Anti - Mouse, CD56 (SCLC) Clone 123C3
- Known as:
- Anti - Mouse, CD56 (SCLC) Clone 123C3
- Catalog number:
- 61-0062
- Product Quantity:
- 1 mL
- Category:
- -
- Supplier:
- Genemed
- Gene target:
- Anti - Mouse CD56 (SCLC) Clone 123C3
Ask about this productRelated genes to: Anti - Mouse, CD56 (SCLC) Clone 123C3
- 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
Related products to: Anti - Mouse, CD56 (SCLC) Clone 123C3
Related articles to: Anti - Mouse, CD56 (SCLC) Clone 123C3
- 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 - Cannabis use is an increasingly common therapeutic for a variety of chronic diseases. In addition, people with sleep problems may self-medicate using cannabis products. However, genetic architecture of cannabis use and its shared genetic predispositions with sleep traits has not been systematically examined. We performed a meta-analysis of cannabis use within the All of Us and UK Biobank cohorts, consisting of 152,807 cases and 220,272 controls. Our meta-analysis identified 39 independent loci, including the previously reported locus associated with cannabis use and replicating previous work. Additionally our associations include neuronal and sleep-regulating genes such as , and . Moreover, tissue-specific analyses revealed that the genetic architecture of cannabis use is heavily enriched within the central nervous system and specific brain cell types. In addition, we observed significant positive genetic correlations with clinical insomnia, insomnia-related medication usage, and objectively measured nighttime physical activity, alongside negative correlations with morningness chronotype and daytime activity. Fine-mapping and colocalization analyses identified shared genetic signals between cannabis use and clinical insomnia including a near-perfect colocalization at and . Together, these results highlight the shared genetic risk between cannabis use and sleep disorders. Additionally, our findings indicate the importance of investigating the genetic effects of cannabis use as its use becomes more widespread, both recreationally and medicinally. - Source: PubMed
Publication date: 2026/04/16
Valliere JesseStrausz SatuTchio CynthiaRisse-Adams Oona ShigenoSinnott-Armstrong NasaOllila Hanna MSaxena Richa - Huoshou black pig (HS) is a well-known indigenous Chinese breed distinguished by superior meat quality compared to Western breeds. To investigate the molecular mechanisms underlying these differences, we performed Data-Independent Acquisition(DIA) proteomic analysis on the longissimus dorsi (LD) muscle from HS and Yorkshire (YY) pigs. We identified 262 differentially expressed proteins (DEPs), including 134 upregulated and 128 downregulated in HS relative to YY. Functional enrichment analysis revealed that these DEPs were significantly involved in small molecule metabolism, oxidoreductase activity, and several key signaling pathways such as the mTOR, AMPK, and PI3K-Akt pathways. Protein -protein interaction network analysis highlighted roles in structural proteins, glycolysis, and ribosome biogenesis. Integrated transcriptomic and proteomic analysis identified five candidate genes (MGST2, PNPO, CALD1, NCAM1, ACSS1) potentially associated with meat quality traits. Parallel reaction monitoring (PRM) and quantitative PCR (qPCR) validated the consistent differential expression of these genes at both the protein and mRNA levels. These findings provide novel insights into the molecular mechanisms regulating pork quality in indigenous pig breeds. - Source: PubMed
Publication date: 2026/04/30
Cao HanyuLi XiaojinXie FeiJiang ChangshengJin MengmengGhonaim Ahmed HRen ManHu QianqianLi Shenghe - - Source: PubMed
Publication date: 2026/04/22
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