Ask about this productRelated genes to: RNASEL antibody
- Gene:
- ABCE1 NIH gene
- Name:
- ATP binding cassette subfamily E member 1
- Previous symbol:
- RNASEL1, RNASELI, RNS4I
- Synonyms:
- RLI, OABP, RLI1
- Chromosome:
- 4q31.21
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-01
- Date modifiied:
- 2016-10-05
- Gene:
- RNASEL NIH gene
- Name:
- ribonuclease L
- Previous symbol:
- RNS4, PRCA1
- Synonyms:
- -
- Chromosome:
- 1q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-09
- Date modifiied:
- 2016-10-05
Related products to: RNASEL antibody
Related articles to: RNASEL antibody
- Tumorigenesis is commonly driven by genetic mutations and disruptions in cellular signalling pathways. Here we show that the oncogenic overexpression of the RNase L inhibitor ABCE1, a component of interferon signalling, leads to distinct and extensive deviations in cancer transcriptomes. RNase L is a cellular endonuclease that cleaves RNA molecules at specific UU and UA dinucleotide sites. Typically, it is activated by viral infections and interferon signalling leading to targeting and destruction of UU/UA-rich viral and cellular mRNA. RNase L has also homoeostatic and tumour suppressive roles. Relying on patient transcriptomic data, we show that ABCE1 is extensively overexpressed in colorectal cancer (CRC) and to a lesser extent in lung cancer. This upregulation was strongly associated with the co-upregulation of almost all UU/UA rich transcripts and downregulation of those that are UU/UA-poor. Many of upregulated mRNAs code for proteins involved in cell cycle regulation and mitosis. Accordingly, the knockdown of ABCE1 in the CRC cell line HT29 led to reduced proliferation. Surprisingly, the very high ABCE1 levels were associated with improved patient survival in CRC. This observation might be related to an anti-ABCE1-specific immune response due to the induction of tumour-reactive cytotoxic T lymphocytes by ABCE1 as previously reported. In lung cancer ABCE1 overexpression is milder and is associated with poor survival. We report a measurable, specific, and extensive modulation of cancer transcriptomes by the oncogenic overexpression of a component of interferon signalling with unexpected outcomes on patient survival. - Source: PubMed
Publication date: 2026/02/16
Hitti EdwardBakheet TalaMahmoud LinahAl-Mutairi NadaAlhaj LatifaAl-Zoghaibi FahadKhabar Khalid S A - Host response to a viral infection includes the production of type I interferon (IFN) and the induction of interferon-stimulated genes that have broad antiviral effects. One of the key antiviral effectors is the IFN-inducible oligoadenylate synthetase/ribonuclease L (OAS/RNase L) pathway, which is activated by double-stranded RNA to synthesize unique oligoadenylates, 2-5A, to activate RNase L. RNase L exerts an antiviral effect by cleaving diverse RNA substrates, limiting viral replication; many viruses have evolved mechanisms to counteract the OAS/RNase L pathway. Here, we show that the ATP-binding cassette E1 (ABCE1) transporter, identified as an inhibitor of RNase L, regulates RNase L activity and RNase L-induced autophagy during viral infections. ABCE1 knockdown cells show increased RNase L activity when activated by 2-5A. Compared to parental cells, the autophagy-inducing activity of RNase L in ABCE1-depleted cells is enhanced with early onset. RNase L activation in ABCE1-depleted cells inhibits cellular proliferation and sensitizes cells to apoptosis. Increased activity of caspase-3 causes premature cleavage of autophagy protein, Beclin-1, promoting a switch from autophagy to apoptosis. ABCE1 regulates autophagy during EMCV infection, and enhanced autophagy in ABCE1 knockdown cells promotes EMCV replication. We identify ABCE1 as a host protein that inhibits the OAS/RNase L pathway by regulating RNase L activity, potentially affecting antiviral effects. - Source: PubMed
Publication date: 2021/02/18
Ramnani BarkhaManivannan PraveenJaggernauth SarahMalathi Krishnamurthy - The 2'-5'-oligoadenylate synthetase (OAS)/RNase L system protects hosts against pathogenic viruses through cleavage of the exogenous single-stranded RNA. In this system, an evolutionally conserved RNA quality control factor Dom34 (known as Pelota (Pelo) in higher eukaryotes) forms a surveillance complex with RNase L to recognize and eliminate the exogenous RNA in a manner dependent on translation. Here, we newly identified that ATP-binding cassette sub-family E member 1 (ABCE1), which is also known as RNase L inhibitor (RLI), is involved in the regulation of exogenous RNA decay. ABCE1 directly binds to form a complex with RNase L and accelerates RNase L dimer formation in the absence of 2'-5' oligoadenylates (2-5A). Depletion of ABCE1 represses 2-5A-induced RNase L activation and stabilizes exogenous RNA to a level comparable to that seen in RNase L depletion. The increased half-life of the RNA by the single depletion of either protein is not significantly affected by the double depletion of both proteins, suggesting that RNase L and ABCE1 act together to eliminate exogenous RNA. Our results indicate that ABCE1 functions as a positive regulator of exogenous RNA decay rather than an inhibitor of RNase L. - Source: PubMed
Publication date: 2020/02/04
Nogimori TakutoOgami KoichiOishi YukaGoda RyoyaHosoda NaoKitamura YoshiakiKitade YukioHoshino Shin-Ichi - This study aims to explore the clinical characteristics of ATP binding cassette E1 (ABCE1) in oral squamous cell carcinomas (OSCC) and its roles in the proliferation, invasiveness, migration and apoptosis of the human oral squamous cell carcinoma cells CAL-27. - Source: PubMed
Publication date: 2014/08/15
Wang LeiZhang MeiLiu Dong-Xu - Breast cancer is the most common type of cancer among females and the adenosine triphosphate (ATP) binding cassette E1 (ABCE1) gene is a member of the ATP‑binding cassette (ABC) family. Studies in lung cancer have shown that overexpression of ABCE1 in tumor cells promotes growth and inhibits apoptosis. However, little is known about whether the ABCE1 gene is associated with breast cancer. In the present study, ABCE1 expression was assessed in breast cancer tissue and adjacent normal breast tissue using immunohistochemistry. Furthermore, small interfering (si)RNA targeting ABCE1 was constructed and transfected into MCF‑7 human breast cancer cells to downregulate ABCE1 expression. The effect of ABCE1 knockdown on cell proliferation, invasion, apoptosis and gene expression was then assessed using MTT assay, Transwell migration assay, flow cytometry and western blot analysis, respectively. ABCE1 was observed to be overexpressed in breast cancer tissue compared with adjacent normal breast tissue. Furthermore, ABCE1‑siRNA was found to inhibit proliferation and invasion in breast cancer cells, significantly induce breast cancer cell apoptosis (P<0.05) in vitro and increase the protein expression of RNase L. These findings showed that ABCE1 had an important role in proliferation, invasion and apoptosis in MCF‑7 human breast cancer cells and that ABCE1 may inhibit intracellular RNase L activity, which inhibits the 2‑5A/RNase L pathway, interfering with the biological characteristics of breast cancer cells. - Source: PubMed
Publication date: 2014/07/28
Huang BoZhou HongliLang XianpingLiu Zhiliang