Human Interleukin-29/Interferon Lambda 1, carrier-free
- Specifications
- Tech Info / Data
- Citations
- Documentation
Specifications
| Formulation | Supplied lyophilized without a carrier protein |
| Molecular Weight | Based on N-terminal sequencing, the mature recombinant IL-29 starts at Gly 20 and has a calculated molecular mass of 21.4 kDa. As a result of glycosylation, the recombinant monomer migrates as an approximately 26-35 kDa protein in SDS-PAGE under reducing conditions. |
| Source | DNA sequence encoding the signal peptide from human CD33 was fused to the carboxyl terminally polyhistidine-tagged mature human IL-29 (Gly 20-Thr 200). The chimeric protein was expressed in a mouse myeloma cell line, NS0. |
| Purity | Greater than 95%Endotoxin level < 1 EU/μg |
| Bioactivity | Human HepG2 cells infected with encephalomyocarditis virus, ED50 1-5 ng/ml |
| Storage | For retention of full activity store at -70°C or below and avoid repeated freeze/thaw cycles |
| Synonyms | Hu IL-29; Hu IFN-λ1 |
| Accession Number | Q8IU54 |
Tech Info / Data
The IFN lambda gene family is composed of three distinct genes: IFN lambda 1 (IL-29), IFN lambda 2 (IL-28A) and IFN lambda 3 (IL-28B). All three are class II cytokine receptor ligands that are distinctly related to members of the IL-10 family and Type I family. Refer to the product specific datasheet for references associated with this information.
IL-28A, IL-28B, and IL-29, also named interferon-λ2 (IFN-λ2), IFN-λ3, and IFN-λ1, respectively, are newly identified class II cytokine receptor ligands that are distantly related to members of the IL-10 family (11-13% aa sequence identity) and type I IFN family (15 - 19% aa sequence identity).1 – 3 The genes encoding these three cytokines are localized to chromosome 19 and each is composed of multiple exons. The exon organization of these genes is also found in the IL-10 family genes but is distinct from the type I IFNs, which are encoded within a single exon. The expression of IL-28A, B, and IL-29 is induced by virus infection or double-stranded RNA. All three cytokines exert bioactivities that overlap those of type I IFNs, including antiviral activity and up-regulation of MHC class I antigen expression. The three proteins signal through the same heterodimeric receptor complex that is composed of the IL-10 receptor β (IL-10 Rβ) and a novel IL-28 receptor α (IL-28 Rα, also known as IFN-λ R1). Ligand binding to the receptor complex induces Jak kinase activation and STAT1 and STAT2 tyrosine phosphorylation. The phosphorylated STAT1 and STAT2 complex with IFN-regulatory factor 9 (IRF-9) to form the IFN-stimulated regulatory factor 3 (ISGF-3) transcription factor complex that is translocated to the nucleus. ISGF-3 binds to the IFN-stimulated response element (ISRE) present in the regulatory regions of the target genes. Human IL-29 cDNA encodes a 200 amino acid (aa) residue precursor protein with a putative 19 aa signal peptide and a 181 aa mature protein, which is a monomer in solution. It shares 67% and 69% aa sequence identity with human IL-28A and human IL-28B, respectively.
Citations
Documentation
11826 Certificate of Analysis (CoA) 11826 Safety Data Sheet (SDS)ebiomall.com
>
>
>
>
>
>
>
>
>
>
>
>
人们知道，人体的生长发育依靠的是生长激素，但科学家研究结果证明：人的脑垂体分泌的生长激素在体内只能存在2分钟左右，经过血液，到达肝脏后迅速转化为生长因子。因此，在研究过程中，只能检测到血液中的生长因子，而检测不到生长激素。同时证明：生长因子随着年龄的增长逐渐减少，人体表现出各种衰老症状。
1、生长因子的由来：
下丘脑----------- 分泌促生长激素释放激素（GHRH）
脑垂体---------- 生长激素(HGH)
经过血液-------
到达肝脏------- 转化为-------- 生长因子(IGF-1)向左转|向右转
抗原是指一种能刺激人或动物机体产生抗体或致敏淋巴细胞，并能与这些产物在体内或体外发生特异性反应的物质。抗原的基本能力是免疫原性和反应原性。免疫原性又称为抗原性，是指能够刺激机体形成特异抗体或致敏淋巴细胞的能力。反应原性是指能与由它刺激所产生的抗体或致敏淋巴细胞发生特异性反应。具备免疫原性和反应原性两种能力的物质称为完全抗原，如病原体、异种动物血清等。只具有反应原性而没有免疫原性的物质，称为半抗原，如青霉素、磺胺等。半抗原没有免疫原性，不会引起免疫反应。但在某些特殊情况下，如果半抗原和大分子蛋白质结合以后，就获得了免疫原性而变成完全抗原。
白细胞介素、
干扰素、
肿瘤坏死因子、
生长因子、每一类里面又可以分为具体的因子。如某种细胞生长因子。
结肠炎是一种影响肠道的严重疾病。对结肠炎病人而言，免疫系统抵抗人体自身的肠道细菌，从而导致炎症产生。为了抵抗这种炎症，科学家们已着重关注一种被称作IL-10的化学信号分子。IL-10是一种抗炎性细胞因子。尽管已知IL-10在控制炎症和阻止肠炎中发挥着至关重要的作用，但是仍不清楚的是，它是如何做到这一点的。
在一项新的研究中，来自美国耶鲁大学医学院和哈佛医学院的研究人员以缺乏这种IL-10信号的小鼠和病人为实验对象，研究了这种炎性反应。他们发现IL-10的作用机制是阻断巨噬细胞（作为这种炎性反应的一部分）的代谢。具体而言，他们发现IL-10抑制脂多糖诱导的葡萄糖摄取和糖酵解，促进氧化磷酸化。再者，他们还证实IL-10通过诱导一种被称作DDIT4的mTOR抑制剂产生来抑制mTOR活性。相关研究结果发表在2017年5月5日的Science期刊上，论文标题为“Anti-inflammatoryeffectofIL-10mediatedbymetabolicreprogrammingofmacrophages”。论文通信作者为耶鲁大学医学院免疫学系研究员RuslanMedzhitov。
这些研究人员也注意到IL-10通过促进线粒体自噬（mitophagy）来清除受损的线粒体。这种细胞损伤的堆积会促进炎症产生。线粒体是细胞内的能量工厂。受损线粒体的特征是较低的膜电势和高水平的活性氧。在结肠炎模式小鼠和炎症性肠病患者体内，当IL-10信号缺乏时，巨噬细胞内堆积着受损的线粒体，这会导致NLRP3炎性体异常激活和IL-1β产生。
这些发现加深了对炎症中的一种关键过程的理解，而且可能导致人们开发出靶向结肠炎中的这个通路的疗法。它也可能在阻止或治疗因细胞损伤导致的经常是在衰老时发生的退行性疾病中发挥着重要作用。
原始出处：
W.K.EddieIp,NamikoHoshi,DrorS.Shouvaletal.Anti-inflammatoryeffectofIL-10mediatedbymetabolicreprogrammingofmacrophages.Science,05May2017,356(6337):513-519,doi:10.1126/science.aal3535
AAgnieszkaM.Kabat,EdwardJ.Pearce.Inflammationbywayofmacrophagemetabolism.Science,05May2017,356(6337):488-489,doi:10.1126/science.aan2691
暂无品牌问答
