RecombinantHumanTGF-beta1(HumanCell-expressed)ProteinSummary
| DetailsofFunctionality | MeasuredbyitsABIlitytoinhibittheIL-4-dependentproliferationofHT‑2mouseT cells.Tsang, M.et al.(1995)Cytokine7:389.TheED50forthiseffectis0.04-0.2ng/mL. |
| Source | Humanembryonickidneycell,HEK293-derivedhumanTGF-beta1proteinAla279-Ser390 |
| Accession# | P01137 |
| N-terminalSequence | Ala279 |
| Structure/Form | Disulfide-linkedhomodimer |
| Protein/PeptideType | RecombinantProteins |
| Gene | TGFB1 |
| Purity | >95%,bySDS-PAGEunderreducingconditionsandvisualizedbysilverstain. |
| EndotoxinNote | <0.01 eu="" per="" 1="" μg="" of="" the="" protein="" by="" the="" lal="">0.01> |
Applications/Dilutions
| TheoreticalMW | 12.8kDa(monomer).Disclaimernote:Theobservedmolecularweightoftheproteinmayvaryfromthelistedpredictedmolecularweightduetoposttranslationalmodifications,posttranslationcleavages,relativecharges,andotherexperimentalfactors. | |
| SDS-PAGE | 11kDa,reducingconditions | |
| Publications |
|
Packaging,Storage&Formulations
| Storage | Useamanualdefrostfreezerandavoidrepeatedfreeze-thawcycles.
|
| Buffer | Lyophilizedfroma0.2μmfilteredsolutioninAcetonitrileandTFAwithBSAasacarrierprotein.*1mgpacksize(01M)issuppliedasa0.2µmfilteredsolutioninAcetonitrileandTFAwithBSAasacarrierprotein. |
| Purity | >95%,bySDS-PAGEunderreducingconditionsandvisualizedbysilverstain. |
| ReconstitutionInstructions | Reconstituteat100μg/mLinsterile4mMHClcontainingatleast0.1%humanorbovineserumalbumin. |
Notes
AlternateNamesforRecombinantHumanTGF-beta1(HumanCell-expressed)Protein
- CEDLAP
- DPD1
- latency-associatedpeptide
- TGFbeta1
- TGFB
- TGFB1
- TGF-beta1protein
- TGFbeta1
- TGF-beta1
- TGFbeta
- TGF-beta-1
- transforminggrowthfactorbeta-1
- transforminggrowthfactor,beta1
Background
- Derynck,R.andK.Miyazono(2008)ColdSpringHarborLaboratoryPressp.29.
- Dunker,N.andK.Krieglstein(2000)Eur.J.Biochem.267:6982.
- Wahl,S.M.(2006)Immunol.Rev.213:213.
- Chang,H.etal.(2002)Endocr.Rev.23:787.
- Lin,J.S.etal.(2006)Reproduction132:179.
- Hinck,A.P.etal.(1996)Biochemistry35:8517.
- Mittl,P.R.E.etal.(1996)ProteinSci.5:1261.
- Derynck,R.etal.(1985)Nature316:701.
- Miyazono,K.etal.(1988)J.Biol.Chem.263:6407.
- Oklu,R.andR.Hesketh(2000)Biochem.J.352:601.
- deCaestecker,M.etal.(2004)CytokineGrowthFactorRev.15:1.
- Zuniga,J.E.etal.(2005)J.Mol.Biol.354:1052.
