Ask about this productRelated genes to: SLA2 Blocking Peptide
- Gene:
- SLA2 NIH gene
- Name:
- Src like adaptor 2
- Previous symbol:
- C20orf156
- Synonyms:
- FLJ21992, SLAP-2
- Chromosome:
- 20q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-19
- Date modifiied:
- 2016-12-12
Related products to: SLA2 Blocking Peptide
Related articles to: SLA2 Blocking Peptide
- Using pigs as tissue donors may eliminate the shortage of replacement organs. As in allotransplantation, antidonor antibodies cause xenotransplant failure. Many antibodies target products of the major histocompatibility complex. Pigs contain a novel major histocompatibility complex gene, swine leukocyte antigen-12 (SLA-12), which has been proposed to behave as a classical class I SLA protein. Though predicted to bind B2m and short peptides, the functionality of the SLA-12 protein remains uncertain. In addition, its similarity to classical class I SLA molecules suggests that the SLA-12 could be a xenoantigen. Here we tested these predictions. - Source: PubMed
Publication date: 2026/04/21
Gennuso Victor NovaraWang Zheng YuReyes Luz MTector MattTector A Joseph - Hepatocellular carcinoma (HCC) is a prevalent and highly aggressive malignancy. Phagocytic regulatory factors (PRFs) play a crucial role in regulating the progression of HCC. This study aimed to investigate the prognostic and immunological features of HCC based on phagocytic regulatory factor-related genes (PFRGs). - Source: PubMed
Publication date: 2025/09/26
Meng XiaodongWang QiufangTian YuanTian FeiLiu SiqingWang YimingCao LiyingMa Xiangming - Understanding the individual- and population-level polymorphisms of major histocompatibility complex (MHC) genes is crucial for identifying associations between MHC variations and immune phenotypes. To support this, we developed NGSMHC, a streamlined bioinformatics tool for efficient and accurate MHC genotyping using nextgeneration sequencing (NGS) data in non-human species. - Source: PubMed
Publication date: 2025/09/30
Kang MingueAhn ByeongyongShin Jae YeolLee JonganCho Eun SeokPark Chankyu - Enoxaparin sodium (ES), a low molecular weight heparin derivative, has recently been recognized for its diverse biological activities. In particular, the ability of heparin to modulate inflammation has been utilized to enhance the biocompatibility of bone implant materials. In this study, we utilized poly (methyl methacrylate) (PMMA), a drug loading bone implant material, as a matrix and combined this with enoxaparin sodium (ES) to create enoxaparin sodium PMMA cement (ES-PMMA) to investigate the regulatory effects of ES on inflammatory responses in bone tissue from an animal model. We established a rabbit model of femoral condyle bone defects to investigate the immunoregulatory mechanisms of ES-PMMA. Rabbits were divided into control (n = 5), model (n = 10), PMMA (n = 10) and ES-PMMA (n = 10) groups. The control group underwent sham surgery as a blank control, while the model group was established with a bone defect model in the rabbit femoral condyle. The PMMA group and ES-PMMA group followed the same modeling procedure as the model group. After successful modeling, the PMMA group and ES-PMMA group were implanted with PMMA bone cement columns and ES-PMMA bone cement columns, respectively. Ten days post-surgery, cancellous bone tissue from the defect site was collected from each group, and the control group was sampled at the same location. Tissue samples were collected from each group for transcriptomic sequencing. RNA sequencing (RNA-seq) was performed and differentially expressed mRNAs were identified between the model and controls, between the PMMA and model groups, and between the ES-PMMA and model groups. Key candidate genes associated with ES-PMMA treatment were identified (304 genes), and Gene Set Variation Analysis (GSVA), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed on the differentially expressed genes and key candidate genes in each group (P < 0.05). The 304 key candidate genes associated with ES-PMMA treatment are involved in functions such as inflammation, cell proliferation, and differentiation. Protein-protein interaction (PPI) network analysis and machine learning revealed three key candidate genes in the ES-PMMA group: recombination activating gene (RAG1), Src-like adaptor 2 (SLA2), S100 calcium binding protein and beta (neural) (S100B). SLA2 and RAG1 are known to be related to inflammation, whereas S100B is related to osteogenic differentiation. Finally, the subcellular localization and functional similarities of the three genes were assessed, and their transcription factors and miRNAs were predicted. Collectively, these findings provide insights into the mechanism of ES in regulating immune responses in the bone; this may facilitate the development of novel bone implant materials. - Source: PubMed
Publication date: 2025/09/08
Shen XiaoyuYao QiangMa Lijie - The accumulation of misfolded proteins inside the cells has been considered to be an important contributor to the development of cigarette smoke-mediated diseases. Since endocytosis plays a crucial role in protein trafficking and clearance, impaired endocytosis may contribute to cigarette smoke-mediated protein accumulation. Therefore, the current study investigated the effects of cigarette smoke extract (CSE) on the endocytosis process in the yeast . The current study demonstrated that treatment of cells with CSE resulted in reduced uptake of the FM4-64 stain, indicating impaired endocytosis. Further analysis revealed that CSE treatment resulted in a defect in the recruitment of proteins involved in endocytosis. Also, aberrant actin filament morphology was found upon CSE treatment, which might interfere with vesicle budding from the membrane. Moreover, the current study showed that the PI(4,5)P2 level in the plasma membrane in CSE-treated cells is reduced due to the failed translocation of MSS4 kinase to the membrane. This reduced PI(4,5)P2 results in aberrant actin filament morphology. Thus, the current study demonstrates that CSE treatment causes endocytosis defects and provides insight into this defective process. - Source: PubMed
Publication date: 2025/08/20
Shukla AdityaSarkar SrimontiSil Alok Kumar