Ask about this productRelated genes to: INTS7 antibody
- Gene:
- INTS7 NIH gene
- Name:
- integrator complex subunit 7
- Previous symbol:
- C1orf73
- Synonyms:
- DKFZP434B168, INT7
- Chromosome:
- 1q32.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-19
- Date modifiied:
- 2014-11-18
Related products to: INTS7 antibody
Related articles to: INTS7 antibody
- The evolutionarily conserved Integrator complex, which is composed of over 10 subunits, orchestrates diverse RNA-processing events such as 3'-end maturation of small nuclear RNAs (snRNAs), transcription termination of RNA Polymerase II, and DNA damage response signaling pathways; however, the functional roles of individual Integrator complex subunits in lung adenocarcinoma (LUAD) remain poorly characterized, and this study aimed to systematically investigate the potential oncogenic functions and prognostic values of these subunits in LUAD. To achieve this goal, the expression profiles of Integrator complex subunits were profiled using transcriptomic data from the The Cancer Genome Atlas (TCGA) database, survival analyses (including Kaplan-Meier and Cox regression models) were performed to evaluate the correlations between subunit expression levels and patient survival outcomes (overall survival (OS) and disease-free survival (DFS)), co-expression network analysis was conducted to annotate the potential biological functions of key subunits, and functional validation was performed using CCK-8 assays and flow cytometry to assess the impact of INTS7 depletion on cell proliferation and cycle progression in LUAD cell lines. The findings of this study showed that Integrator complex subunits were significantly overexpressed in LUAD tissues compared to normal lung parenchyma; among these subunits, INTS7 expression was most strongly associated with shortened OS and DFS, indicating its pivotal role in LUAD pathogenesis, while bioinformatics analyses revealed that INTS7 is involved in regulating critical biological processes including cell cycle progression, transcriptional regulation, and RNA metabolism, and loss-of-function experiments demonstrated that genetic silencing of INTS7 significantly inhibited cell proliferation and induced cell cycle arrest in LUAD cells. Ultimately, this study provides the first evidence that INTS7, a core component of the Integrator complex, serves as a functional and prognostic regulator in LUAD, highlighting its potential as a therapeutic target for this malignancy. - Source: PubMed
Liu YamingHuang TengfeiZeng DehuaZhang MeiqingLian DuohuanZhou ShunkaiChen MengmengZeng ZhiyongLi Huizhong - The murine endogenous retrovirus MERVL is dynamically activated in a small population of in vitro cultured mouse embryonic stem cells (mESCs) exhibiting totipotent-like features. Yet, the relationship between MERVL activation and cell fate decisions of mESCs is incompletely understood. Through a genome-wide knockout screen, we discovered that MERVL activity is intrinsically linked to DNA damage response pathways. Loss of Ints7, a backbone subunit of the Integrator complex, increased DNA damage and triggered MERVL expression. Mechanistically, Ints7 depletion induced phosphorylation of Kap1, increased chromatin accessibility at MERVL loci, and activated the p53-Dux axis to drive MERVL transcription. Intriguingly, DNA damage-induced MERVL resurgence followed the cleavage of caspase-3, often accompanying a process known as anastasis-cell survival after transient apoptotic signaling. Collectively, our study uncovered that MERVL activation in mESCs is integrated into the cellular circuit for decision-making in response to DNA damage, suggesting that sublethal caspase activation can influence the developmental potential of stem cells. - Source: PubMed
Shen YunfanLi LiNi HuilingLi HuiXu MingruiTan XiaoyangLi ZhangjieLi PishunChen FangMao SongSun GongpingYuan Kai - Intracranial large artery stenosis (ILAS) is one of the most common causes of stroke worldwide and is associated with the risk for future vascular events. Asymptomatic ILAS is a frequent finding on neuroimaging and shares many risk factors with atherosclerotic vascular disease. Whether asymptomatic ILAS is driven by genetic variants is not well-understood. - Source: PubMed
Publication date: 2025/08/24
Liu MinghuaKhasiyev FaridSpagnolo-Allende AntonioSanchez Danurys LAndrews HowardYang QiongBeiser AlexaQiao YeRomero Jose RafaelRundek TatjanaBrickman Adam MManly Jennifer JElkind Mitchell SvSeshadri SudhaChen ChristopherDel Brutto Oscar HHilal SaimaWasserman Bruce ATosto GiuseppeFornage MyriamGutierrez Jose - Intracranial large artery stenosis (ILAS) is one of the most common causes of stroke worldwide and is associated with the risk for future vascular events. Asymptomatic ILAS is a frequent finding on neuroimaging and shares many risk factors with atherosclerotic vascular disease. Whether asymptomatic ILAS is driven by genetic variants is not well-understood. - Source: PubMed
Publication date: 2025/05/07
Liu MinghuaKhasiyev FaridSpagnolo-Allende AntonioSanchez Danurys LAndrews HowardYang QiongBeiser AlexaQiao YeRomero Jose RafaelRundek TatjanaBrickman Adam MManly Jennifer JElkind Mitchell SvSeshadri SudhaChen ChristopherDel Brutto Oscar HHilal SaimaWasserman Bruce ATosto GiuseppeFornage MyriamGutierrez Jose - Lung adenocarcinoma (LUAD) is the most common lung cancer, accounting for 19.4% of all cancer deaths. Our previous study discovered that INTS7 expression was upregulated in LUAD, while the precise mechanism by which INTS7 exerts pro-cancer effects remains unknown. In our study, shRNA was used to knockdown the expression of INTS7 in A549 cells. Cancer behaviors in vitro were determined by CCK8 and transwell assays. Xenograft mice models were constructed to detect the tumorigenesis in vivo. Immunofluorescence and toluidine blue staining were used to test the immune infiltration. Bioinformatics analysis was adopted to predict the potential signaling pathways and construct INTS7-derived genomic prognostic model. Western blot was utilized to confirm the molecular pathways. In total, downregulation of INTS7 suppressed proliferation, invasion and migration of A549 cells, as well as tumor growth. Bioinformatics and western blot analysis indicated that p38MAPK pathway participated in the regulatory mechanism of INTS7. Moreover, INTS7 expression was negatively correlated with infiltration of memory B cells and mast cells, while positively correlated with infiltration of macrophages M2. A nomogram, including INTS7-derived risk score, was used to estimate individual's survival probability. Generally, our findings provided comprehensive understanding of the molecular mechanisms about INTS7, and targeting INTS7 may represent a potential therapy for LUAD. - Source: PubMed
Publication date: 2024/10/27
Li XiangLu FeifeiCao ManYao YiyongGuo JingjingZeng GangQian Jinxian