CD86, Clone 24F, Mab anti_Rat, PE
- Known as:
- CD86, Clone 24F, Mab anti_Rat, PE
- Catalog number:
- ACL086PE
- Product Quantity:
- 50 µg.
- Category:
- -
- Supplier:
- Accu
- Gene target:
- CD86 Clone 24F Mab anti_Rat
Related genes to: CD86, Clone 24F, Mab anti_Rat, PE
- Gene:
- CD86 NIH gene
- Name:
- CD86 molecule
- Previous symbol:
- CD28LG2
- Synonyms:
- B7.2, B7-2
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1994-12-07
- Date modifiied:
- 2016-10-05
Related products to: CD86, Clone 24F, Mab anti_Rat, PE
Alkaline Phosphatase Conjugated Affinity Purified anti-Swine IgG (H&L) [Goat] Secondary_Antibodiesα - Calcitonin Gene Related Peptide, α - CGRP, rat'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(2_Furoyl)_PAR_2 (2_6)_Orn amide (mouse, rat) Salt Trifluoroacetate Binding _ Synonym (2_Furoyl)_LIGRLOamide SumFormula C36H63N11O8(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala11·22·28)_VIP (human, bovine, porcine, rat) Salt Trifluoroacetate Binding _ Synonym (Ala11·22·28)_Aviptadil SumFormula C139H231N43O39S(Ala13)-Apelin-13 (human, bovine, mouse, rat) 98% C63H107N23O16S CAS: 568565-11-7(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala13)_Apelin_13 (human, bovine, mouse, rat) Salt Trifluoroacetate Binding _ Synonym SumFormula C63H107N23O16S(Ala96)-Myelin Basic Protein (87-99) (human, bovine, rat) 98% C70H110N20O17 CAS:(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Ala96)_Myelin Basic Protein (87_99) (human, bovine, rat) Salt _ Binding _ Synonym SumFormula C72H112N20O17(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2 Related articles to: CD86, Clone 24F, Mab anti_Rat, PE
- Duchenne muscular dystrophy (DMD) is an X-linked recessive disorder caused by dystrophin gene mutations. This study investigated the therapeutic effects of leflunomide, a STAT1 inhibitor on dystrophic muscles. - Source: PubMed
Publication date: 2026/06/26
Hu WantingTong HaoweiZhu MaolinWang HunaHuang XiaofeiFan ShushengGuo GuangyaoIsmail MohammedZhao LeiLi XihuaZhang LuyongYu QinweiJiang Zhenzhou - Diabetic foot ulcer (DFU) represents a significant challenge in clinical management due to its complexity and the impaired wound-healing process associated with diabetes. The role of MAF bZIP transcription factor B (MAFB) in regulating macrophage polarization and its potential impact on DFU healing is an area of growing interest. This study investigates the molecular mechanisms by which MAFB influences diabetic wound healing. MAFB and WD repeat domain 74 (WDR74) protein levels were evaluated using western blotting. mRNA expression of target genes was quantified through quantitative real-time polymerase chain reaction. Flow cytometry was utilized to analyze the proportion of cluster of differentiation 206 (CD206) and CD86-positive cells. Enzyme-linked immunosorbent assays were conducted to measure the concentrations of interleukin-6, tumor necrosis factor-alpha, and interleukin-10. Malondialdehyde production and superoxide dismutase activity were determined using colorimetric assays. Reactive oxygen species levels were quantified with a fluorometric assay. Chromatin immunoprecipitation and dual-luciferase reporter assays were performed to examine the interaction between MAFB and WDR74. Furthermore, a rat model of DFU was established to validate in vivo findings regarding MAFB's role in M2 polarization, inflammation, and oxidative stress. Histological evaluation of wound tissues was performed using hematoxylin and eosin (H&E)and Masson's trichrome staining. The results showed that elevated MAFB levels in LPS-stimulated RAW264.7 macrophages led to a shift towards an M2 phenotype, alongside decreased inflammatory responses and oxidative stress. Mechanistically, MAFB was found to activate the transcription of WDR74 in these macrophages. Notably, WDR74 upregulation promoted M2 polarization and mitigated inflammation and oxidative stress in LPS-treated cells, whereas silencing WDR74 reversed the beneficial effects of MAFB overexpression. Further, in vivo, MAFB promoted wound healing of DFU rats by repressing inflammatory and oxidative stress responses. Thus, MAFB overexpression promoted diabetic foot ulcer healing by fostering a tissue repair phenotype and suppressing inflammation and oxidative stress through the transcriptional activation of WDR74. These findings underscore the potential of MAFB as a therapeutic target for improving diabetic wound healing, which could lead to novel clinical strategies for treating DFUs. - Source: PubMed
Publication date: 2026/06/26
