CD86, Clone 24F, Mab anti_Rat, Biotin
- Known as:
- CD86, Clone 24F, Mab anti_Rat, Biotin
- Catalog number:
- ACL086B
- Product Quantity:
- 100 µg.
- Category:
- -
- Supplier:
- Accu
- Gene target:
- CD86 Clone 24F Mab anti_Rat Biotin
Related genes to: CD86, Clone 24F, Mab anti_Rat, Biotin
- 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, Biotin
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(+)-Biotin (+)-Sulfoxide CAS: 10406-89-0 Formula: C10H16N2O4S(+)-Biotin 4-Amidobenzoic Acid, Sodium Salt C17H20N3NaO4S CAS: 102418-74-6(+)-Biotin 4-Amidobenzoic Acid, Sodium Salt CAS: 102418-74-6 Formula: C17H20N3NaO4S(+)-Biotin-PFP-ester CAS: 120550-35-8(-)-Biotin Sulfoxide CAS: 3376-83-8 Formula: C10H16N2O4S(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 Related articles to: CD86, Clone 24F, Mab anti_Rat, Biotin
- Triple-negative breast cancer (TNBC) is characterized by aggressive behaviors, limited treatment options, and poor prognosis. Adipocytes, the predominant cellular component in the tumor microenvironment (TME) of breast cancer, interact bidirectionally with tumor cells, influencing tumor progression and immune evasion. Understanding the interactions between TNBC cells and adipocytes within TME is crucial for identifying new therapeutic targets. We employed murine models and co-culture systems to investigate the effects of adipocyte-TNBC cell interactions on lipid metabolism, signaling pathways, and immune evasion mechanisms. Our findings revealed that TNBC cells utilized PCSK9-enriched exosome transfer to induce the formation of cancer-associated adipocytes (CAAs) from adipocytes. These CAAs, characterized by altered lipid content and a pro-inflammatory secretory profile, contributed to a tumor-promoting environment. Additionally, CAAs enhanced the immune evasion properties of TNBC by modifying the metabolic pathways of tumor cells. In depth, CAAs induced fatty acid oxidation (FAO) in TNBC cells, which facilitated G3BP1-induced stabilization of PCSK9 and promoted OPTN-mediated autophagic degradation of the co-stimulatory molecules CD80 and CD86, which are essential for T cell activation. Our study identifies PCSK9 as a central mediator in the bidirectional interactions between TNBC cells and adipocytes, influencing tumor progression and immune evasion. These insights suggest that targeting the PCSK9 pathway could provide new therapeutic opportunities for TNBC, potentially transforming treatment approaches and improving patient outcomes. Further investigation into the mechanisms by which PCSK9 regulates these processes may yield novel combination strategies to enhance the efficacy of immunotherapy in TNBC. - Source: PubMed
Publication date: 2026/07/03
Zhai DuanyangShi YaweiFan YuanjianZheng ShaoquanZhang MengmengZhou ShulingShao NanZhang YunjianCui JihongLin Ying - To investigate the protective effects of epigallocatechin gallate (EGCG) on sepsis-induced myocardial injury (SIMI) in mice and elucidate its underlying mechanisms. - Source: PubMed
Publication date: 2026/07/01
Han HuiLi SiyuFang ShanshanZhang LinlinYang RuiMehmood ShomailaJia Qiang - Osteoporosis is a prevalent skeletal disorder marked by reduced bone strength and increased fragility, especially in postmenopausal women and older adults. Icariin (ICA), a natural flavonoid, has been reported to stimulate osteoblastogenesis and suppress osteoclast activity. - Source: PubMed
Publication date: 2026/07/03
