CD56 (NCAM) Antibody
- Known as:
- CD56 (NCAM) Antibody
- Catalog number:
- MAB352P
- Product Quantity:
- 5 ml
- Category:
- -
- Supplier:
- INNOVEX
- Gene target:
- CD56 (NCAM) Antibody
Related genes to: CD56 (NCAM) Antibody
- Gene:
- CADM1 NIH gene
- Name:
- cell adhesion molecule 1
- Previous symbol:
- TSLC1, IGSF4
- Synonyms:
- NECL2, ST17, BL2, SYNCAM, IGSF4A, Necl-2, SYNCAM1, RA175
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-02
- Date modifiied:
- 2016-10-05
- Gene:
- NCAM1 NIH gene
- Name:
- neural cell adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- NCAM, CD56
- Chromosome:
- 11q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
- Gene:
- NCAM2 NIH gene
- Name:
- neural cell adhesion molecule 2
- Previous symbol:
- -
- Synonyms:
- NCAM21, MGC51008
- Chromosome:
- 21q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-25
- Date modifiied:
- 2016-10-05
Related products to: CD56 (NCAM) Antibody
Related articles to: CD56 (NCAM) Antibody
- Multiple myeloma (MM) remains incurable, with drug resistance being a key clinical challenge. Impaired natural killer T (NKT) cell function may contribute to MM immune escape, while the significance of the inhibitory receptor CD161 expression on NKT cells is unclear. This study investigated the association between the peripheral blood CD3⁺CD56⁺CD161⁺ NKT cell proportion and response to bortezomib plus dexamethasone therapy in newly diagnosed MM (NDMM) patients. - Source: PubMed
Zhou SutaoXu XueqingCuo JuanSun ChaoHou YaliWang XiaNana DuanWeixun Shi - Recent revisions to acute leukemia classification systems increasingly emphasize genetic drivers of disease; however, critical immunophenotypic features remain essential for accurate diagnosis and risk assessment. CD56, an isoform of the neural cell adhesion molecule, is expressed on natural killer (NK) cells but is aberrantly present across multiple acute leukemias, where it may contribute to diagnostic complexity and adverse clinical outcomes. This review highlights the diagnostic and clinical significance of CD56 expression in acute leukemias. - Source: PubMed
Siddon Alexa JKahlow ChristineWeinberg Olga K - (Lm) is an important zoonotic foodborne pathogen that causes severe rhombencephalitis in ruminants. The trigeminal ganglion is a critical node for Lm invasion of the central nervous system via neural pathways. However, the roles of key virulence factors InlA, InlB, and LLO from ovine-derived Lm in trigeminal ganglion neuron infection remain unclear. In this study, LM90SB2, an ovine-derived Lm strain isolated from a sheep with encephalitis in Xinjiang, China, was used as the wild type, and its Δ double-gene deletion and Δ triple-gene deletion mutants were constructed. Primary mouse trigeminal ganglion cells (TGCs) were infected with these strains, and cell-association and invasion assays, bacterial colonization analysis, cell scratch tests, Western blotting, and qRT-PCR were performed to explore the effects of InlA, InlB, and LLO on Lm infection of TGCs and their regulatory roles in host adhesion molecules N-cadherin and NCAM1. The results showed that the wild-type LM90SB2 had significantly stronger cell-association, invasion, and colonization abilities in TGCs than the Δ and Δ mutants ( < 0.01 or < 0.0001). LM90SB2 infection significantly upregulated the mRNA and protein expression levels of N-cadherin and NCAM1 in TGCs and enhanced TGC migration, while these effects were gradually attenuated with the sequential deletion of , and . This study clarifies the synergistic roles of InlA, InlB, and LLO in mediating the infection of trigeminal ganglion neurons by ovine-derived Lm and reveals the molecular mechanism by which Lm promotes neural invasion by regulating the expression of host cell adhesion molecules. Our findings provide important experimental data for elucidating the neural invasion pathway of Lm in ruminants and lay a theoretical foundation for the development of targeted prevention and control strategies for ruminant listeriosis in veterinary clinical practices. - Source: PubMed
Publication date: 2026/04/30
