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 >  Protein>IL-34 >IL4-H82E5

Biotinylated Human IL-34 Protein, His,Avitag™

分子别名(Synonym)

IL34,C16orf77,IL-34,Interleukin-34,MGC34647

表达区间及表达系统(Source)

Biotinylated Human IL-34, His,Avitag (IL4-H82E5) is expressed from human 293 cells (HEK293). It contains AA Asn 21 - Pro 242 (Accession # Q6ZMJ4-1).

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蛋白结构(Molecular Characterization)

IL-34 Structure

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

The protein has a calculated MW of 29.0 kDa. The protein migrates as 33-40 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.

标记(Labeling)

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(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 PBS, pH7.4 with trehalose as protectant.

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)

IL-34 SDS-PAGE

Biotinylated Human IL-34, 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%.

 

活性(Bioactivity)-ELISA

IL-34 ELISA

Immobilized Human M-CSF R, Fc Tag, low endotoxin (Cat. No. CSR-H5258) at 5 μg/mL (100 μL/well) can bind Biotinylated Human IL-34, His,Avitag (Cat. No. IL4-H82E5) with a linear range of 0.2-10 ng/mL (QC tested).

Protocol

IL-34 ELISA

Immobilized Human M-CSF R, Mouse IgG2a Fc Tag (MALS verified) (Cat. No. CSR-H5255) at 5 μg/mL (100 μL/well) can bind Biotinylated Human IL-34, His,Avitag (Cat. No. IL4-H82E5) with a linear range of 0.2-10 ng/mL (Routinely tested).

Protocol

IL-34 ELISA

Immobilized Biotinylated Human IL-34, His,Avitag (Cat. No. IL4-H82E5) at 1 μg/mL (100 μL/well) on streptavidin (Cat. No. STN-N5116) precoated (0.5 μg/well) plate can bind Human TREM2, Fc Tag (Cat. No. TR2-H5254) with a linear range of 0.002-0.078 μg/mL (Routinely tested).

Protocol

 
评论(0)
  1. 198XXXXXXX5
  2. 0人赞
  3. 在试剂盒开发过程中,elisa的方法开发与优化使用了S1N C52Hv 这个蛋白,很顺利的完成了方法开发并交付。
  4. 2024-3-11
 
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背景(Background)

nterleukins (IL) are a group of cytokines that play an important role in the immune system. They modulate inflammation and immunity by regulating growth, mobility and differentiation of lymphoid and other cells.This entry represents interleukin-34 (IL-34), it was identified via functional screening of a library of secreted proteins [1]. This cytokine promotes the differentiation and viability of monocytes and macrophages through the colony-stimulating factor-1 receptor (CSF1R)

 

