Anti-Mouse CD314 (NKG2D) PE 200 ug
- Known as:
- Antibody toMouse CD314 (NKG2D) PE 200 ug
- Catalog number:
- 12-5873-83
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD314 (NKG2D) 200
Related genes to: Anti-Mouse CD314 (NKG2D) PE 200 ug
- Gene:
- KLRK1 NIH gene
- Name:
- killer cell lectin like receptor K1
- Previous symbol:
- D12S2489E
- Synonyms:
- NKG2D, KLR, NKG2-D, CD314
- Chromosome:
- 12p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-12
- Date modifiied:
- 2016-10-05
Related products to: Anti-Mouse CD314 (NKG2D) PE 200 ug
Related articles to: Anti-Mouse CD314 (NKG2D) PE 200 ug
- Stem cell-derived β (SC-β) cells are a promising therapy for type 1 diabetes (T1D), but their long-term efficacy is limited by immune-mediated graft rejection. Platelet-derived exosome product (PEP) has emerged as a novel immunomodulatory agent, although its effect on SC-β cell xenograft rejection remains unclear. Here, we evaluated PEP in stimulated human peripheral blood mononuclear cells (PBMCs) and in an immunocompetent mouse model of SC-β cell transplantation under the kidney capsule. Immune-related gene expression was assessed by quantitative PCR, immune cell infiltration by immunofluorescence, and graft function by circulating human insulin. In vitro, PEP reduced NK-cell-associated gene expression, including NK1.1, EOMES, and KLRK1, and increased IL-10 expression. In vivo, untreated SC-β cell xenografts showed progressive immune infiltration and loss of detectable human insulin by day 14, whereas PEP-treated grafts retained detectable insulin through day 14 across co-transplantation, pretreatment, and systemic administration strategies. PEP co-transplantation delayed, but did not prevent, xenograft rejection, with graft loss observed by day 21. This delay was associated with reduced NK1.1+ cell infiltration and lower expression of selected inflammatory and rejection-associated markers, including NK1.1, Nos2, and Nlrp3. These findings suggest that PEP modulates graft-associated immune responses and may serve as an adjunct immunomodulatory strategy for stem cell-based therapies for type 1 diabetes. Further studies are needed to evaluate sustained graft durability, safety, and translational efficacy. - Source: PubMed
Publication date: 2026/07/29
Khashim ZenithShrestha SwikritiHassoun ShaimaaLaw Ethan WSchornack Anna Marie RLacap JessicaBeetler Danielle JWeigel Gabriel JJennings Lauren TBecher LauraParadise ChrisBehfar AttaFairweather DeLisaPeterson Quinn P - The aim of this study was to detect genomic regions and genes associated with gastrointestinal nematodes (GIN) resistance in Pelibuey sheep, based in deworming necessity (NOD) estimated by fecal egg count (FEC). During a ten-months period, deworming criterion was based on GIN eggs per gram (EPG), then animals exceeding 1000 EPG were dewormed, and individuals were classified as cases (dewormed at least once) or controls (non-deworming at all). Animals were genotyped with the GGP Ovine50k genome profiler microarray. Quality control of dataset and case-control GWAS were carried to identify associated candidate genes and quantitative trait loci (QTL). Two genome-wide strongly associated SNPs were detected on chromosomes 2 and 3, located near FEC associated QTLs and immune-related genes: GALNT6, KLRK1, KLRD1, CLEC1B, FGF13, TMEM52B, OLR1, and CLEC7A. The identified genes are involved in key defense mechanisms such as mucus synthesis, immune signaling, and natural-killer cell activation, supporting their relevance as candidate genes for GIN-resistance selection in Pelibuey hair-sheep. - Source: PubMed
Publication date: 2026/07/04
