登录 | 注册    关注公众号  
微信公众号
搜索
 >  Protein>MIF >MIF-H82E7

Biotinylated Human MIF Protein, His,Avitag™

分子别名(Synonym)

MIF,GLIF,MMIF,GIF

表达区间及表达系统(Source)

Biotinylated Human MIF, His,Avitag (MIF-H82E7) is expressed from human 293 cells (HEK293). It contains AA Pro 2 - Ala 115 (Accession # P14174-1).

Predicted N-terminus: Pro 2

Request for sequence

蛋白结构(Molecular Characterization)

Online(Pro 2 - Ala 115) P14174-1

This protein carries a polyhistidine tag at the C-terminus, followed by an Avi tag (Avitag™).

The protein has a calculated MW of 16.0 kDa. The protein migrates as 20 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

标记(Biotinylation)

Biotinylation of this product is performed using Avitag™ technology. Briefly, the single lysine residue in the Avitag is enzymatically labeled with biotin.

蛋白标记度(Biotin:Protein Ratio)

Passed as determined by the HABA assay / binding ELISA.

内毒素(Endotoxin)

Less than 1.0 EU per μg by the LAL method.

纯度(Purity)

>90% as determined by SDS-PAGE.

制剂(Formulation)

Lyophilized from 0.22 μm filtered solution in 25 mM MES, 500 mM NaCl, pH6.5. Normally trehalose is added as protectant before lyophilization.

Contact us for customized product form or formulation.

重构方法(Reconstitution)

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

存储(Storage)

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:

  1. -20°C to -70°C for 12 months in lyophilized state;
  2. -70°C for 3 months under sterile conditions after reconstitution.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
 

电泳(SDS-PAGE)

Biotinylated Human MIF, His,Avitag (Cat. No. MIF-H82E7) SDS-PAGE gel

Biotinylated Human MIF, His,Avitag on SDS-PAGE under reducing (R) condition. The gel was stained with Coomassie Blue. The purity of the protein is greater than 90%.

 
评论(0)
 
ACRO质量管理体系
 
 

背景(Background)

Macrophage migration inhibitory factor(MIF) is also known as Glycosylation-inhibiting factor(GIF), L-dopachrome isomerase, L-dopachrome tautomerase, Phenylpyruvate tautomerase. Interacts with CXCR2 extracellular domain, CD74 extracellular domain, COPS5 and BNIPL. The expression of MIF at sites of inflammation suggests a role as mediator in regulating the function of macrophages in host defense. Counteracts the anti-inflammatory activity of glucocorticoids. Has phenylpyruvate tautomerase and dopachrome tautomerase activity (in vitro), but the physiological substrate is not known. It is not clear whether the tautomerase activity has any physiological relevance, and whether it is important for cytokine activity.

 

 

