CD162
- Known as:
- CD162
- Catalog number:
- 11-312-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD162
Related genes to: CD162
- Gene:
- SELPLG NIH gene
- Name:
- selectin P ligand
- Previous symbol:
- -
- Synonyms:
- PSGL-1, CD162
- Chromosome:
- 12q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 1995-01-31
- Date modifiied:
- 2016-10-25
Related products to: CD162
Related articles to: CD162
- Glaucoma is a leading cause of irreversible blindness worldwide with an unclear pathogenesis. Accumulating evidence has indicated that adhesion molecule-mediated transvascular migration of T cells into the retina is involved in the disease process. Because P-selectin mediates adhesive interactions between leukocytes and endothelial cells, we sought to determine whether it participates in retinal immune cell recruitment and contributes to glaucoma pathogenesis. - Source: PubMed
Xiu WenboCheng JingZhang GaoChen YangSun ChaonanGao YanpingLi AnXiao XiaoDeng BolinWang Jinxia - Plasma membrane lipid asymmetry is tightly regulated and fundamental to mammalian cell physiology. TMEM30A is the β-subunit of P4-ATPases, flippase enzymes that maintain strict phosphatidylserine (PS) asymmetry by pumping it from the outer to the cytosolic leaflet. Loss of TMEM30A function causes constitutive PS externalization and has been implicated in diseases such as diffuse large B-cell lymphoma and tumor immune evasion. Here, we systematically define the biophysical and molecular consequences of TMEM30A deletion in immune cells. Using a live-cell lipid reporter, membrane order probe, and surface proteome mapping, we show that TMEM30A-knockout cells display robust PS externalization accompanied by faster lateral diffusion of membrane constituents and decreased plasma membrane order. Surface proteome reorganization includes increased abundance of tetraspanins and CD47. Furthermore, TMEM30A loss triggers glycocalyx remodeling via ADAM10-dependent shedding, which removes major transmembrane mucins, including CD43 and CD162 (also known as SPN and SELPLG, respectively). Together, these data reveal a coordinated reorganization of lipids, glycans and proteins upon TMEM30A loss, suggesting mechanistic links between flippase dysfunction and increased plasma membrane dynamics and potential sensitization to immune therapy. Furthermore, our study provides an integrated surfaceome framework that might shed light on the relationship between TMEM30A expression and clinical outcomes in cancer. - Source: PubMed
Publication date: 2026/08/14
Gurdap Cenk ORagaller FranziskaMuller MarionSjule EllenSych TarasBlomén LinneaThorén Fredrik BLevental IlyaLevental Kandice RSattentau Quentin JSezgin Erdinc - Polymorphonuclear (PMN) leukocyte recruitment to activated pulmonary endothelium is a central mechanism in acute respiratory distress syndrome (ARDS). This process is mediated by selectins and their counter-ligand, P-selectin glycoprotein ligand-1 (PSGL-1), encoded by SELPLG. Genetic variation in SELPLG has been associated with ARDS susceptibility, while disruption of PSGL-1/P-selectin interactions attenuates lung injury in preclinical models. Because inflammatory stimuli increase both SELPLG expression and circulating PSGL-1 levels, PSGL-1 represents a promising biomarker and therapeutic target. We sought to define the genetic determinants of plasma PSGL-1 levels and evaluate their causal relationships with key inflammatory and endothelial biomarkers. - Source: PubMed
Publication date: 2026/07/16
Bime ChristianKlimentidis Yann CSun XiaoguangFloyd Chilton HStandage-Beier Carrie SSaad SammaniCasanova Nancy GHufford Mathew KCamp Sara MGarcia Joe G N - X-linked hypophosphatemia (XLH) is a rare hereditary disorder characterized by gene mutations, elevated levels, and impaired bone mineralization. Burosumab, a monoclonal antibody targeting , has demonstrated clinical efficacy; however, the immunological dynamics during treatment remain unexplored. This study employed longitudinal single-cell RNA sequencing (scRNA-seq) to characterize peripheral blood immune cell alterations across multiple treatment stages in pediatric XLH. We performed scRNA-seq on peripheral blood mononuclear cells from pediatric patients with XLH at five time points spanning pretreatment and burosumab therapy phases, along with healthy pediatric controls. A total of 93,112 cells were analyzed using comprehensive bioinformatic pipelines, including unsupervised clustering, pseudotime trajectory analysis, temporal gene expression profiling, and cell-cell communication inference. Eleven major immune cell populations were identified, with notable dynamic alterations in T cells and natural killer (NK) cell subtypes across treatment stages. The cellular proportion of T helper 2 (Th2) cells and regulatory T (Treg) cells were elevated before treatment and normalized during therapy, whereas T helper 17 (Th17) cells exhibited reciprocal patterns. Genes upregulated in Treg cells during early treatment were enriched in osteoclast differentiation pathway. Natural killer subtype 2 cells showed enrichment in osteoclast differentiation and interleukin-12 response pathways. Cell-cell communication analysis identified dynamic interactions among Th2 cells, Th17 cells, Treg cells, and NK cell subtypes mediated by KLRB1-CLEC2D and SELL-SELPLG ligand-receptor pairs. This longitudinal transcriptomic study provides the first comprehensive characterization of peripheral immune dynamics during burosumab therapy in XLH, offering new insights into the immunological mechanisms underlying treatment response. - Source: PubMed
Publication date: 2026/06/27
Xie YueLi LiLi RongSun YihongZhou TingCun YupengZhu Gaohui - Disulfidptosis is a novel form of glucose starvation-induced cell death, yet its prognostic implications in gastric cancer (GC) remain largely undefined. - Source: PubMed
Publication date: 2026/06/26
Xu YuxuanKong XianmingLi JinXiang Dongxi