Polyclonal Rabbit ALDH1B1 Antibody
- Known as:
- Polyclonal Rabbit ALDH1B1 Antibody
- Catalog number:
- KA0185
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit ALDH1B1 Antibody
Related genes to: Polyclonal Rabbit ALDH1B1 Antibody
- Gene:
- ALDH1B1 NIH gene
- Name:
- aldehyde dehydrogenase 1 family member B1
- Previous symbol:
- ALDH5
- Synonyms:
- ALDHX
- Chromosome:
- 9p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-13
- Date modifiied:
- 2018-05-03
Related products to: Polyclonal Rabbit ALDH1B1 Antibody
Related articles to: Polyclonal Rabbit ALDH1B1 Antibody
- Oxidative alcohol metabolism in the liver relies on sequential enzymatic reactions involving alcohol dehydrogenase (ADH), cytochrome P450 2E1 (CYP2E1), and aldehyde dehydrogenase (ALDH) isozymes. However, the circadian regulation of these enzymes, their susceptibility to genetic, environmental, and metabolic disruption, and their functional implications toward alcohol-mediated tissue injury remain incompletely defined. To address this gap, we performed a comprehensive integrative analysis of the publicly available circadian transcriptome datasets spanning genetic clock disruption, acute sleep deprivation, chronic high-fat diet feeding, and occupational shift work to systematically characterize the temporal regulation and disruption vulnerability of the major alcohol-metabolizing enzymes. Mouse tissue-cycling analyses revealed pronounced gene- and tissue-specific diurnal regulation, with oscillating primarily in adipose tissues; and mitochondrial cycling broadly across kidney, aorta, lung, adrenal gland, and liver; and cytosolic being uniformly arrhythmic. In the liver, and exhibited robust ~24 h oscillations that peaked during the light/resting phase, while showed inconsistent rhythmicity and remained arrhythmic. Notably, and rhythms persisted in knockout and mutant livers under light-dark conditions, despite complete loss of core clock gene oscillations, yet were abolished in constant darkness, revealing that systemic zeitgeber cues can mask the loss of intrinsic clock function to maintain apparent rhythmicity in these metabolic genes. Systematic cross-paradigm comparison established a novel gene-specific vulnerability hierarchy. was found to be most disrupted by environmental and metabolic perturbations, with acute sleep deprivation eliminating its rhythmicity and temporal expression pattern and a Western-style high-fat diet inducing pronounced phase delays and rhythm loss relative to low-fat diet controls. Both disruptions paralleled alterations in hepatocyte nuclear factor 4α (), newly implicating HNF4α as a potential mediator of ALDH2 circadian instability. In humans, ALDH2 and CYP2E1 exhibited conserved but phase-inverted circadian rhythms across multiple tissues relative to mice, and, importantly, night-shift workers showed markedly dampened and phase-shifted ALDH2 rhythms in peripheral blood mononuclear cells, providing the molecular link between occupational circadian misalignment and impaired acetaldehyde detoxification. Collectively, our detailed and innovative analytical approach reveals gene- and tissue-specific circadian regulation of alcohol-metabolizing enzymes, identifies ALDH2 as uniquely vulnerable to circadian misalignment, underscores the importance of circadian timing for optimal hepatic detoxification and resistance to tissue injury, and suggests that monitoring circadian rhythms could help tailor individualized advice on alcohol consumption for shift workers and populations with irregular sleep schedules, informing precision medicine approaches for alcohol-related disorders. - Source: PubMed
Publication date: 2026/02/22
