Recombinant Human CD48 /SLAMF2 Protein
- Known as:
- Recombinant Human CD48 /SLAMF2 Protein
- Catalog number:
- cd-795
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human CD48 /SLAMF2 Protein
Related genes to: Recombinant Human CD48 /SLAMF2 Protein
- 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: Recombinant Human CD48 /SLAMF2 Protein
Related articles to: Recombinant Human CD48 /SLAMF2 Protein
- Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), exhibits marked racial disparities in incidence, progression, and clinical outcomes. While diet, lifestyle, and socioeconomic factors have been shown to influence these disparities, biological mechanisms underlying racial differences in MASLD risk remain poorly understood. We hypothesized that race-associated variation in hepatic gene expression may contribute to differential susceptibility and progression of MASLD. To test this hypothesis, we analyzed publicly available gene expression data from liver biopsies obtained from over 300 Black and White individuals undergoing bariatric surgery. Gene expression profiles were compared across four histological stages: normal liver, MASLD, metabolic dysfunction-associated steatohepatitis (MASH) without fibrosis, and MASH with fibrosis. We identified more than 200 genes that were significantly differentially expressed between Black and White individuals. Genes associated with MASLD progression were significantly enriched among race-specific genes, supporting the hypothesis that racial differences in hepatic gene expression contribute to disease risk and progression. Using histologically normal liver as a reference, we identified race-specific candidate genes potentially driving MASLD progression. These included UCN3 and PRSS3 in Black individuals, and MMP15, LAMB2, LEPR, ELOVL2, CD48, COL5A2, and ICAM1 in White individuals. Notably, divergence in gene expression profiles between racial groups became more pronounced with advancing disease stages, suggesting that race may play an increasingly important role in later phases of MASLD progression. Our findings indicate that differential modulation of hepatic gene expression represents a potential biological mechanism contributing to racial disparities in MASLD. These results highlight the importance of considering race-specific molecular signatures in understanding MASLD pathogenesis and in developing targeted prevention and therapeutic strategies. - Source: PubMed
Publication date: 2026/05/04
Gorlov Ivan PGorlova Olga YThrift Aaron P - Classic Hodgkin lymphoma (cHL) shares mutations with primary mediastinal B cell lymphoma (PMBL) but differs in histology, clinical behavior, and phenotype. To define transcriptional programs underlying these differences, we performed flow cytometric cell sorting and low-input RNA sequencing of Hodgkin and Reed-Sternberg (HRS) cells from eighteen primary tumors, paired intra-tumoral B cells, and four cHL cell lines, and compared them with RNA-sequencing data from 40 PMBL cases. Transcriptomic profiling revealed that HRS cells undergo abortive plasma cell differentiation with robust activation of the unfolded protein response (UPR), a feature shared with multiple myeloma but absent in diffuse large B cell lymphoma and PMBL. HRS cells also demonstrated profound immune evasion, including suppression of B cell identity genes and loss of natural killer cell recognition through downregulation of SLAM family ligands such as CD48. Comparative analysis with PMBL highlighted shared oncogenic programs and key distinctions: HRS cells exhibited greater loss of B cell identity, absence of GCB- and plasma cell markers, and unique upregulation of cytoskeletal and mitotic pathways consistent with their multinucleated morphology. These findings establish HRS cells as aberrantly differentiated GCB cells with partial plasmacytic features, UPR activation and distinct immune evasion strategies. - Source: PubMed
Publication date: 2026/04/22
Roshal MikhailKong Isabella YDinalankara WikumReichel Jonathan BTeater MatthewBinder BhavneetZairis SakellariosBrody Joshua DPark Sunita IKovach Alexandra EGulati NityaOberley Matthew JLim Megan SBarth Matthew JElemento OlivierMelnick AriRabadan RaulChadburn AmyMarchionni LuigiGiulino-Roth LisaCesarman Ethel - - Source: PubMed
Publication date: 2026/04/21
Zhang XiaoluRoehlen Natascha - 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 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
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