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干扰素(Interferon,IFN),是由英国科学家Isaacs于1957年利用鸡胚绒毛尿囊膜研究流感病毒干扰现象时首先发现的,是一种细胞因子,具有抑制细胞分裂、调节免疫、抗病毒、抗肿瘤等多种作用。其本质是蛋白质,类型可分为α、β、γ、ω等几种。IFN能诱导细胞对病毒感染产生抗性,它通过干扰病毒基因转录或病毒蛋白组分的翻译,从而阻止或限制病毒感染,是目前最主要的抗病毒感染和抗肿瘤生物制品。
CristinaAlberini教授的个人主页:http://www.mountsinai.org/profiles/cristina-alberini
全文下载:
nature09667.pdf(558.65k)
单核吞噬细胞系统(mononeuclear phagocyte system)又称单核巨噬细胞系统,是高等动物体内具有强烈吞噬能力的巨噬细胞,及其前身细胞所组成的一个细胞系统,是机体防御结构的重要组成部分。
巨噬细胞细胞质内含丰富溶酶体、线粒体及粗糙内质网,细胞表面形成小突起和胞膜皱褶。静止时称固着巨噬细胞,有趋化因子时便成为游走巨噬细胞,能进行变形运动及吞噬活动。人的巨噬细胞能生活数月至数年。许多疾病能引起单核吞噬细胞系统大量增生,表现为肝、脾淋巴结肿大。功能为吞噬清除体内病菌异物及衰老伤亡细胞;活化T.B.淋巴细胞免疫反应。在细菌或其他因子刺激下能分泌酸性水解酶、中性蛋白酶、溶菌酶和其他内源性热原等。该系统包括单核细胞,结缔组织跟淋巴组织中的巨噬细胞、肝的库普佛细胞、肺的尘细胞、神经组织的小胶质细胞、骨组织的破骨细胞、表皮的朗格汉斯细胞和淋巴组织中的交错突细胞,单核细胞穿出血管壁进入其他组织中,分别分化为上述各种细胞。
(1)绝大多数细胞因子为分子量小于25kDa的糖蛋白,分子量低者如IL-8仅8kDa。多数细胞因子以单体形式存在,少数细胞因子如IL-5、IL-12、M-CSF和TGF-β等以双体形式发挥生物学作用。大多数编码细胞因子的基因为单拷贝基因(IFN-α除外),并由4-5个外显子和3-4个内含子组成。
(2)主要与调节机体的免疫应答、造血功能和炎症反应有关。
(3)通常以旁分泌(paracrine)或自分泌(autocrine)形式作用于附近细胞或细胞因子产生细胞本身。在生理状态下,绝大多数细胞因子只有产生的局部起作用。
(4)高效能作用,一般在pM(10-12M)水平即有明显的生物学作用。
(5)存在于细胞表面的相应高亲和性受体数量不多,在10-10000/每个细胞。细胞因子受体的研究进展相当迅速,根据细胞因子受体基因DNA序列以及受体胞膜外区氨基酸序列、同源性和结构,可分为四个类型:免疫球蛋白超家族、造血因子受体超家族、神经生长因子受体超家族和趋化因子受体。
(6)多种细胞产生,一种IL可由许多种不同的细胞在不同条件下产生,如IL-1除单核细胞、巨噬细胞或巨噬细胞系产生外,B细胞、NK细胞、成纤维细胞、内皮细胞、表皮细胞等在某些条件下均可合成和分泌IL-1。
(7)多重的调节作用(multipleregulatoryaction),细胞因子不同的调节作用与其本身浓度、作用靶细胞的类型以及同时存在的其它细胞因子种类有关。有时动物种属不一,相同的细胞因子的生物学作用可有较大的差异,如人IL-5主要作用于嗜酸性粒细胞,而鼠IL-5还可作用于B细胞。
(8)重叠的免疫调节作用(overlappingregulatoryaction),如IL-2、IL-4、IL-9和IL-12都能维持和促进T淋巴细胞的增殖。
(9)以网络形式发挥作用,细胞因子的网络作用主要是通过以下三种方式:(1)一种细胞因子诱导或抑制另一种细胞因子的产生,如IL-1和TGF-β分别促进或抑制T细胞IL-2的产生;(2)调节同一种细胞因子受体的表达,如高剂量IL-2可诱导NK细胞表达高亲和力IL-2受体;(3)诱导或抑制其它细胞因子受体的表达,如TGF-β可降低T细胞IL-2受体的数量,而IL-6和IFN-γ可促进T细胞IL-2受体的表达。
(10)与激素、神经肽、神经递质共同组成了细胞间信号分子系统。
(11)自限性分泌。向左转|向右转
而对于大多数革兰阳性细菌,喹诺酮类药物主要抑制细菌的拓扑异构酶Ⅳ,拓扑异构酶Ⅳ为解链酶,可在DNA复制时将缠绕的子代染色体释放。向左转|向右转
研究人员将多效生长因子注入骨髓生长因受到辐射而被抑制的实验鼠体内,后者的骨髓干细胞生长速度与未注射多效生长因子的实验鼠相比提高了10倍。在实验室培养皿中,多效生长因子还被确认可促进人类脐带血干细胞的生长。研究人员还证实,多效生长因子不会导致实验鼠出现癌变。
研究人员说,这项成果将来有望使更广泛的人群受益于脐带血移植,更重要的是,对正在接受化疗或放疗的患者而言,利用多效生长因子进行的治疗或许具有加速患者血液和免疫系统恢复的潜力。
【原文见附件】
ellsNatureMedicineNaturePublishingGroup.pdf(1020.57k)
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




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