前沿进展

New soluble CSF-1R-dimeric mutein with enhanced trapping of both CSF-1 and IL-34 reduces suppressive tumor-associated macrophages in pleural mesothelioma
Joalland, Quéméner, Deshayes et al
J Immunother Cancer (2025) 13 (3)
Abstract: Colony stimulating factor-1 receptor (CSF-1R) and its ligands CSF-1 and interleukin (IL)-34 have tumorigenic effects through both induction of suppressive macrophages, and survival/proliferation of tumor cells. In addition, the IL-34 tumorigenic effect can also be mediated by its other receptors, protein-tyrosine phosphatase zeta, Syndecan-1 (CD138) and triggering receptor expressed on myeloid cells 2. Small tyrosine kinase inhibitors are used to block CSF-1R signaling but lack specificity. Neutralizing anti-CSF-1 and/or IL-34 antibodies have been proposed, but their effects are limited. Thus, there is a need for a more specific and yet integrative approach.A human mutated form of the extracellular portion of CSF-1R was in silico modelized to trap both IL-34 and CSF-1 with higher affinity than the wild-type CSF-1R by replacing the methionine residue at position 149 with a Lysine (M149K). The extracellular portion of the mutated CSF-1R M149K was dimerized using the immunoglobulin Fc sequence of a silenced human IgG1 (sCSF-1RM149K-Fc). Signaling through CSF-1R, survival of monocytes and differentiation of suppressive macrophages were analyzed using pleural mesothelioma patient's samples and mesothelioma/macrophage spheroids in vitro and in vivo in the presence of sCSF-1RM149K-Fc or sCSF-1R-Fc wild type control (sCSF-1RWT-Fc).We defined that the D1 to D5 domains of the extracellular portion of CSF-1R were required for efficient binding to IL-34 and CSF-1. The mutein sCSF-1RM149K-Fc trapped with higher affinity than sCSF-1RWT-Fc both CSF-1 and IL-34 added in culture and naturally produced in mesothelioma pleural effusions. sCSF-1RM149K-Fc inhibited CSF-1R signaling, survival and differentiation of human suppressive macrophage in vitro and in vivo induced by pleural mesothelioma cells. Neutralization of IL-34 and CSF-1 by sCSF-1RM149K-Fc also resulted in higher killing of pleural mesothelioma cells by a tumor-specific CD8+ T cell clone in mesothelioma/macrophage spheroids.sCSF-1RM149K-Fc efficiently traps both CSF-1 and IL-34 and inhibits CSF-1R signaling, monocyte survival and suppressive macrophage differentiation induced by pleural mesothelioma cells producing CSF-1 and IL-34, as well as restores cytotoxic T-cell responses. sCSF-1RM149K-Fc has therapeutic potential vs other therapies under development targeting single components of this complex cytokine pathway involved in cancer.© Author(s) (or their employer(s)) 2025. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ Group.
IL-34/TREM2 modulates microglia-mediated inflammation and provides neuroprotection in a mouse model of sporadic Alzheimer's disease
Wang, Huang, Duan et al
J Alzheimers Dis (2025)
Abstract: As a recently identified cytokine, interleukin-34 (IL-34) is predominantly produced by neurons and functions as a modulator for glial functions. Emerging evidence indicates that IL-34 exerted neuroprotective effects in Alzheimer's disease (AD), but the underlying mechanism remained elusive.To uncover the mechanisms by which IL-34 provides neuroprotection in AD.Using senescence-accelerated mouse prone substrain 8 (SAMP8) mice, a well-established model for sporadic AD, we investigated the dynamic changes in brain IL-34 concentrations during AD progression. Afterwards, SAMP8 mice received a 4-week continuous intracerebroventricular infusion of IL-34. Morris water maze test was employed to assess the spatial cognitive functions. Neuronal and synaptic markers, oxidative stress makers, pro-inflammatory cytokines and glial activation markers in the brains of SAMP8 mice were measured. Finally, amyloid-β (Aβ)42-stimulated primary microglia, lentivirus-mediated gene knockdown strategy and co-immunoprecipitation assay were utilized to uncover the possible mechanisms by which IL-34 exerted neuroprotection in AD.In SAMP8 mice, we revealed that brain IL-34 concentrations gradually decreased during AD progression. A 4-week continuous intracerebroventricular infusion of IL-34 rescued spatial cognitive impairments, ameliorated neuronal and synaptic damage, and suppressed oxidative stress and microglia-mediated inflammation in the brains of SAMP8 mice. Using Aβ42-stimulated primary microglia, we demonstrated for the first time that IL-34 suppressed microglial NLRP3 inflammasome activation and pro-inflammatory cytokines release by interacting with triggering receptor expressed on myeloid cells 2 (TREM2), a key regulator of microglial functions.These findings uncover the mechanisms by which IL-34 provides neuroprotection in AD, indicating that IL-34/TREM2 signaling may represent a novel therapeutic strategy for this devastating disease.