Esparza-Acebo Leilany MargaritaOjeda-Robertos Nadia FlorenciaDe La Rosa-Reyna Xochitl FabiolaParra-Bracamonte Gaspar Manuel - Chimeric antigen receptor T-cell (CAR-T) therapies have shown potential in clinical trials for glioblastoma, yet treatment responses vary due to heterogeneous antigen expression and post-treatment immune escape. NKG2D-based CAR-T cells have exhibited a favorable safety profile in patients with hematologic malignancies and demonstrated potent antitumor activity in xenograft models, including those of glioblastoma. Nevertheless, glioma cells could evade immune recognition by downregulating or proteolytically shedding NKG2D ligands. To enhance the efficacy of NKG2D CAR-T therapy, we investigated its combination with preclinical agents capable of penetrating the blood-brain barrier that could upregulate NKG2D ligands on glioma cells. Our study revealed that resveratrol (RSV), a bioactive polyphenol, significantly increased the surface expression of NKG2D ligands on glioblastoma cells. RSV pretreatment sensitized these cells to NKG2D CAR-T-mediated killing . Additionally, the combination of RSV with NKG2D CAR-T cells demonstrated potent antitumor activity Mechanistically, RSV potentially induced NKG2D ligand expression via activation of the p53 signaling pathway. These preclinical findings identify RSV as a promising pharmacological adjuvant that enhances NKG2D CAR-T efficacy in glioblastoma, supporting further translational and clinical evaluation of this combinatory approach. - Source: PubMed
Publication date: 2026/07/06
Liang WeiTang YexiaoSaliu Muhammad AuwalSalisu Mansur DabaiChen CuimeiXu ZhimingXu ShuLiu MaoxuanWan Xiaochun - Clear cell renal cell carcinoma (ccRCC) is a prevalent malignancy, representing 80-90% of kidney cancer cases. This study aimed to identify potential prognostic genes to improve patient survival prediction and provide new insights into the pathogenesis and treatment of ccRCC through comprehensive whole transcriptome sequencing analysis. - Source: PubMed
Publication date: 2026/07/08
Chang PengchengQin ZitongLiu RunzhangWang BinxianLu HuaiquanJing SuoshiGuo ChenhaoLi Weiping - Immune surveillance is increasingly recognized as a modifier of myeloproliferative neoplasm (MPN) initiation and evolution, yet the contribution of the NKG2D receptor and its ligands MICA/MICB to CALR-mutated disease remains unclear. We performed high-resolution next-generation sequencing genotyping of MICA and MICB in 43 patients with CALR-mutated MPN (WHO 2022 criteria) and compared the allele and haplotype distributions with those of 156 healthy Bulgarian controls and 85 patients with JAK2 V617F-positive MPN. Associations were tested using age- and sex-adjusted additive generalized linear models; bi-locus haplotypes were evaluated using haplotype score methods. In a genotyped subgroup (35 CALR-mutated MPN patients and 105 controls), functional KLRK1 (NKG2D) polymorphisms were analyzed for haplotype-level associations. We also performed 700 ns molecular dynamics simulations of selected MICA variants in complex with NKG2D and reanalyzed publicly available single-cell RNA-sequencing data (GSE117826) and RNA-sequencing data from CRISPR/Cas9-edited CALR-mutant iPSC-derived megakaryocytes to evaluate MICA/MICB expression. MICA*004:001 was significantly associated with CALR-mutated MPN versus controls ( = 0.004; Bonferroni-adjusted = 0.047), while MICB*008:001 showed only nominal association. Exploratory haplotype analyses identified a MICA*009:01-MICB*004:001 haplotype associated with CALR-mutated status ( = 0.008) and a KLRK1 G-A-G-T haplotype (rs1049174-rs2617160-rs2246809-rs2617170) associated with increased CALR-mutated MPN risk (OR = 3.61; = 0.029). Transcriptomic reanalysis indicated a higher fraction of CALR-mutant stem and progenitor cells expressing detectable MICA/MICB transcripts, and heterozygous CALR-mutant megakaryocytes exhibited higher MICA expression than the wild type. Together, these data support an exploratory immunogenetic and transcriptomic link between the NKG2D-MICA/MICB axis and CALR-mutated MPN, but direct protein-level and functional studies are required before mechanistic or therapeutic conclusions can be drawn. - Source: PubMed
Publication date: 2026/06/24
Shivarov VelizarTsvetkova GerganaMicheva IlinaHadjiev EvgueniyPetkova JasminaMadjarova GaliaIvanova Milena