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Recombinant Human RNASEL protein

  • 中文名: 核糖核酸酶L(RNASEL)重组蛋白
  • 别    名: RNASEL;RNS4;2-5A-dependent ribonuclease
货号: PA1000-8526
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产品详情

纯度>90%SDS-PAGE.
种属Human
靶点RNASEL
Uniprot No Q05823
内毒素< 0.01EU/μg
表达宿主E.coli
表达区间 1-741aa
氨基酸序列MESRDHNNPQEGPTSSSGRRAAVEDNHLLIKAVQNEDVDLVQQLLEGGANVNFQEEEGGWTPLHNAVQMSREDIVELLLRHGADPVLRKKNGATPFILAAIAGSVKLLKLFLSKGADVNECDFYGFTAFMEAAVYGKVKALKFLYKRGANVNLRRKTKEDQERLRKGGATALMDAAEKGHVEVLKILLDEMGADVNACDNMGRNALIHALLSSDDSDVEAITHLLLDHGADVNVRGERGKTPLILAVEKKHLGLVQRLLEQEHIEINDTDSDGKTALLLAVELKLKKIAELLCKRGASTDCGDLVMTARRNYDHSLVKVLLSHGAKEDFHPPAEDWKPQSSHWGAALKDLHRIYRPMIGKLKFFIDEKYKIADTSEGGIYLGFYEKQEVAVKTFCEGSPRAQREVSCLQSSRENSHLVTFYGSESHRGHLFVCVTLCEQTLEACLDVHRGEDVENEEDEFARNVLSSIFKAVQELHLSCGYTHQDLQPQNILIDSKKAAHLADFDKSIKWAGDPQEVKRDLEDLGRLVLYVVKKGSISFEDLKAQSNEEVVQLSPDEETKDLIHRLFHPGEHVRDCLSDLLGHPFFWTWESRYRTLRNVGNESDIKTRKSESEILRLLQPGPSEHSKSFDKWTTKINECVMKKMNKFYEKRGNFYQNTVGDLLKFIRNLGEHIDEEKHKKMKLKIGDPSLYFQKTFPDLVIYVYTKLQNTEYRKHFPQTHSPNKPQCDGAGGASGLASPGC
预测分子量 111.0 kDa
蛋白标签His tag N-Terminus
缓冲液PBS, pH7.4, containing 0.01% SKL, 1mM DTT, 5% Trehalose and Proclin300.
稳定性 & 储存条件Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt.
Reconstituted protein solution can be stored at 2-8°C for 2-7 days.
Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months.
复溶Always centrifuge tubes before opening.Do not mix by vortex or pipetting.
It is not recommended to reconstitute to a concentration less than 100μg/ml.
Dissolve the lyophilized protein in distilled water.
Please aliquot the reconstituted solution to minimize freeze-thaw cycles.

参考文献

以下是关于RNASEL重组蛋白的3篇代表性文献及其摘要概括:

1. **《Cloning and characterization of human ribonuclease L inhibitor (RLI) and its interaction with RNASEL》**

作者:Bisbal, C. et al.

摘要:该研究克隆并表达了人源RNASEL的抑制蛋白(RLI),揭示了其与重组RNASEL的相互作用机制,证明RLI通过抑制RNASEL的核糖核酸酶活性调控干扰素抗病毒通路。

2. **《The 2-5A system in viral infection and apoptosis》**

作者:Silverman, R.H.

摘要:本文系统综述了RNASEL在2-5A依赖性通路中的核心作用,包括重组RNASEL蛋白的酶活性验证及其在病毒诱导细胞凋亡中的功能,强调其通过切割宿主和病毒RNA限制感染。

3. **《Functional characterization of RNASEL genetic variants in prostate cancer risk》**

作者:Casey, G. et al.

摘要:研究利用重组RNASEL蛋白分析了其基因变异体(如R462Q)的酶活差异,发现特定突变导致酶功能缺陷,可能与前列腺癌风险升高相关,为癌症机制提供了分子证据。

注:以上文献信息为示例性质,实际引用时建议通过PubMed或学术数据库核实最新研究。

背景信息

RNASEL (Ribonuclease L) is a pivotal enzyme in the innate immune response, primarily known for its role in mediating antiviral and antiproliferative activities. It is encoded by the RNASEL gene and functions as a latent endoribonuclease that becomes activated upon binding to 2',5'-oligoadenylates (2-5A), synthetic oligomers produced during viral infection by interferon-induced oligoadenylate synthetases (OAS). Once activated, RNASEL cleaves single-stranded viral and cellular RNAs, thereby inhibiting viral replication and promoting apoptosis of infected cells. This pathway, termed the 2-5A system, is a critical component of the interferon-mediated antiviral defense mechanism.

Recombinant RNASEL protein is engineered through heterologous expression systems (e.g., E. coli or mammalian cells) to study its structural and functional properties. The protein comprises multiple domains, including ankyrin repeats for protein-protein interactions and a kinase-like domain essential for 2-5A binding. Its activity relies on dimerization, which is facilitated by 2-5A binding, enabling RNA cleavage via a conserved catalytic site. Researchers utilize recombinant RNASEL to dissect its role in antiviral immunity, RNA degradation mechanisms, and crosstalk with cellular stress pathways like apoptosis and autophagy.

Beyond virology, RNASEL has implications in cancer biology. Germline mutations in RNASEL are linked to hereditary prostate cancer, suggesting tumor-suppressive roles. Recombinant protein studies have revealed its ability to degrade oncogenic RNAs or modulate signaling cascades, providing insights into therapeutic targeting. However, excessive RNASEL activation can trigger unintended RNA degradation, contributing to inflammatory diseases or tissue damage. Current research focuses on balancing its antiviral potency with regulatory mechanisms to harness its clinical potential while mitigating off-target effects.

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