Mendelian randomization reveals causal relationships between cytokines and male reproductive diseases
Ding
J Reprod Immunol (2025) 169, 104465
Abstract: This study aims to explore the causal links between cytokines and four male reproductive disorders, namely abnormal spermatozoa (AS), male infertility, erectile dysfunction (ED), and hyperplasia of prostate (HP), employing a two-sample Mendelian randomization (MR) approach. Genetic associations with male reproductive diseases were derived from the IEU OpenGWAS project, with cytokine data from two GWASs focused on the human proteome and cytokines. Estimations were derived using inverse variance weighting, MR-Egger regression, weighted median, weighted model, and simple mode. Furthermore, the robustness of the findings was evaluated through Cochran's Q-test, MR-Egger regression, and leave-one-out sensitivity analysis. Fifteen unique cytokines were identified as having causal relationships with the risk of four male reproductive disorders. Specifically, for AS, interleukin-22 (IL-22), IL-12, and macrophage migration inhibitory factor were negatively correlated with AS, while tumor necrosis factor β levels were positively correlated with AS. In the context of male infertility, IL-2 receptor antagonist levels, IL-34, and granulocyte-colony stimulating factor levels were positively linked to male infertility, whereas IL-21 showed a negative relationship. Regarding ED, IL-19, IL-1β, and eotaxin levels were negatively associated with ED risk, while macrophage inflammatory protein 1β (MIP-1β) levels and interferon gamma-induced protein 10 levels were positively associated. As for HP, stromal-cell-derived factor 1α levels and MIP-1α levels revealed negative associations with HP. In conclusion, this MR analysis revealed that several cytokines were causally associated with male reproductive diseases and could be valuable in offering new insights for further mechanistic and clinical investigations of cytokines-associated male reproductive diseases.Copyright © 2025. Published by Elsevier B.V.
Integration and functionality of human iPSC-derived microglia in a chimeric mouse retinal model
Tang, Zhou, Huang et al
J Neuroinflammation (2025) 22 (1), 53
Abstract: Microglia, the resident immune cells of the central nervous system, play a pivotal role in maintaining homeostasis, responding to injury, and modulating neuroinflammation. However, the limitations of rodent models in accurately representing human microglia have posed significant challenges in the study of retinal diseases.PLX5622 was used to eliminate endogenous microglia in mice through oral and intraperitoneal administration, followed by transplantation of human induced pluripotent stem cell-derived microglia (hiPSC-microglia, iMG) into retinal explants to create a novel ex vivo chimeric model containing xenotransplanted microglia (xMG). The number and proportion of xMG in the retina were quantified using retinal flat-mounting and immunostaining. To evaluate the proliferative capacity and synaptic pruning ability of xMG, the expression of Ki-67 and the phagocytosis of synaptic proteins SV2 and PSD95 was assessed. The chimeric model was stimulated with LPS, and single-cell RNA sequencing (scRNA-seq) was used to analyze transcriptomic changes in iMG and xMG. Mouse IL-34 antibody neutralization experiments were performed, and the behavior of xMG in retinal degenerative Pde6b-/- mice was examined.We demonstrated that xenotransplanted microglia (xMG) successfully migrated to and localized within the mouse retina, adopting homeostatic morphologies. Our approach achieved over 86% integration of human microglia, which maintained key functions including proliferation, immune responsiveness, and synaptic pruning over a 14-day culture period. scRNA-seq of xMG revealed a shift in microglial signatures compared to monoculture iMG, indicating a transition to a more in vivo-like phenotype. In retinal degenerative Pde6b-/- mice, xMG exhibited activation and migrated toward degenerated photoreceptors.This model provides a powerful platform for studying human microglia in the retinal context, offering significant insights for advancing research into retinal degenerative diseases and developing potential therapeutic strategies. Future applications of this model include using patient-derived iPSCs to investigate disease-specific microglial behaviors, thereby enhancing our understanding of microglia-related pathogenesis.© 2025. The Author(s).
Showing 1-4 of 470 papers.
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