CD56 (NCAM) Antibody
- Known as:
- CD56 (NCAM) Antibody
- Catalog number:
- MAB352C
- Product Quantity:
- 0.5 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
- 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
Abati ElenaSaccomanno DomenicaAlberti ClaudiaAnastasia AlessiaGagliardi DeliaFerri EvelynArosio BeatriceD Angelo GraziaCima RossellaBassi Maria TeresaOldoni SamantaComi Giacomo PietroRizzo PaolaCorti Stefania Paola - In C. elegans, the epidermis and its overlying extracellular matrix form a primary protective barrier, functioning as the first line of defense against environmental factors. To properly develop those cellular boundaries, a tightly controlled interaction of many molecules and pathways is needed. Mutant alleles of paqr-2 and iglr-2 (lipid homeostasis), dpy-21 (membrane trafficking), and sma-1 (actin-binding spectrin) result in hermaphrodite tail tip defects suggesting that this simple 4-cell structure can serve as a sensitive model for the identification of pathways responsible for the establishment of cellular boundaries. With this in mind, we performed a small forward genetics screen of ∼800 ethyl methanesulfonate-mutagenized haploid genomes and identified 21 mutants with a Tail End Defects in the hermaphrodite phenotype. Whole genome sequencing of these mutants identified mutations in genes encoding either structural constituents of the cuticle itself (mostly collagen genes) or protein with regulatory functions. By using CRISPR/Cas9 we confirmed 6 novel alleles of ptr-18, paqr-2, nab-1, ncam-1, vab-9 and efn-4. We further characterized the loss of function allele ptr-18(et70), which encodes a patch domain-containing (PTCHD) protein homologous to human PTCHD1. ptr-18(et70) has a significant effect on growth and development of the worms, while also increasing membrane permeability. Lipidomics analysis revealed no major alterations in membrane lipid composition, implicating cuticle defects as the primary cause of the observed permeability phenotype. - Source: PubMed
Publication date: 2026/04/22
Radović UrošHenricsson MarcusBorén JanPilon Marc - Charcot Marie Tooth neuropathies arise from diverse genetic disturbances that impair axonal structure or myelin integrity. Variants in NEFL, encoding the light chain of neurofilaments, represent a rare cause of CMT and may disrupt filament assembly, axonal transport, and cytoskeletal stability. Because NEFL variants are uncommon and phenotypes variable, the pathogenic relevance of individual substitutions is often difficult to determine. Here, we identified a previously unreported missense variant, p.(Leu97Ile), in three affected individuals. In two, a second variant, p.(Arg206Ser), was present in cis. We therefore aimed to investigate the pathogenic impact of this allele constellation using clinical, biochemical, and structural approaches. - Source: PubMed
Oeztuerk MenekseWalli SaraMuhmann DavidChoueiri CatherineDobelmann VeraAbicht AngelaLeube BarbaraSchara-Schmidt UlrikeMeuth Sven GHorvath RitaLochmueller HannsRoos AndreasRuck Tobias