Capp pipette, fixed vol. 10 ml, Bravo
- Known as:
- Capp pipette, fixed vol. 10 milliliter, Bravo
- Catalog number:
- B10000-1F *
- Category:
- -
- Supplier:
- Capp
- Gene target:
- Capp pipette fixed vol. 10 Bravo
Related genes to: Capp pipette, fixed vol. 10 ml, Bravo
- Gene:
- NRCAM NIH gene
- Name:
- neuronal cell adhesion molecule
- Previous symbol:
- -
- Synonyms:
- KIAA0343, Bravo
- Chromosome:
- 7q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-06-19
- Date modifiied:
- 2016-10-05
Related products to: Capp pipette, fixed vol. 10 ml, Bravo
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- The damage of ferroptosis is related to the pathogenesis of intervertebral disc degeneration (IDD). N6-methyladenosine (m6A) modification accounts for more than 80% of RNA modifications in eukaryotic cells. However, the key role of m6A related ferroptosis-related genes (FRGs) in IDD remain explorable. Firstly, batch correction between datasets was performed. Weighted gene co-expression network analysis (WGCNA) was then conducted to acquire the most relevant module genes. Differentially expressed genes (DEGs) between the IDD and Normal Group were obtained by differential analysis subsequently. Next, according to the Pearson correlation and the intersection of m6A and FRGs related genes, m6A-FRGs related genes were selected. Additionally, we intersected module genes, DEGs and m6A-FRGs related genes to obtain DEGs of m6A-FRGs related module genes (m6A-FRGs-DEGs). Least absolute shrinkage and selection operator (LASSO) was applied to get HUBgenes. After, we conducted gene set enrichment analysis (GSEA) to gain function items and related pathways of HUBgenes. Single sample gene set enrichment analysis (ssGSEA) and wilcox.test were proceeded to analyse differences in relative abundance of immune cells between the IDD and Normal Groups, and a nomogram was constructed based on significantly different HUBgenes. The Comparative Toxicogenomics Database (CTDbase) was then applied to predict potential drugs or molecular compounds that could modulate HUBgenes. Last but not least, we performed the quantitative real-time fluorescence PCR (qRT-PCR) to verify HUBgenes. 181 m6A-FRGs-DEGs were acquired by the intersection of key module genes (from MEtan, MEsalmon, MEbrown and MEgreen), 362 DEGs and 15,678 m6A-FRGs related genes. Subsequent analysis showed that HUBgenes (ZNF595, PLXDC1, FNBP1L, KLRB1, NRCAM, PPCDC, C9orf139, SIGLEC17P, RRAS2 and DPRXP4) significantly participated in positive regulation of cytokine production, mitochondrial inner membrane and organellar ribosome. Besides, the relative abundance of neutrophils was found significantly different between IDD and normal groups. A nomogram was constructed based on ZNF595 and RRAS2, and there were 11 drugs targeted on ZNF595, while 118 drugs predicted based on RRAS2 such as Tetrachlorodibenzodioxin, Bisphenol A and Benzo(a)pyrene. Lastly, ZNF595 and RRAS2 were both obviously up-regulated in IDD according to the qRT-PCR. Our research suggested 10 HUBgenes were significantly associated with IDD, providing more evidence about the vital role of HUBgenes in IDD. - Source: PubMed
Publication date: 2025/09/29
Che ZhenChen RuibingLi MingLiao ZhuangyaoWang KunYao DengboLiang YuweiLi YuxiWen GuomingXing TongSu KaihuiLiang ChangchunHuang LinZhao Qun - Neuron-related cell adhesion molecule (NrCAM) has been implicated in tumor progression, but its role in small-cell lung cancer (SCLC) remains unclear. This study examined the clinical significance of NrCAM in SCLC and its impact on cellular processes. - Source: PubMed
Publication date: 2025/08/20
