Anti_Mouse, mab 4_1BBL Source Rat
- Known as:
- Anti_Mouse, mab 4_1BBL Source Rat
- Catalog number:
- 103-M209
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Reliatech
- Gene target:
- Anti_Mouse mab 4_1BBL Source Rat
Related products to: Anti_Mouse, mab 4_1BBL Source Rat
Related articles to: Anti_Mouse, mab 4_1BBL Source Rat
- CD161CD8 T cells, a cytotoxic T cell subset, remain poorly defined in terms of their clinical significance and functional role in esophageal squamous cell carcinoma (ESCC), which has limited the advancement of precision immunotherapy strategies. - Source: PubMed
Publication date: 2026/07/09
Xu Shao-JunChen ChaoYe Ming-QiangHuang JinTu Jia-HuaShen Yan-MingLuo Yun-FanSun Zhao-MinChen JieLin Ji-HongGuan JunHuang Han-XingChen Shu Chen - Compared to lean pig genotypes, the local Krškopolje pig is characterised by a greater capacity for lipid and lower capacity for protein deposition, along with lower dietary protein requirements. The aim of the present study was to unravel the transcriptomic differences in subcutaneous adipose tissue between the local Krškopolje pig and modern hybrids, as well as to study the impact of the reduced protein diet in both genotypes. Differential gene expression analysis between local and modern pigs revealed 375 differentially expressed genes, with 189 upregulated and 186 downregulated in Krškopolje pig. Among the upregulated genes, several suggested more pronounced adipogenesis (SLC7A10, ADIRF, INHBB, and SFRP2) in the Krškopolje pig. In addition, genes encoding collagen proteins and extracellular matrix remodelling (e.g., COL6A5, COL4A5, COL2A1), calcium signalling (TRPV4, CAMK2A, CALML5), pro-inflammatory cytokines (e.g., IL1A, TNFSF9, CXCL8, PTGS2 etc.) and cholesterol metabolism (CYP1A1, CYP2A19, CES1 etc.) were differentially expressed. The reduced protein diet induced only minor changes in gene expression at the individual gene level. However, gene set enrichment analysis revealed that, in Krškopolje pigs, dietary effects were associated with biological processes related to immune response, intracellular protein transport, and extracellular matrix organisation. In the case of modern hybrids, a reduced protein diet resulted in enrichment of gene sets related to oxidative phosphorylation, mitochondrial function, and energy metabolism. In conclusion, this study demonstrated that the adipose tissue of Krškopolje pigs compared with modern hybrids exhibited greater adipogenic potential, being also supported by higher expression of genes involved in extracellular matrix remodelling and inflammation. The impact of a reduced protein diet on adipose-tissue gene expression was relatively small in both breeds, particularly in Krškopolje pig, suggesting a metabolic adaptability of this breed. - Source: PubMed
Publication date: 2026/05/27
Poklukar KČandek-Potokar MSavić BŠkrlep M - Immune escape is a hallmark of lung cancer, and limited responsiveness to PD-1/PD-L1 blockade highlights the need to identify additional immunoregulatory mechanisms in the mediastinal tumor microenvironment (TME). Non-classical immune checkpoints, including CD137/CD137L and CD200/CD200R, may interact with classical pathways but remain insufficiently defined in metastatic lymph nodes (LNs). We evaluated their expression on tumor cells and lymphocytes and their associations with PD-L1 and PD-L2. - Source: PubMed
Publication date: 2026/05/26
Kwiecień IwonaRaniszewska-Borys AgataRutkowska ElżbietaSokołowski RafałJahnz-Różyk KarinaRzepecki Piotr - Fragile histidine triad (FHIT) is a well-known tumor suppressor frequently downregulated in gastric cancer (GC), yet its molecular mechanisms remain insufficiently understood. In this study, we reveal that FHIT expression is significantly reduced during carcinogen-induced malignant transformation of gastric epithelial cells, independent of its diadenosine triphosphate hydrolase activity. Ribosome profiling and polysome analysis demonstrate that FHIT regulates the translation of lysine-specific demethylase 6B (KDM6B), a key epigenetic modulator, without altering its transcription. KDM6B promotes expression of proapoptotic genes, including PUMA, NOXA, GADD45, and TP53, by demethylating H3K27me3 at their promoters. In addition, KDM6B negatively regulates cytokine-related genes, such as TNFRSF12A, TNFSF9, and TNFRSF21. Functional assays, including colony formation, micronucleus assays, and xenograft tumor growth studies, confirm that FHIT's tumor-suppressive effects are independent of its enzymatic activity but rely on translational regulation. Our findings reveal a novel FHIT-KDM6B axis that integrates translational and epigenetic regulation to inhibit GC progression. Targeting this pathway may offer promising therapeutic strategies for early stage GC intervention. - Source: PubMed
Publication date: 2026/03/26
Hu HaoruiWang YumingQi HongyanLiu GuilingWang RunanShen Jing - Brain microvascular endothelial cells (BMECs) constitute the core component of the Blood-Brain Barrier (BBB), whose structural and functional integrity is crucial for maintaining central nervous system homeostasis. In recent years, ferroptosis-a novel iron-dependent lipid peroxidation-driven cell death pathway-has been demonstrated to play a pivotal role in secondary brain injury following stroke. However, current research predominantly focuses on ferroptosis in neurons and glial cells, with insufficient attention given to the mechanisms underlying BMEC ferroptosis in stroke pathogenesis. This review systematically examines the pivotal role of BMEC ferroptosis in the development of both ischemic and hemorrhagic strokes, elucidating its multiple pathways for exacerbating brain injury: compromising BBB integrity, triggering vasogenic cerebral edema, intensifying neuroinflammation, and promoting hemorrhagic transformation. The article highlights the molecular mechanisms of signaling pathways-including Meg3/p53/GPX4, TEAD1/MMP3, SESN2/System Xc-/GPX4, and SP1/TNFSF9/SLC3A2-in regulating BMEC ferroptosis. It summarizes multidimensional therapeutic strategies encompassing iron chelators, genetic/molecular interventions (e.g., FGF2, p23, METTL3, lncRNA H19), novel nanodelivery systems (e.g., RosA-LIP), and selenium compounds (SeMC). This study aims to provide new insights into vascular unit injury after stroke and establish theoretical foundations and translational directions for developing neuroprotective therapies targeting ferroptosis in BMECs. - Source: PubMed
Publication date: 2026/02/26
Qin WenxiuZhao YiranDu JianqiangZhang QiaoliWei GangWang ShaokangYu ZiruXu JunfengYang JianGao Ying