Anti_Mouse, mab NKG2D Source Rat
- Known as:
- Anti_Mouse, mab NKG2D Source Rat
- Catalog number:
- 103-M441
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab NKG2D Source Rat
Related genes to: Anti_Mouse, mab NKG2D Source Rat
- 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, mab NKG2D Source Rat
Related articles to: Anti_Mouse, mab NKG2D Source Rat
- Intestinal barrier (IB) dysfunction contributes to metabolic endotoxemia and associated diseases. Specifically, intestinal inflammation upregulates natural killer cell receptor 2D ligands (NKG2DLs) in intestinal epithelial cells (IECs), which triggers excessive immune responses and exacerbates IB injury. The prebiotic xylooligosaccharides (XOS) hold promise for ameliorating such injury by regulating NKG2DLs, yet the underlying mechanisms remain elusive. This study aimed to investigate the efficacy of XOS in improving IB injury and explore its role and molecular mechanisms in mitigating IB damage via NKG2DLs modulation. IB injury models were established in differentiated Caco-2 and MODE-K cells by treatment with 20 ng/mL tumor necrosis factor-α (TNF-α), followed by XOS intervention at concentrations of 50, 100, 150, and 200 μg/mL. Tight junction (TJ) proteins (ZO-1, Occludin) were detected using Western blotting (WB) and immunofluorescence, while barrier permeability was evaluated via transepithelial electrical resistance (TEER), phenol red permeability assay, and transmission electron microscopy (TEM). Additionally, the RhoA/ROCK/MLCK signaling pathway, apoptosis-related factors (Caspase-3, Bcl-2), and the expression of human NKG2DLs (MICA, MICB, ULBP-1) and murine NKG2DLs (Rae-1ε, H60, MULT-1) were analyzed by quantitative real-time PCR (qRT-PCR) or WB, and apoptotic cells were labeled using the TUNEL assay. To further investigate the involvement of NKG2DLs in the protective effect of XOS, RNA interference (RNAi) was performed to knock down NKG2DLs in Caco-2 and MODE-K cells. This conserved mechanism relies on Argonaute (Ago) family proteins that associate with small RNAs to mediate sequence-specific degradation of complementary target RNAs. Subsequently, both cell lines were treated with TNF-α and XOS, and the expression levels of NKG2DLs, ZO-1, and Occludin were determined by qRT-PCR or WB. Compared with TNF-α treatment alone, XOS at the concentrations used in this study significantly attenuated the downregulation and mislocalization of ZO-1 and Occludin in both Caco-2 and MODE-K cells (p < 0.05), increased TEER in Caco-2 cell (p < 0.05), reduced phenol red permeability (p < 0.05), and improved the ultrastructure of TJs and the integrity of microvilli. XOS at the tested concentrations also inhibited the activation of the RhoA/ROCK/MLCK signaling pathway (p < 0.05), suppressed Caspase-3 (p < 0.05) and the number of TUNEL-positive apoptotic cells, and alleviated TNF-α-induced overexpression of both human and murine NKG2DLs (p < 0.05). Notably, RNAi-mediated knockdown of Rae-1ε or H60 in MODE-K cells abrogated the XOS-induced restoration of ZO-1 and Occludin expression under TNF-α challenge. Collectively, under the experimental conditions of this study, XOS mitigate IB injury by inhibiting apoptosis, RhoA/ROCK/MLCK signaling and NKG2DLs in IECs. - Source: PubMed
Publication date: 2026/04/26
Yang JunyiGuo LeiRen ShijingLai QiuyuYang ShunyuWu YanhuaYing ShihaoMeng YitingLi Qing - Psoriasis is a chronic inflammatory skin disease that is characterized by abnormal keratinocyte proliferation and differentiation. This study aimed to explore potential regulatory mechanisms and key genes related to autophagy in the pathogenesis of psoriasis. - Source: PubMed
Publication date: 2026/05/04
Zhou YingChen BingjieChen JunmingFang LingluZhang LitianDou ShuhuiLi FangguHuang JingtongChen Chongyang - Sciatica is a debilitating condition characterized by pain radiating along the sciatic nerve, often manifesting due to underlying neuroinflammatory processes. Understanding the molecular mechanisms linking neuroinflammation to sciatica is essential for developing targeted therapeutic interventions. Recent studies have suggested that specific neuroinflammatory genes may play a pivotal role in the pathophysiology of sciatica, offering a potential avenue for understanding this condition. - Source: PubMed
Publication date: 2026/03/05
Jiang FeiXu YangYe Xi-HongZheng BinZhang Guang-LeiLi Ren-Hu - Glucocorticoids, interferon-2α, colchicine, and azathioprine are recommended by EULAR for various manifestations of Behçet syndrome (BS). Curcumin is a natural compound with anti-inflammatory activities. NKG2D is a receptor expressed by NK, NKT, and CD8pos T cells implicated in recognizing stressed cells. This study aimed to: (i) evaluate the effects of selected drugs used in the management of BS plus curcumin on NKG2D expression by lymphocytes; (ii) test the effects of these drugs on immune cell subsets; and (iii) determine whether immune cells from BS patients respond differently to those from healthy controls (CTR). Peripheral blood mononuclear cells from BS patients and CTR were treated with dexamethasone, interferon-2α, colchicine, azathioprine, or curcumin for 48 h in the presence or absence of IL-15. NKG2D expression on NK, NKT, and CD8pos T cells and the percentages/absolute counts of NK, NKT, T, and B cells were evaluated by flow cytometry. All drugs down-regulated NKG2D expression. The reduction was more pronounced in CTR than in BS patients following dexamethasone treatment, in BS patients than in CTR following colchicine treatment. Dexamethasone reduced NK cells in the absence of IL-15, but increased them in its presence. Colchicine reduced B cells regardless of IL-15 stimulation. Azathioprine also down-regulated B cells, but only in the presence of IL-15 stimulation. Drugs used in the management of BS reduced NKG2D expression, potentially decreasing the activation of cytotoxic cells. Immune cells from BS patients responded differently to dexamethasone and colchicine compared to those from CTR. - Source: PubMed
Bonacini MartinaMuratore FrancescoAlbertazzi LauraCimino LucaColla RossanaZerbini AlessandroSalvarani CarloCroci Stefania - Pulmonary fibrosis (PF) is a progressive, fatal interstitial lung disease with limited therapeutic options. Emerging evidence implicates immune-fibrotic crosstalk in PF pathogenesis, although the underlying molecular mechanisms remain poorly defined. While Natural Killer (NK) cells and their activating receptor NKG2D have been linked to fibrotic processes, their functional role in PF is unclear. This study investigates the NKG2D-DAP12-SYK-p53-p21 signaling axis as a potential driver of PF through immune-fibroblast interactions. - Source: PubMed
Publication date: 2026/03/02
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