GAL3ST4 Over-expression Lysate Product
- Known as:
- GAL3ST4 Over-expression Lysate Product
- Catalog number:
- GWB-5872BE
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- GAL3ST4 Over-expression Lysate Product
Related genes to: GAL3ST4 Over-expression Lysate Product
- Gene:
- GAL3ST4 NIH gene
- Name:
- galactose-3-O-sulfotransferase 4
- Previous symbol:
- -
- Synonyms:
- FLJ12116
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-23
- Date modifiied:
- 2014-11-18
Related products to: GAL3ST4 Over-expression Lysate Product
(META) Human Metapneumovirus Type 16 (A1) Lysate(META) Human Metapneumovirus Type 18 (B2) Lysate(META) Human Metapneumovirus Type 20 (A2) Lysate(META) Human Metapneumovirus Type 27 (A2) Lysate(META) Human Metapneumovirus Type 3 (B1) Lysate(META) Human Metapneumovirus Type 4 (B2) Lysate(META) Human Metapneumovirus Type 5 (B1) Lysate(META) Human Metapneumovirus Type 8 (B2) Lysate(META) Human Metapneumovirus Type 9 (A1) Lysate0 day neonate eyeball cDNA. RIKEN full-length enriched library. clone E130107M17 product hypothetical protein. full insert seque - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4831434J02 product nuclear factor of activated T-cells. cytop - N_A Polyclonal0 day neonate head cDNA. RIKEN full-length enriched library. clone 4832421E02 product myocyte enhancer factor 2C. full insert se - N_A Polyclonal1,2,3,4-Tetrahydro-1,2-dimethyl-4,6-isoquinolinediol
(Major Product) CAS: 102830-16-0 Formula: C11H15NO21,2,3,4-tetrahydro-1,2-dimethyl-4,8-isoquinolinediol
(Minor Product) CAS: 102830-20-6 Formula: C11H15NO210 days embryo whole body cDNA. RIKEN full-length enriched library. clone 2610510L15 product poly(A)-specific ribonuclease (dead - N_A Polyclonal Related articles to: GAL3ST4 Over-expression Lysate Product
- Pectus excavatum (PE) is the most common congenital chest wall deformity, affecting approximately 1 in 400 live births. Although familial clustering supports a genetic contribution, the molecular basis of PE remains poorly defined. This systematic review synthesizes existing evidence on genetic variants associated with PE to guide future genome-wide association studies (GWAS) and Mendelian randomization (MR) analyses. - Source: PubMed
Publication date: 2026/01/22
Ranjan RedoyImtiaz NafizWaterhouse BenjaminPaul IanBrunswicker AnnemarieDunning Joel - Many cancers upregulate the expression of sialic acid-containing glycans. These oligosaccharides engage inhibitory sialic acid-binding immunoglobulin-like lectin (Siglec) receptors on immune cells, allowing cancer cells to evade immune surveillance. The genetic mechanisms underlying this process remain poorly defined. In this study, we performed gain-of-function CRISPR activation (CRISPRa) screens to define genetic pathways that regulate expression of Siglec-binding glycans. We show that Siglec ligand expression is controlled through genetic competition between genes that catalyze α2-3 sialylation and GlcNAcylation of galactose residues. Cancer glycome remodeling is also aided by the overexpression of "professional ligands" that facilitate Siglec-glycan binding. Notably, we also find that expression of the CD24 gene is genetically dispensable for cell surface binding of the inhibitory receptor Siglec-10. Finally, we identify the sulfotransferase enzyme GAL3ST4 as a potential driver of immune evasion in glioma cells. Our study provides a unique genomic atlas of cancer-associated glycosylation and identifies immediately actionable targets for cancer immunotherapy. - Source: PubMed
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Daly JohnPiatnitca LidiaAl-Seragi MohammedKrishnamoorthy VigneshWisnovsky Simon - The aim of this study is to investigate the pathophysiology of cataract by analyzing signaling pathways in three sample types obtained from four different lens groups: age-related (ARC), diabetic (DC), post-vitrectomy cataract (PVC) and clear control lenses. - Source: PubMed
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