ADH1B Blocking Peptide, Blocking Peptides
- Known as:
- ADH1B Blocking Peptide, Blocking Peptides
- Catalog number:
- 33R-6775
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- ADH1B Blocking Peptide Peptides
Related genes to: ADH1B Blocking Peptide, Blocking Peptides
- 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 Blocking Peptide, Blocking Peptides
Related articles to: ADH1B Blocking Peptide, Blocking Peptides
- 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: 2026/05/13
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 - Genetic polymorphisms of alcohol-metabolizing enzymes influence drinking behavior and susceptibility to alcohol-related liver disease (ALD). This study aimed to clarify the distribution of ALDH2 and ADH1B genotypes in liver transplant recipients with ALD, and to explore associations with post-transplant drinking behavior using a recipient-donor paired design. - Source: PubMed
Publication date: 2026/05/02
Yamashiki NoriyoUeda YoshihideIto TakashiHatano Etsuro - Colorectal cancer (CRC) is one of the most commonly diagnosed and globally spread malignant diseases. Cancer-associated fibroblasts (CAFs) are key architects of the tumor microenvironment, yet their origin, stability, and interconvertibility remain poorly understood. Using transcriptomic profiling of fibroblasts from colorectal cancer (CRC) patients, we identify highly expressed (HEX) markers that define fibroblast subpopulations and uncover mechanisms governing their plasticity. We find that ADH1B marks normal colon-associated fibroblasts (NAFs), which consist of PI16-NAFs and ADAMDEC1-NAFs. ITGA3 delineates the total CAF population, which comprises myofibroblastic CAFs (myCAFs), whose characterizing markers were associated with poor prognosis and proteolytic inflammatory CAFs (piCAFs), characterized by markers not associated with prognosis. An AGT/TGM2-expressing fibroblast subset is present in both healthy and tumor tissues, suggesting alternative trajectories to the classical NAF-to-CAF transition model. While PI16-NAFs, AGT/TGM2-fibroblasts, and myCAFs maintain stable identities in long-term culture, the ADAMDEC1-NAF and piCAF phenotypes are lost in vitro. ITGA3-CAFs demonstrate dynamic plasticity, with TGF-β stably inducing myCAF formation and TNF-α or inhibition of DNA methylation promoting transient piCAF emergence. These findings redefine fibroblast heterogeneity in CRC and reveal a coexisting stable and plastic fibroblast network that may be amenable to modulation and provides a framework for future functional and translational studies. We identified highly expressed markers (HEX markers) to distinguish CAFs, NAFs and corresponding subpopulations in CRC. ADH1B characterized NAFs, which consisted of stable (solid outline) PI16-NAFs and unstable (dashed outline) ADAMDEC1-NAFs. ITGA3 identified CAFs consisting of stable myCAFs associated with poor prognosis and unstable piCAFs not associated with prognosis. AGT/TGM2 fibroblasts did not express ADH1B or ITGA3, were stable in culture and could be detected in both healthy colon and CRC. Treatment of PI16-NAFs with LPS or IFN-γ induced ADAMDEC1-NAFs, TGF-β the formation of myCAFs, while treatment with TNF-α led to the formation of piCAFs. Reduced DNA methylation converted myCAFs and PI16-NAFs into piCAFs. - Source: PubMed
Publication date: 2026/04/28
Demmler RichardAnchang Charles GYong YongsongRamming AndreasRauber SimonSchellerer Vera SSchmid BenjaminHartmann ArndtMerkel SusanneImkeller KatharinaNaschberger ElisabethStürzl Michael