interactions between the gene encoding the nuclease APOLLO and the core non-homologous end joining (NHEJ) genes , , and , suggesting that NHEJ impairs the fitness of APOLLO-deficient cells. This work provides a functional map of the DDR network and demonstrates the power of Cas12a-based screens for identifying synthetic lethal and buffering interactions with therapeutic potential. - Source: PubMed
Publication date: 2026/06/08
Hayward Samuel BVaitsiankova AlinaLama-Diaz TomasChou JuihsuanTaglialatela AngeloHuang Jen-WeiWijesekarahanthi YodharaudshaniHeyza Joshua RLeuzzi GiuseppeChen ChuanyuanWong NancyLhakhang TenzinFu XiBuendia Alejandro LGheorghe VeronicaAnvar Nazanin EsmaeiliSchmidt Jens CNussenzweig AndreRabadan RaulCostanzo VincenzoGuérois RaphaëlHart TraverCiccia Alberto - Inborn errors of immunity (IEIs) are rare diseases that affect the immune system. Variants in over 500 genes have been identified as causative of 555 IEIs, with clinical phenotypes that can be heterogeneous within the same gene or even within the same variant. Therefore, these challenges make it difficult to determine the cause of IEI in individuals with immune disorders and to link clinical phenotypes to the precise genetic damage. An incorrect diagnosis can miss approximately 25% of IEI patients with overlapping initial manifestations. Accurate diagnosis and timely treatment are essential to improving quality of life and prolonging the lives of patients, as these patients often suffer from severe, life-threatening infections if left untreated. - Source: PubMed
Publication date: 2026/05/28
Kim Lien Nguyen ThiVan Tung NguyenMinh Huong Le ThiVan Anh Nguyen ThiPhuong Mai Nguyen ThiDien Tran MinhHien Nguyen ThanhTao Nguyen ThienHoang Nguyen Huy - The Yunlong Short-Leg chicken is a local dual-purpose breed in the Dali Bai Autonomous Prefecture of Yunnan Province, China, characterized phenotypically by notably shortened shank and a compact body stature. Nevertheless, the genetic mechanisms responsible for its short-legged phenotype have yet to be elucidated. - Source: PubMed
Publication date: 2026/05/18
Xu KuoweiZhang KaiLi JinyanHuang YuxinGou JunlanZhou JielongWang YuChen FenfenXiao Ping - External stressors, particularly heat stress, induce DNA damage and genomic instability in cells. However, the mechanisms by which cells rapidly respond to such DNA damage remain largely unknown. In this study, we found that heat shock factor 1 (HSF1), the major transcription factor in the heat shock response, activated several non-homologous end joining (NHEJ) pathway-associated genes, particularly NHEJ1, through puncta formation, thereby maintaining the stability of NHEJ pathway and alleviating the repair burden of DNA double-strand breaks caused by heat stress. Furthermore, N6-methyladenosine (m6A) RNA modification and its reader YTH domain-containing protein 1 (YTHDC1) contributed to this process by promoting the splicing of NHEJ1. Knockdown of HSF1 or YTHDC1 increased nuclear intensity of phosphorylation of histone variant H2AX at Ser-139 (γH2AX) in heat-stressed cells, whereas NHEJ1 overexpression rescued this effect. Moreover, HSF1 or YTHDC1 overexpression increased NHEJ repair efficiency in heat-stressed cells, supporting the existence of an HSF1/YTHDC1-NHEJ1-DNA double-strand repair axis. Our findings reveal a mechanism by which cells repair DNA damage during the heat shock response, providing new insights into how cells maintain genomic stability under external stress conditions. - Source: PubMed
Ding WenqingDeng QidongWang TianyuLiu RuoqianXiang YunfanHuang LuluLiu Jun