CD48 Mouse Monoclonal Antibody
- Known as:
- CD48 Mouse Monoclonal Antibody
- Catalog number:
- BIN-000962-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CD48 Mouse Monoclonal Antibody
Related genes to: CD48 Mouse Monoclonal Antibody
- Gene:
- CD48 NIH gene
- Name:
- CD48 molecule
- Previous symbol:
- BCM1
- Synonyms:
- BLAST, mCD48, hCD48, SLAMF2
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: CD48 Mouse Monoclonal Antibody
Related articles to: CD48 Mouse Monoclonal Antibody
- CD48 is a surface molecule with immunoregulatory functions. Following our initial report of a patient with a de novo heterozygous variant at amino acid S220 in the CD48 gene, we describe a second, unrelated patient with similar features of immune dysregulation and a missense change affecting the same residue. To further elucidate the specific pathogenic mechanisms of the identified variants, we reviewed patient records, analyzed patient-derived cells, and employed complementary in vitro and in vivo model systems, including transfected cell lines and CD48-deficient mice. We demonstrate that the variants are associated with altered distribution of CD48, characterized by diminished CD48 surface expression, intracellular retention, and activation of endoplasmic reticulum stress signaling. Patient T cells display increased susceptibility to apoptosis, reduced antiviral responses, and enhanced inflammation. Both patients exhibit T-cell lymphopenia, a restricted TCR repertoire diversity, and oligoclonal expansions consistent with antigen-driven selection. In parallel, virally-infected CD48-deficient mice recapitulate key aspects of the human phenotype, including delayed antiviral immune responses, impaired viral clearance and pronounced inflammation. We conclude that identified variants compromise CD48 cell-surface localization, impair T-cell survival and function, and predispose to inflammation, thereby highlighting the role of CD48 in immune regulation and the prevention of excessive inflammation. - Source: PubMed
Publication date: 2026/04/14
Milanesi SamanthaLorenzini TizianaMarchetti TommasoTintor DianaPlanas RaquelSabet OlaMalmström LarsAcharya SudipWilliams Carson DManning Zoe ERoser Jack HEhler Angelica CHuber MichaelPrader SerainaVavassori StefanoDutmer Cullen MAbbott Jordan KPachlopnik Schmid Jana - Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by type 2 (T2) inflammation with elevated IL-5 and IL-13. Although group 2 innate lymphoid cells (ILC2s) drive T2 inflammation, their subset diversity and clinical relevance in nasal polyps (NPs) remain unclear. - Source: PubMed
Publication date: 2026/04/07
Kidoguchi MasanoriIwasaki NaruhitoPoposki Julie AOgasawara NorikoOka AikoKlingler Aiko ISuh LydiaAgrwal AditiBai JunqinStevens Whitney WPeters Anju TGrammer Leslie CWelch Kevin CSmith Stephanie SJohnson MicahRadwan AmrConley David BSchleimer Robert PKern Robert CTan Bruce KOkano MitsuhiroFujieda ShigeharuKato Atsushi - HO-1 (HMOX1) is a stress-inducible, rate-limiting heme catabolic enzyme aberrantly upregulated across hematologic malignancies and frequently associated with progression, relapse, and poor therapeutic response. This review integrates clinical and experimental evidence and frames HO-1 as a multidimensional resistance hub operating through three interconnected axes. (1) Enzymatic axis: heme degradation products (CO, biliverdin/bilirubin, and Fe) buffer therapy-induced oxidative stress, modulate apoptosis/autophagy, and tune ferroptosis susceptibility in a context- and dose-dependent manner. (2) Non-enzymatic axis: stress-induced truncation and nuclear translocation of HO-1 rewire transcriptional programs by stabilizing NRF2 and engaging epigenetic regulators, converting transient stress cues into durable resistance states. (3) Microenvironmental axis: HO-1 activity in stromal and immune compartments reshapes cytokine networks and suppresses immune recognition (e.g., HLA-C and CD48), reinforcing immune-evasive niches. We systematically summarize translational strategies at three levels: (1) agents directly targeting the HO-1 protein, (2) therapies targeting upstream regulatory pathways, and (3) approaches targeting downstream effectors and the HO-1-shaped immunosuppressive microenvironment. - Source: PubMed
Publication date: 2026/01/22
Lei WenbinHu TianzhenWang Jishi - HML-2 subgroup mobile genetic elements of the HERV-K family were described to participate in carcinogenesis processes, but their expression and epigenetic regulation in molecular subtypes of colorectal cancer (CRC) remain partly characterized. The present study aimed to evaluate the expression of HML-2 elements using RNA-sequencing data in paired tumor and normal intestinal tissue samples from 63 patients with CRC to identify patterns of the retrotransposons' activity in different molecular subtypes (CMSs). - Source: PubMed
Publication date: 2026/02/12
Obrezanenko Valentina SShulga Polina MVolkova Anastasia GPrimova Anastasia ARemizova Yulia AMeshkov Ivan OKikot Alexandra DTarasova Daria ABolashova Ekaterina SIvashechkin Alexey AMakhotenko Antonida VSnigir Ekaterina AMasyukova Yulia ARadion Elizaveta IKuznetsova Olesya ACheporova Maria SFedyanin Michail YTryakin Alexey AMakarov Valentin VYudin Vladimir SKeskinov Anton AMakarova Anna S - BACKGROUND Acute lung injury (ALI) after liver transplantation (LT) is a critical complication negatively affecting transplant outcomes and patient survival. However, effective biomarkers for early diagnosis remain unidentified. This study aimed to identify hub biomarkers and signaling pathways involved in post-LT ALI through integrated bioinformatics and machine-learning analyses and to validate their diagnostic potential. MATERIAL AND METHODS Differential gene expression analysis identified 27 differentially expressed genes (DEGs). Functional enrichment analyses revealed significant involvement in cytokine-mediated signaling, particularly within the NF-kB and TNF pathways. Single-sample gene set enrichment analysis (ssGSEA) evaluated immune infiltration. Machine-learning algorithms identified crucial biomarkers for ALI prediction. Transcription factor-hub gene and competitive endogenous RNA (ceRNA) networks were constructed. Single-cell RNA sequencing (scRNA-seq) and enzyme-linked immunosorbent assay (ELISA) analyses validated biomarker expression patterns in relation to ALI. RESULTS Hub biomarkers identified included CXCL3, CD48, and IRAK3. ssGSEA revealed prominent macrophage and neutrophil infiltration associated with ALI. Machine-learning models confirmed CXCL3, CD48, and IRAK3 as reliable predictive biomarkers, which were incorporated into a robust diagnostic nomogram. scRNA-seq analysis showed cell-type-specific expression patterns for CXCL3, CD48, and IRAK3, with heterogeneous associations across datasets. ELISA validated significantly altered protein levels of CXCL3, CD48, and IRAK3 in post-transplant ALI cases compared with controls. CONCLUSIONS CXCL3, CD48, and IRAK3 are novel and promising diagnostic biomarkers for predicting post-LT ALI. These findings provide foundational insights that could support improved diagnosis, prevention strategies, and targeted therapeutic interventions, ultimately enhancing patient outcomes after liver transplantation. - Source: PubMed
Publication date: 2026/02/17
Guiting YangZhang ShengfengJi LiuLv ChengmeiZhao ChenLing MaoyaoLiao XiaotingPan Linghui