Monkey IP-10 ELISA kit
- Known as:
- Monkey IP-10 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- CT157A
- Product Quantity:
- 5-plate*
- Category:
- -
- Supplier:
- U-CyTech
- Gene target:
- Monkey IP-10 ELISA kit
Related genes to: Monkey IP-10 ELISA kit
- Gene:
- BBIP1 NIH gene
- Name:
- BBSome interacting protein 1
- Previous symbol:
- NCRNA00081
- Synonyms:
- bA348N5.3, BBIP10, BBS18
- Chromosome:
- 10q25.2
- Locus Type:
- gene with protein product
- Date approved:
- 2008-09-02
- Date modifiied:
- 2016-10-05
- Gene:
- CXCR3 NIH gene
- Name:
- C-X-C motif chemokine receptor 3
- Previous symbol:
- GPR9
- Synonyms:
- CKR-L2, CMKAR3, IP10-R, MigR, CD183
- Chromosome:
- Xq13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-01
- Date modifiied:
- 2016-10-05
- Gene:
- MED24 NIH gene
- Name:
- mediator complex subunit 24
- Previous symbol:
- THRAP4, CRSP4
- Synonyms:
- TRAP100, KIAA0130, DRIP100, CRSP100, MED5
- Chromosome:
- 17q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-30
- Date modifiied:
- 2016-10-05
- Gene:
- PPIAP10 NIH gene
- Name:
- peptidylprolyl isomerase A pseudogene 10
- Previous symbol:
- PPIAL2, PPIP10
- Synonyms:
- CRP
- Chromosome:
- 20q13.2
- Locus Type:
- pseudogene
- Date approved:
- 1998-10-12
- Date modifiied:
- 2017-08-21
- Gene:
- PRPF40A NIH gene
- Name:
- pre-mRNA processing factor 40 homolog A
- Previous symbol:
- FNBP3
- Synonyms:
- FLJ20585, FBP11, HYPA, NY-REN-6, HIP10, FBP-11, FLAF1, Prp40
- Chromosome:
- 2q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-08-28
- Date modifiied:
- 2018-11-19
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- The extracellular cyclic GMP-AMP (cGAMP)-ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1) axis is an emerging pharmacological target that links tumor-intrinsic DNA stress to antitumor immunity. Tumor cells can generate cGAMP in response to chromosomal instability, micronuclear rupture, replication stress, and therapy-induced DNA damage. After export into the tumor microenvironment, extracellular cGAMP may be transferred to antigen-presenting cells and activate stimulator of interferon genes (STING)-dependent type I interferon and C-X-C motif chemokine ligand 10 (CXCL10) programs, thereby supporting dendritic-cell activation, immune priming, and cytotoxic T-cell recruitment. ENPP1 restricts this process by degrading extracellular cGAMP and by contributing to nucleotide catabolism associated with AMP- and adenosine-dependent immunosuppression. Accordingly, pharmacological ENPP1 inhibition differs from direct STING agonism by preserving endogenous tumor-derived cGAMP rather than imposing exogenous receptor activation. This Review summarizes the mechanistic basis, pharmacological rationale, and translational challenges of targeting the extracellular cGAMP-ENPP1 axis in cancer. We discuss ENPP1 inhibitors and cGAMP-stabilizing approaches, focusing on mechanism of action, pharmacokinetic/pharmacodynamic (PK/PD) relationships, target engagement, therapeutic window, and potential immunotoxicological constraints. We also propose a biomarker-guided framework incorporating cGAMP-generating capacity, ENPP1 expression and enzymatic activity, STING-response competence, and on-treatment pharmacodynamic conversion. Finally, we evaluate rational combinations with radiotherapy, chemotherapy, DNA damage response-targeted agents, immune checkpoint blockade, and immune-metabolic modulators. Clinical translation will require patient stratification, schedule-aware combination design, and robust pharmacodynamic validation in early-phase studies. - Source: PubMed
Publication date: 2026/07/29
Mu Kai-LangLiao Rui-QiXie Jun-LiTang Xiao-MinLiu Yu-ChenLiu GangJu Zhi-GangZhang LuYuan YuanPang Yu-Xin - Type 1 diabetes (T1D) is an autoimmune disease that destroys insulin-producing β-cells. Extracellular vesicles (EVs), including exosomes, are now recognized as important mediators of intercellular communication in immune regulation and metabolic homeostasis. Yet how immune cell-derived circulating EVs contribute to metabolic dysfunction across the disease spectrum-from preclinical to clinical T1D-has not been systematically examined. - Source: PubMed
Publication date: 2026/07/29