Lv YueDeng QiuyanLi YeLu YuxuanXie JiahuiRen JingjingJiang Jianjun - Glioblastoma (GBM) remains a lethal malignancy characterized by therapeutic resistance and recurrence. Emerging evidence suggests that senescent niches may shape tumor progression, support tumor stemness, and modulate immune engagement. We integrated transcriptomic data from the Glioma Longitudinal Analysis Consortium (GLASS; 118 primary and 113 recurrent IDH-wildtype GBM samples) with protein-level analysis from an independent cohort of 37 GBM patients (25 primary, 12 recurrent), including 6 matched primary-recurrent pairs. Senescence-, stemness-, and immune-related pathways were assessed using single-sample gene set enrichment analysis (ssGSEA), while immunohistochemistry quantified the expression of Lamin B1, Ki67, p53, SOX2, HLA-DRA, B2M, and CD56. Transcript-level validation was performed using matched-pair Wilcoxon testing in 101 GLASS pairs. Recurrent tumors demonstrated increased enrichment of senescence-associated transcriptional programs, including upregulated KAMMINGA_SENESCENCE and reduced TANG_SENESCENCE_TP53_TARGETS_DN scores. Lamin B1 and Ki67 protein levels were significantly lower in recurrent tumors (p = 0.004 and p = 0.016), while p53 expression increased overall (p = 0.001), suggestive of a senescence enrichment upon recurrence. In the matched analysis (6 pairs; 12 samples total), Lamin B1 and Ki67 generally trended lower at recurrence, although paired differences were not statistically significant. SOX2 expression remained broadly stable at the protein level but showed a modest decrease in RNA expression. Immune markers (HLA-DRA, B2M, CD56) exhibited minimal differences, although HLA-DRA increased significantly overall at recurrence (p = 0.025). Matched transcriptomic analysis in GLASS pairs supported recurrent-specific reductions in LMNB1, MKI67, and SOX2, with no consistent changes in TP53, HLA-DRA, B2M, or NCAM1. Recurrent IDH-wildtype GBM exhibits a transcriptional and protein expression shift towards a senescence-associated state with no concomitant changes in SOX2 and select immune markers. - Source: PubMed
Publication date: 2026/05/06
Al Shboul SofianAlrjoub MoathAl Karsaneh Ola AbuSurakhy MirvatAlhesa AhmadEl-Sadoni MohammadAl-Sheyab MaramAlsoud AnoudFriehat KholoudKhasawneh Ashraf IAbabneh Nidaa AAlotaibi Moureq RHupp TedSaleh Tareq - Natural killer (NK) cells are effector cells of the innate immune system. The cytokine microenvironment influences NK cell function. Dysregulation of NK cell cytotoxicity can manifest in reproductive disorders and is also observed in tumor-transformed tissues. The search for immunotherapies capable of regulating NK cell activity is therefore relevant. This study aimed to evaluate the effect of the TGFβ signaling pathway inhibitor and the cyclin-dependent kinase (CDK) 7/12/13 inhibitor on the transcriptional profile of NK-92 cell line. In the study, the cytokines TGFβ1, IL-12, IL-15, IL-18, and TNFα, and the TGFβ receptor type 1 (TGFβR1) inhibitor LY3200882 and the CDK7/12/13 inhibitor THZ1 were used. The cells were cultured sequentially in the presence of inhibitors and cytokines, followed by assessment of the gene expression of , , , , , , , , , , and We observed direct effects of the inhibitors on NK cells. LY3200882 increased the expression of and , and reduced . THZ1 increased the expression of , , and , while it reduced and . IL-12, IL-15, IL-18, and TNFα modified the gene expression of some phenotypic and cytotoxic receptors and transcription factors. TGFβ1 increased the expression of , , and . Blocking TGFβ-dependent signaling with LY3200882 abolished TGFβ1 effects. We assessed CD56 presence on NK-92 cell membrane and found its increase in the presence of LY3200882. After LY3200882 treatment, in the presence of TGFβ1 and choriocarcinoma cell line JEG-3, the expression of CD56 receptor on NK cell membrane decreased. Pretreating NK cells with THZ1 decreased the expression of , , and in the presence of TGFβ1. Thus, LY3200882 partially neutralized TGFβ1 effects on the expression of NK cell receptor genes. THZ1 followed by TGFβ1 treatment promoted NK cell transcriptional profile characteristic for CD56dim NK cells. Both LY3200882 and THZ1 affected the NK cell transcription even without cytokine treatment. The independent effects of synthetic inhibitors on NK cells, as well as their influence in the presence of tumor cells, should be considered. - Source: PubMed
Publication date: 2026/04/17
Mikhailova ValentinaMarko OksanaMkrtchyan EdgarSokolov Dmitry