Ask about this productRelated genes to: ERCC6L antibody
- Gene:
- ERCC6L NIH gene
- Name:
- ERCC excision repair 6 like, spindle assembly checkpoint helicase
- Previous symbol:
- -
- Synonyms:
- FLJ20105, PICH, RAD26L
- Chromosome:
- Xq13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2007-08-02
- Date modifiied:
- 2016-05-23
Related products to: ERCC6L antibody
Related articles to: ERCC6L antibody
- Lung adenocarcinoma (LUAD) is prone to metastasis and exhibits a poor prognosis. The DNA repair-related protein ERCC6L is implicated in tumorigenesis, but its role in LUAD invasion and metastasis remains unclear. The expression, function, and underlying mechanisms of ERCC6L were investigated using bioinformatics analysis, cellular assays, and animal experiments. ERCC6L was significantly upregulated in LUAD tissues and cell lines, and its high expression was associated with poor overall and recurrence-free survival. Functional experiments demonstrated that ERCC6L overexpression promoted the migration, invasion, and epithelial-mesenchymal transition (EMT) of LUAD cells. Mechanistically, ERCC6L activated the E3 ubiquitin ligase PJA2, which mediated K48-linked polyubiquitination and subsequent degradation of p53, thereby attenuating its tumor-suppressive function. In vivo studies confirmed that ERCC6L knockout suppressed tumor growth, metastasis, and EMT progression by regulating the PJA2/p53 signaling axis. ERCC6L promotes migration, invasion, and EMT in LUAD by facilitating PJA2-mediated ubiquitination and degradation of p53. The ERCC6L/PJA2/p53 axis represents a potential novel therapeutic target for inhibiting metastasis in LUAD. - Source: PubMed
Publication date: 2026/04/30
Jiang LingyuZhou HuaihaiLiang ShengjingWen ZhaokeQin JunqiLei ZhenniuLi RonglingMa YunzhiPeng ShucongZhou YifanZhong Yonglong - Somatic cell reprogramming to induced pluripotent stem cells (iPSCs) holds great promise for revolutionizing tissue repair and regenerative medicine. However, achieving high reprogramming efficiency remains challenging due to various endogenous or exogenous barriers. One major obstacle is DNA replication stress arising from rapid cell proliferation during iPSC reprogramming, which results in genomic instability and markedly reduced reprogramming efficiency. The Plk1-interacting checkpoint helicase [PICH; also known as DNA excision repair protein ERCC-6-like (ERCC6L)], a member of the SNF2 ATPase family, is pivotal in maintaining genomic stability by promoting sister chromatid disjunction upon replication stress. Our previous work revealed that PICH is essential for maintaining the genomic stability of embryonic hematopoietic stem cells, but whether and how PICH participates in iPSC reprogramming remains elusive. We show that PICH deficiency induces genomic instability and drastically reduces the efficiency of iPSC generation. Overexpression of Pich improves iPSC reprogramming efficiency by alleviating replication stress. Furthermore, PICH cooperates with telomere-associated protein RIF1, another protein required for sister chromatid disjunction, to maintain genomic stability in iPSCs, thereby enhancing reprogramming efficiency. Taken together, these results reveal a previously unknown role of PICH in facilitating the reprogramming of iPSCs via maintaining genomic stability under replication stress, and provide a new strategy for improving iPSC reprogramming efficiency. - Source: PubMed
Publication date: 2026/04/14
Zhang FengjiaoJi ChaoranJi FangZhang ChaoLiao HongweiShao ZhehuaJia FangGeng XinweiYing Songmin - To elucidate the oncogenic role and mechanistic basis of ERCC6L in cutaneous melanoma, focusing on its impact on tumor metabolism and progression. - Source: PubMed
Publication date: 2026/01/19
Zhang MengdiZhou ShengboHan BingGe Yining - The impact of biological sex on treatment response and prognosis in lung cancer remains poorly understood. This study investigates the relationship between sex-linked genes, DNA repair, senescence, and survival in male and female patients with lung cancer. - Source: PubMed
Publication date: 2025/09/20
Kinsella APrina-Mello AMarignol L - The ataxia telangiectasia mutated (ATM) kinase orchestrates the early stages of DNA double-strand break repair by promoting hyperphosphorylation of CtIP, a key step in the initiation of DNA end resection. However, the regulatory mechanisms controlling resection extent remain incompletely understood. Here we identify ERCC6L2 as a key regulator of DNA end resection in response to ATM inhibition. ERCC6L2 undergoes liquid-liquid phase separation via its intrinsically disordered regions, forming dynamic nuclear condensates that regulate CtIP stability. Disruption of these condensates renders CtIP susceptible to RNF138-mediated ubiquitination and degradation, thereby mitigating the heightened chromatin recruitment of CtIP induced by ATM inhibition. Intriguingly, ERCC6L2 is frequently downregulated in multiple cancer types and correlates with resistance to ATM inhibitors in both in vitro and in vivo settings. Our findings unveil the crucial role of ERCC6L2-CtIP condensates in governing the extent of DNA end resection and underscore the potential significance of ERCC6L2 as a predictive biomarker for ATM inhibitor response. - Source: PubMed
Publication date: 2025/09/05
Yin YixinLin JinlongCai XiaoxiaNie RuncongLin JiliangLi ShutingXiang ZhichengLing YihongZhang YiyangZhou JieChen JieweiLin WenpingDuan JinlingZheng XueyiXie DanCai Muyan