Qu BingbingZeng BingjunYuan YuruiHe XiulingRen LinaZhu HangGuan Xuanke - Alopecia areata (AA) is an autoimmune hair disorder characterized by interferon-gamma (IFN-γ)-driven inflammation and collapse of hair follicle immune privilege. Although Janus kinase (JAK) inhibitors are effective, incomplete or delayed responses remain common. Minoxidil is frequently combined with JAK inhibitors in clinical practice, yet its immunomodulatory mechanisms in AA are unclear. We investigated the effects of minoxidil sulfate (MXS) on inflammatory signalling, immune privilege-associated features and mitochondrial stress responses, and evaluated whether MXS enhances the anti-inflammatory effects of the JAK inhibitor baricitinib. Clinical observations of patients receiving combination therapy were descriptively assessed. Mechanistic studies were conducted in human outer root sheath (ORS) cells stimulated with IFN-γ and polyinosinic:polycytidylic acid to model the AA inflammatory microenvironment. Representative clinical observations suggested accelerated hair regrowth after addition of oral minoxidil to baricitinib. In inflamed ORS cells, MXS enhanced baricitinib-mediated suppression of STAT1 phosphorylation and IFN-γ-inducible chemokines (CXCL9, CXCL10, CXCL11). MXS also exerted baricitinib-independent anti-inflammatory effects by inhibiting STAT1 and STAT3 activation. Furthermore, MXS reduced inflammatory induction of MHC class I expression and partially restored insulin-like growth factor-1 expression. MXS attenuated cytosolic and mitochondrial reactive oxygen species accumulation, mitochondrial DNA damage and loss of mitochondrial membrane potential, accompanied by suppression of NOX1 and NOX4 expression. These findings suggest that MXS modulates inflammatory signalling, preserves immune privilege-associated features and protects mitochondrial integrity, providing a mechanistic rationale for adjunctive use with JAK inhibitors without additional systemic immunosuppression. - Source: PubMed
Shin Jung-MinGo BogyeongJung Kyung EunKim Chang DeokSeo Young-JoonLee Young - Fc-gamma receptors (FcγRs) regulate IgG antibody activity, and Fc-engineering is a proven method to improve the efficacy of tumor-targeting antibodies. Here, we explore tailored FcγR blockade to enhance the therapeutic efficacy and tolerability of immune checkpoint-blocking (ICB) antibodies. - Source: PubMed
Publication date: 2026/07/25
Oldham Robert JMårtensson LindaSemmrich MonikaYoosuf NiyazHolmkvist PetraGraham Lara VTaylor Martin CCleary Kirstie L SYazdani MonaBuckingham Josephine FRoghanian AliKarlsson IngridBeers Stephen ATeige IngridCragg Mark SFrendéus Björn - A case-control study was conducted in Basrah, Iraq, between September 2023 and December 2024. Stool samples from 110 symptomatic individuals were examined microscopically using direct wet mounts, concentration methods, and permanent staining techniques. Confirmed cases included 43 patients infected with Entamoeba spp. and 30 patients infected with Giardia duodenalis, while 50 apparently healthy individuals served as controls. Hemoglobin and leukocyte differential counts, serum total protein, albumin, interleukin-1 beta (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), C-X-C motif chemokine ligand 10 (CXCL10), malondialdehyde (MDA), glutathione (GSH), and lactate dehydrogenase (LDH) were evaluated. The results demonstrated significant hematological, biochemical, inflammatory, and oxidative stress alterations among infected individuals. Hemoglobin, serum total protein, and albumin levels were significantly reduced in both amoebiasis and giardiasis patients compared with healthy controls, with more pronounced alterations observed in amoebiasis. IL-1β, IL-6, IL-8, CXCL10, MDA, and LDH levels were significantly elevated, whereas increased GSH levels may reflect a compensatory antioxidant response rather than antioxidant depletion, particularly among amoebiasis patients. Giardiasis patients exhibited inflammatory and oxidative stress changes, although these alterations were less pronounced than those observed in amoebiasis. Comparative analysis indicated that amoebiasis induced stronger inflammatory, oxidative, and tissue injury responses than giardiasis, due to the invasive nature of amoebic infection. Overall, Entamoeba spp. infection elicited stronger inflammatory, oxidative stress, and tissue injury responses than giardiasis, providing further insight into the distinct host-parasite interactions associated with these intestinal protozoan infections. - Source: PubMed
Publication date: 2026/07/28
Al-Hilfi SufyanAl-Hilfi AthraaThamer Sanaa