Yang YongdongLuo ChuanRen XingyuTan QiushengDeng Caifu - is a traditional medicinal herb used for inflammatory and infectious diseases, but its mechanisms against endotoxin‑induced systemic inflammation remain unclear. The present study investigated the protective effects of total phenolics from (TPLA) on lipopolysaccharide (LPS)‑induced inflammatory injury and explored the involvement of PTEN‑induced putative kinase 1 (PINK1)/Parkin‑associated mitophagy and macrophage polarization. LPS‑induced inflammatory models were established in RAW264.7 macrophages and C57BL/6 mice. Cell viability, apoptosis, mitochondrial membrane potential (MMP), cytokine production, macrophage polarization and mitophagy‑related protein expression were evaluated. Mdivi‑1 was used to assess the involvement of mitophagy‑related signaling. , core body temperature, serum cytokines, and lung and liver histopathology were examined. TPLA improved the viability of LPS‑stimulated macrophages, reduced apoptosis, restored MMP, decreased p62 expression, and increased PINK1, Parkin and the LC3‑II/LC3‑I ratio. TPLA also suppressed M1‑associated indicators, including inducible nitric oxide synthase, IL‑12 and CD80/CD86, while enhancing M2‑associated indicators, including arginase 1, IL‑10 and CD206/CD163. In addition, TPLA reduced IL‑1β, IL‑6 and TNF‑α release. Mdivi‑1 partially reversed the effects of high‑dose TPLA on mitophagy‑related protein expression and macrophage polarization. In LPS‑challenged mice, TPLA alleviated hypothermia, reduced systemic cytokine levels, and attenuated hepatic and pulmonary injury. These findings suggest that TPLA protects against LPS‑induced systemic inflammation and hepatic‑pulmonary injury by modulating PINK1/Parkin‑associated mitophagy‑related signaling and macrophage polarization. - Source: PubMed
Publication date: 2026/07/03
Wei JiangcunZhong WenZhou GuangyunHuang MingtaoHuang XiaodongLiang Jing - Trichinella spiralis, a food-borne zoonotic parasitic nematode with global distribution, poses a significant hazard to both public health and the safety of animal-derived meat products. Previous studies have identified a trypsin from T. spiralis, designated as TsTryp, within the excretory-secretory antigens (ESA) of intestinal infective larvae (IIL). Notably, the recombinant TsTryp (rTsTryp) was found to facilitate the T. spiralis larva invasion of gut epithelia, whereas anti-rTsTryp antibodies exerted a clear inhibitory effect on this larval invasion process. However, whether TsTryp regulates macrophage polarization in experimental T. spiralis infection and its molecular mechanisms are not clear. This present research intends to explore the functional significance of rTsTryp in macrophage polarization and cytotoxicity killing newborn larvae (NBL). The indirect immunofluorescence test verified specific binding between rTsTryp and RAW264.7 cells. qPCR, Western blot, and flow cytometry exhibited that rTsTryp induced the marked upregulation of iNOS expression, increased expression levels of p-NF-κB p65 and p-IκB-α, and elevated the proportion of CD86 cells and drove the macrophage M1 polarization. qPCR and ELISA results further demonstrated pronounced elevation in proinflammatory cytokine (IL-6 and TNF-α) expression levels of macrophages following rTsTryp stimulation. Pretreating macrophages by the NF-κB inhibitor pyrrolidinecarbodithioic acid (PDTC) significantly abolished and reduced rTsTryp-increased expression levels of iNOS, p-NF-κB p65, and p-IκB-α and proinflammatory cytokine production. rTsTryp treatment also prominently strengthened macrophages' antibody-dependent cellular cytotoxicity (ADCC) killing NBL, whereas PDTC pretreatment significantly decreased this cytotoxicity. The findings indicated that rTsTryp specifically bound to macrophages and activated the NF-κB signal pathway, drove M1 polarization and increased proinflammatory cytokine expression, and enhanced the ADCC activity killing larvae. - Source: PubMed
Cong Pei KunZhang YaoZhang RuZhang Xin ZhuoLong Shao RongLiu Ruo DanXu JiaCui JingWang Zhong Quan