前沿进展

No Distinct Cytokine, Chemokine, and Growth Factor Blood Profile Associated With Monkeypox Virus Clade IIb Infected Patients
Bangwen, Berens-Riha, de Vrij et al
J Med Virol (2025) 97 (4), e70320
Abstract: Previous studies indicated Clade I monkeypox virus infection to be associated with marked elevation of proinflammatory cytokines. This remains unexplored for Clade II-associated disease, which has different clinical manifestations and prognosis. We used a 65-plex cytokine, chemokine, and growth factor (CCG) panel to analyze serum samples of 100 male acute Clade IIb mpox patients and 26 healthy controls in Belgium. Cluster analyses revealed no strong or distinct CCG profiles distinguishing mpox patients from controls but suggested trends in certain cytokine modulation. Individual CCG analyses found elevated levels of cytokines (MIF, CD30, IL2R, IL18, APRIL, and TNFRII), chemokines (CCL4, CCL8, CCL22, CCL24, CXCL9, CXCL10, CXCL11, CXCL12, and CXCL13), and growth factors (HGF and VEGFA) in patients, while CCL11 and CXCL5 were significantly suppressed. We detected no differences in key proinflammatory cytokines, IL-1α, IL-1β, IL-6, IL-8 or anti-inflammatory cytokines, IL-4, IL-10, IL-13. In patients living with HIV, comparison with pre-outbreak samples showed an increase in CXCL13 and a decrease in CXCL5, CCL2, CCL24, HGF, SCF, and TWEAK. The absence of discriminatory CCG profiles in Clade IIb mpox patients compared to healthy controls suggests there may be limited clinical applications of those markers.© 2025 The Author(s). Journal of Medical Virology published by Wiley Periodicals LLC.
In vivo synergistic enhancement of MIF-mediated inflammation in acute lung injury by the plant ortholog Arabidopsis MDL1
Spiller, Zhang, Gerra et al
FASEB J (2025) 39 (6), e70489
Abstract: Recent research has uncovered Arabidopsis thaliana proteins that are similar to the human inflammatory cytokine MIF. Plant MIF/D-dopachrome tautomerase (D-DT)-like proteins (MDLs) can interact with human MIF, yet the significance of these findings in living organisms has not been investigated. Given MIF's key role in acute respiratory distress syndrome promoting pulmonary inflammation, pathology, and leukocyte infiltration, here we set out to investigate the interplay between MIF and MDL1, one of three A. thaliana MIF orthologs, in an in vivo mouse model of MIF-induced acute lung injury (ALI). Human MIF and MDL1 were administered to C57BL/6 mice via inhalation, individually or in combination. Inhalation of MIF promoted various parameters of lung injury as evaluated by flow cytometry, immunofluorescence microscopy, RT-qPCR, and ELISA, while MDL1 inhalation alone had no effect. Intriguingly, combined treatment with MIF and MDL1 synergistically enhanced pulmonary infiltration of neutrophils and monocytic cells, accompanied by an upregulation of pro-inflammatory cytokine genes. Thus, the plant-derived MIF ortholog MDL1 potentiates MIF-induced inflammation in ALI. These data support the growing evidence of interactions between plant-derived compounds and human inflammatory mediators and illustrate how they may impact human health.© 2025 The Author(s). The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.
In-vitro immune-modulation of triple-negative breast cancer through targeting miR-30a-5p/MALAT1 axis using nano-PDT combinational approach
Ramzy, Abdel-Halim, Manie et al
Transl Oncol (2025) 55, 102365
Abstract: Triple negative breast cancer (TNBC) is an immunogenic tumor; however, its tumor immune microenvironment (TIME) is densely packed with immune suppressive cytokines and immune checkpoints. The immune-suppressive features of TNBC TIME represent a considerable obstacle to any immunotherapeutic approach. The objective of this study was to develop a multimodal in-vitro strategy to manipulate the TNBC TIME and enhance patients' outcomes by employing carefully tailored hybrid chitosan-lipid Nanoparticles (CLNPs), metformin and chlorin e6 (Ce-6)-mediated PDT, alone or combined. Special focus is directed towards evaluation of the role of the selected treatment agents on the non-coding RNAs (ncRNAs) involved in tuning the immuno-oncogenic profile of TNBC, for instance, the miR-30a-5p/MALAT1 network.This study enrolled 30 BC patients. CLNPs and ce-6-loaded CLNPs with different physicochemical features were synthesized and optimized using ionotropic gelation. The intracellular concentration and effects on MDA-MB-231 cellular viability were investigated. UHPLC was used to quantify ce-6. MDA-MB-231 cells were transfected with miR-30a-5p oligonucleotides and MALAT1 siRNAs using lipofection to investigate the interaction between MIF, PD-L1, TNF-α, IL-10, and the miR-30a-5p/MALAT1 ceRNA network. qRT-PCR was used to evaluate IL-10, TNF-α, and MIF expression levels, whereas flow cytometry was used for PD-L1.Immunophenotyping of BC biopsies revealed significantly elevated levels of immunosuppressive markers, including IL-10, TNF-α, PD-L1, and MIF in BC biopsies compared to its normal counterparts. Upon patient stratification, it was shown that MIF and IL-10 are upregulated in TNBC patients compared to non-TNBC patients. Nonetheless, immune suppressive biomarkers expression investigated in the current study was generally correlated with signs of poor prognosis. CLNPs with mean particle size ranging from 50-150 nm were obtained. CLNPs exhibited different patterns of intracellular uptake, cytotoxicity and modulation of the immunosuppressive markers based on their physicochemical properties and composition. In particular, CLNP4 in-vitro effectively reduced IL-10, TNF-α, MIF, and PD-L1. Loading of Ce-6 into CLNP4 (Ce6-CLNPs) improved the in-vitro cytotoxic effects via PDT. In addition, PDT with Ce6-CLNP4 enhanced the expression of tumor-suppressive miR-30a-5p and decreased oncogenic lncRNA MALAT1 expression in MDA-MB-231 cells, suggesting a potential for modulating the TNBC immuno-oncogenic profile.This study demonstrated that CLNPs and Ce-6-mediated PDT can modulate several key immunosuppressive factors and the miR-30a-5p/MALAT1 axis in TNBC cells. These findings provide a rationale for further in-vivo investigation of this multimodal therapeutic strategy.Copyright © 2025. Published by Elsevier Inc.
MIF as an oncogenic driver of low-heterogeneity melanomas
Tran, Sánchez-Zuno, Kulkarni et al
Mol Oncol (2025)
Abstract: Identifying targets involved in tumor evolution and immune escape is an active area of research in oncology. Macrophage migration inhibitory factor (MIF) is an upstream immunoregulatory cytokine that promotes transformed cell proliferation and survival, and generates a tumor-permissive immune landscape of immunosuppressive myeloid and T cells. Shvefel and colleagues have identified a key role for MIF in tumor progression in melanoma clones with low tumor heterogeneity. These findings provide important insights into the potential therapeutic utility of MIF antagonists and support ongoing research to utilize MIF pathway inhibitors for improved therapeutic outcomes.© 2025 The Author(s). Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.
Showing 1-4 of 7011 papers.
Powered by BizGenius
 
 
货号/价格
产品推荐
文档
联系电话:
+86 400-682-2521(全国)
010-53681107(北京)
021-50850665(上海)
运输方式
订单邮箱:
order.cn@acrobiosystems.com
技术支持邮箱:
tech.cn@acrobiosystems.com
MIF靶点信息
英文全称:Macrophage migration inhibitory factor
中文全称:巨噬细胞移动抑制因子
种类:Homo sapiens
上市药物数量:1详情
临床药物数量:2详情
最高研发阶段:批准上市
查看更多信息
前沿进展
点击查看详细

消息提示

请输入您的联系方式,再点击提交!

确定