Li TaoLiu PeilongWang YanXu Hong - To overcome the paucity of known tumor-specific surface antigens in pediatric high-grade glioma (pHGG), we contrasted splicing patterns in pHGGs and normal brain samples. Among alternative splicing events affecting extracellular protein domains, the most pervasive alteration was the skipping of ≤30-nt-long exons. Several of these skipped microexons mapped to L1-immunoglobulin cell adhesion molecule (IgCAM) family members, such as neuronal CAM (NRCAM). Bulk and single-nuclei short- and long-read RNA-seq revealed uniform skipping of NRCAM microexons 5 and 19 in virtually every pHGG sample. Importantly, the Δex5Δex19 (but not the full-length) NRCAM proteoform was essential for pHGG cell migration and invasion in vitro and tumor growth in vivo. We developed a monoclonal antibody selective for Δex5Δex19 NRCAM and demonstrated that "painting" pHGG cells with this antibody enables killing by T cells armed with an FcRI-based universal immune receptor. Thus, pHGG-specific NRCAM and possibly other L1-IgCAM proteoforms are promising and highly selective targets for adoptive immunotherapies. - Source: PubMed
Publication date: 2025/08/07
Sehgal PriyankaNaqvi Ammar SHiggins MakennaLiu JiagengHarvey KyraJarroux JulienKim TaewooMankaliye BerkMishra PamelaWatterson GraceFine JustynDavis JacintaHayer Katharina ECastro AnnetteMogbo AdannaDrummer CharlesMartinez DanielKoptyra Mateusz PAng ZhiweiWang KaiFarrel AlvinQuesnel-Vallieres MathieuBarash YosephSpangler Jamie BRokita Jo LynneResnick Adam CTilgner Hagen UDe Raedt ThomasPowell Daniel JThomas-Tikhonenko Andrei - Placental insufficiency underpins pregnancy complications, fetal growth restriction (FGR) and preeclampsia, yet predictive biomarkers are limited. Neuronal Cell Adhesion Molecule (NrCAM) may be a promising biomarker of placental dysfunction. This study investigated whether NrCAM can predict diseases of placental insufficiency. - Source: PubMed
Publication date: 2025/07/21
Bartho Lucy AWalker Susan PIdzes DanicaHeazell Alexander E PHiggins Lucy ESferruzzi-Perri Amanda NHannan Natalie JCluver Catherine ABergman LinaWong Georgia PKandel ManjuCannon PingNguyen Tuong-ViNguyen AnnaTong StephenKaitu'u-Lino Tu'uhevaha J - is a high confidence autism spectrum disorder (ASD) gene encoding the spectrin-actin scaffold protein Ankyrin B (AnkB). The 220 kDal isoform of AnkB has multiple functions including developmental spine pruning through L1 family cell adhesion molecules (L1-CAMs) and class 3 Semaphorins on dendrites of pyramidal neurons to achieve an appropriate excitatory balance in the neocortex. Molecular modeling employing AlphaFold was used to predict the structure and interactions of AnkB with the cytoplasmic domain of Neuron-glial Related L1-CAM (NrCAM), and with β2-Spectrin. The validity of the models was assessed by analyzing protein-protein interactions by co-immunoprecipitation from HEK293 cell lysates after mutating key residues in AnkB predicted to impair these associations. Results revealed a pocket with critical residues in the AnkB membrane-binding domain that engages NrCAM at the conserved cytoplasmic motif FIGQY. Alphafold modeling of the AnkB/β2-Spectrin complex also identified key interactions between the AnkB spectrin-binding domain and β2-Spectrin repeats 14-15. Selected ASD-linked mutations in AnkB predicted to impact binding to NrCAM or β2-Spectrin were then assayed for protein interactions. Maternally inherited ASD missense mutations AnkB A368G located in the NrCAM binding pocket and AnkB R977Q in the Zu51 subdomain disrupted associations with NrCAM and β2-Spectrin, respectively. Moreover, AnkB A368G impaired the neuronal function of 220 kDal AnkB in Semaphorin 3F-induced spine pruning in mouse cortical neuron cultures. These new findings provide structural insights into the L1-CAM/AnkB complex and the molecular basis of ASD etiology associated with AnkB missense mutations. - Source: PubMed
Publication date: 2025/05/05
Chirasani Venkata RHaberman Victoria AOldre Erik NWebb Barrett DPereira Ernest BYang WonsukManess Patricia F