ADH1B antibody
- Known as:
- ADH1B (anti-)
- Catalog number:
- orb135010
- Product Quantity:
- 200 ug
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- ADH1B antibody
Related genes to: ADH1B antibody
- Gene:
- ADH1B NIH gene
- Name:
- alcohol dehydrogenase 1B (class I), beta polypeptide
- Previous symbol:
- ADH2
- Synonyms:
- -
- Chromosome:
- 4q23
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-01-18
Related products to: ADH1B antibody
Related articles to: ADH1B antibody
- To investigate the effect of ethanol for promoting oxaliplatin resistance in colorectal cancer (CRC) and the underlying molecular mechanisms. - Source: PubMed
Tan BinWeng NuozhouZeng WentaoGu JiayuWeng LianjiWen HuilinXiao HaochengZheng Kehong - Single-nucleotide variants (SNVs) are the most common type of genetic variation and are associated with some diseases. Accurate detection of SNVs is of great significance in multiple fields. Despite the rapid development of SNV detection technologies, most methods suffer from limitations in detection specificity, which may lead to false positive results, especially for low-frequency SNVs. Here, we report a novel mutation detection method, the ribonucleotide-modified primer (r-primer) overlapping blocker elongation (PROBE) method. The PROBE method combines RNase H2-mediated r-primer-specific cleavage and blocker-mediated blocking to achieve selective amplification of the mutant (MUT) templates and efficient suppression of wild-type (WT) template amplification. The PROBE method requires allele-specific (AS)- and non-AS-r-primers, along with one peptide nucleic acid (PNA) or locked nucleic acid (LNA) blocker, all of which are blocked by a 3'-C3 spacer. The AS-r-primer and the blocker completely match the MUT and WT, respectively. They overlap and competitively bind to the SNV-containing region. The PROBE method can completely inhibit WT amplification, achieving a sensitivity of 200 copies per reaction and a selectivity of 0.1%. We developed PROBE assays for single-tube discrimination of homozygous (WT and MUT) and heterozygous genotypes of alcohol dehydrogenase 1B () rs1229984 and aldehyde dehydrogenase 2 () rs671 polymorphisms. Clinical evaluation revealed that the PROBE assay achieved accuracies of 100% for rs1229984 and 99.1% for rs671, with the latter slightly exceeding 98.1% accuracy of Sanger sequencing. - Source: PubMed
Publication date: 2026/05/23
Zhao YongjuanWang ZiyanZhang MinZhao XiuliYan BeibeiMa YingyingSong Zhi-GangWan ZhenzhouZhang Chiyu - The pathogenic mechanisms underlying rheumatoid arthritis (RA) remain elusive. Lactylation, a novel post-translational modification, may regulate immune and metabolic reprogramming, underscoring the imperative to delineate lactylation-related genes (LRGs) driving RA progression. - Source: PubMed
Publication date: 2026/05/14
Hu XiaoliXiao QianWang LizhouXu YuanGou QiaoqiaoWen JingZhou Shi - Alcohol and heroin are classified as central nervous depressants. Their addiction has a strong genetic component, although the specific genetic variations involved are not fully understood. This study investigates the roles of alcohol metabolic enzyme genes (ADH1B and ALDH2) in patients with alcohol use disorder (AUD) and heroin use disorder (HUD) that co-occur with AUD. - Source: PubMed
Publication date: 2026/05/14
Wu Yao-ChengChen Chun-YenKuo Shin-ChangYeh Yi-WeiLin Chun-LongHuang Chih-YunHuang San-Yuan - Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a systemic disorder shaped by genetic variants and network-level interactions beyond obesity and insulin resistance. This study aimed to define the genetic and proteomic architecture of MASLD by integrating GWAS and plasma proteomic profiling from the UK Biobank. Genome-wide association analyses were conducted under additive and dominant models, with functional annotations performed using SIFT, PolyPhen-2, PROVEAN, REVEL, CADD, MutationTaster, and conservation metrics (GERP++, phyloP, phastCons, and B-statistic). Differential protein expression was assessed using the Olink platform, and STRING was applied for protein-protein interaction analysis. MASLD patients showed male predominance and significant differences in hepatic (AST, ALT, GGT, PDFF), metabolic (glucose, triglycerides, TyG index), and inflammatory markers (CRP, neutrophils, NLR, CAR). GWAS confirmed (rs738409, I148M) and (rs58542926, E167K) as major risk variants, while and showed weaker but conserved associations. Proteomics revealed downregulation of IGFBP2, IGFBP1, PON3, CKB, and APOF and upregulation of CPM, IGSF9, GUSB, ACY1, AFM, LEP, and GSTA1/3. PPI analysis identified ADIPOQ, LEP, FGF21, and ADH1B as central hubs in metabolic and inflammatory regulation. MASLD should be regarded as a network disease involving lipid metabolism, insulin/IGF signaling, mitochondrial function, and ECM-inflammatory pathways. These findings highlight and as major genetic drivers, while , , and peripheral proteins contribute regulatory roles, suggesting novel biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/04/28
Kang Sang WookKim Su KangBan Ju YeonPark Min Su