Lee YoolKeshavarzian AliSong Byoung-Joon - Vascular calcification (VC) is a major contributor to cardiovascular morbidity and mortality, yet effective therapies are lacking. Here, we show that alternate-day intermittent fasting (IF1:1) attenuates vitamin D-induced VC in mice, whereas a 5:2 regimen is ineffective. The protective effect of IF1:1 is gut microbiota-dependent, particularly through enrichment of Akkermansia muciniphila (Akk). Microbiota-derived extracellular vesicles (EVs) function as nano-scale mediators that bypass the spatiotemporal constraints of bacterial survival to facilitate long-distance communication with host cells, providing a crucial pathway for downstream mechanistic investigation. Akk-derived EVs (Akk-EVs) are internalized by vascular smooth muscle cells (VSMCs), suppressing osteogenic differentiation and calcification in vitro and in vivo. Proteomic analysis identified B2URF3 as a highly enriched functional protein in Akk-EVs and Akk, which interacts with Aldehyde Dehydrogenase 1 Family Member B1 (ALDH1B1) to inhibit VSMC osteogenic transdifferentiation. Clinically, reduced fecal Akk abundance and lower serum B2URF3 levels were observed in patients with coronary calcification. These findings define a gut-vascular axis by which IF1:1 mitigates VC and nominate Akk-EVs and B2URF3 as potential therapeutic targets and biomarkers. - Source: PubMed
Publication date: 2026/01/07
Zeng Shi-YuLiu Jiang-HuaXiang Ying-YingZeng Zhao-LinZhao Zhi-BoZheng JieLiu Yi-FuLin Zhi-RouWang Yi-YiHong Chun-GuJin LingZhu Guo-QiangLiu Yi-WeiWang XinLi Xiao-XueGuan ZheWang Zhen-XingSun TingXie HuiLiu Jiang-Hua - Metastasis remains the primary cause of cancer-related mortality. During dissemination, cancer cells must navigate spatially confined microenvironments, yet the underlying metabolic adaptations that facilitate this process remain unclear. Here, through an in vivo CRISPR screen targeting metabolic enzymes, we identify aldehyde dehydrogenase 1 family member B1 (ALDH1B1) as essential for tumor cell survival in confining capillaries. Mechanistically, compressive force induces casein kinase 2 alpha 3 (CSK23) to phosphorylate kappa-B kinase subunit beta (IKKβ) at Ser177/181, which activates the nuclear factor kappa B (NF-κB) pathway and upregulates ALDH1B1. The upregulation of ALDH1B1 enhances aldehyde detoxification, which suppresses ferroptosis and promotes tumor cell survival during migration through the capillaries, thereby facilitating metastasis. Importantly, genetic or pharmacological inhibition of CSK23 or ALDH1B1 effectively impairs metastasis. In lung cancer patients, confined tumor cells exhibit higher levels of ALDH1B1 and NF-κB activation, which correlates with metastatic recurrence. Our findings reveal a mechano-metabolic pathway that promotes metastasis and suggest CSK23 and ALDH1B1 as potential therapeutic targets. - Source: PubMed
Publication date: 2025/12/14
Liu BingLiu MinZhang YajuanZhu YifeiZhou DingpeiGao HongYang FanGao DongZhao YunTao BangBaoYao FengYang Weiwei - Aldehyde dehydrogenases (ALDHs) are responsible for the NAD(P)-dependent oxidation of aldehydes into carboxylic acids, fulfilling key roles in detoxification, antioxidant defense, biosynthesis, and regulatory processes. Elevated expression and activity of ALDH isoenzymes have been documented in various human cancers, where they are linked to cancer recurrence. While the human genome encodes 19 functional ALDH genes, aldehyde dehydrogenase 1B1 (ALDH1B1) has emerged as a critical enzyme in diverse human pathologies. ALDH1B1 is a major mitochondrial enzyme involved in detoxifying lipid peroxidation by-products and metabolizing various aldehyde substrates. Notably, both low and high ALDH1B1 expression levels contribute to tumor progression and with marked variability observed across different tumor types. This review summarizes the essential functions and potential ALDH1B1 mechanisms in the tumor initiation, progression, metastasis, and therapeutic responses across cancer types. Our analysis indicates that ALDH1B1 is a potential therapeutic target for cancer therapy. - Source: PubMed
Publication date: 2025/11/19
Zhao TingtingSun ZhihongLi ZhenguoQu LiujingLi YulanLiu Jie - Congenital pulmonary airway malformation (CPAM) is a rare lung abnormality characterized by the formation of cystic or solid masses in lung tissues. To date, the genetic etiology of CPAM has not been well described. The objective of this study is to explore the potential genetic etiology of CPAM through trio-based whole exome sequencing (WES). - Source: PubMed
Publication date: 2025/08/26
Yu QiChen JunxianLi HaiboXue JiangyangMeng CuijuHong HaifaQin WenjunChen Changshui