Lin HaiCai QiWang TingtingZheng LiYu MeizhenWen Yinwei - Lindl. (SOL) has long been used in traditional medicine for inflammatory disorders, yet its molecular actions in reproductive tract inflammation remain poorly defined. This study investigated the phytochemical composition and anti-inflammatory mechanisms of an aqueous SOL leaf extract using murine and cellular models of endometritis. Ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) analysis revealed major constituents including rutin, salidroside, and esculetin. In a murine model of bacterial endometritis induced by and , SOL markedly attenuated uterine edema, epithelial disruption, leukocyte infiltration, and bacterial burden. Mechanistic analyses demonstrated that SOL suppressed the Toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88) axis and decreased the uterine expression of interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α). In lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages, SOL and its principal monomers significantly reduced nitric oxide (NO) and reactive oxygen species (ROS) production both in the presence and absence of the TLR4 inhibitor TAK-242, suggesting additional modulation of redox-responsive pathways beyond canonical TLR4 signaling. Moreover, SOL selectively decreased the M1 macrophage marker CD86 in uterine tissue without altering CD163, consistent with partial inhibition of pro-inflammatory macrophage polarization. Collectively, these findings indicate that SOL exerts potent antimicrobial, anti-inflammatory, and antioxidative effects through coordinated regulation of innate immune signaling and macrophage activation, supporting its potential as a natural therapeutic candidate for inflammation-associated reproductive disorders. - Source: PubMed
Publication date: 2026/05/28
Zhang YangShen JinjinLi JiawenZhu TongFu JiahaoChen XueyingSu JingHao JingyouLi YanhuaLiu Yanyan - Preeclampsia (PE) is a severe pregnancy-specific hypertensive disorder characterized by immune microenvironment dysregulation at the maternal-fetal interface, with decidual macrophage phenotypic imbalance being a key pathological feature. The Ghrelin/growth hormone secretagogue receptor-1a (GHSR-1a) axis exerts immunomodulatory and anti-inflammatory effects, but its role in regulating decidual macrophage infiltration and phenotypic marker expression in PE remains unclear. In this study, we first detected the expression of the Ghrelin/GHSR-1a axis in decidual tissues from 10 healthy pregnant women and 12 PE patients via immunohistochemistry (IHC). We then established a lipopolysaccharide (LPS)-induced PE-like rat model to investigate the axis's functional role and underlying mechanisms. Intriguingly, clinical analysis revealed a severity-dependent compensatory escalation of the Ghrelin/GHSR-1a axis in PE decidual tissues, potentially representing an endogenous antagonistic response to pregnancy-associated pathological stress. In the animal model, exogenous Ghrelin supplementation reversed LPS-induced PE-like phenotypes, including hypertension, proteinuria, fetal growth restriction (FGR), and placental dysfunction, and alleviated pathological damage to the maternal liver, kidney, and placenta. Mechanistically, Ghrelin modulated decidual macrophage phenotypic marker expression by downregulating the M1 marker CD86 and upregulating the M2 marker CD163 and promoted trophoblast invasion and spiral artery remodeling by restoring laminin, α-cytokeratin 7 (α-CK7), and α-smooth muscle actin (α-SMA) expression in placental tissue. All protective effects of Ghrelin were abrogated by co-administration of D-lys-3-GHRP-6, a specific GHSR-1a antagonist, confirming the dependence on the Ghrelin/GHSR-1a axis. Collectively, our findings suggest that the Ghrelin/GHSR-1a axis is compensatorily upregulated in PE and may exert a protective role by regulating decidual macrophage phenotypic marker expression and improving placental function, providing preliminary evidence that this axis merits further investigation as a potential research target for PE. - Source: PubMed
Publication date: 2026/05/29
Zhang LinglingYuan JianiHu NingningYu JianZhang LiwenChen RujunWang Xiaoqin - The tumor microenvironment (TME), especially tumor-associated macrophages (TAMs), plays a critical role in prostate cancer (PCa) progression. Cathepsin Z (CTSZ) is a lysosomal protease implicated in various malignancies, but its specific function and mechanism within the PCa-associated TAMs remain largely unexplored. - Source: PubMed
Publication date: 2026/06/25
Liu YouxinChen SaipengXu JieYuan HangYang HanziDeng BingqianFeng JieLiu HetingXie LanglangHuang GangShen Wenhao