Mouse polyclonal to AKR1C3, Host Mouse
- Known as:
- Mouse pab AKR1C3, Host Mouse
- Catalog number:
- YF-PA15761
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal AKR1C3 Host
Related genes to: Mouse polyclonal to AKR1C3, Host Mouse
- Gene:
- AKR1C3 NIH gene
- Name:
- aldo-keto reductase family 1 member C3
- Previous symbol:
- HSD17B5
- Synonyms:
- KIAA0119, DDX, HAKRB, PGFS
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-29
- Date modifiied:
- 2016-10-05
Related products to: Mouse polyclonal to AKR1C3, Host Mouse
Related articles to: Mouse polyclonal to AKR1C3, Host Mouse
- Arachidonic acid (AA), a membrane-abundant polyunsaturated fatty acid, is primarily liberated from membrane phospholipids by phospholipase A (PLA), and is subsequently metabolized into bioactive eicosanoids involved in vascular tone and inflammation. With lipidomics advances, AA metabolism's multifaceted roles in the tumor microenvironment (TME) have emerged, and it is recognized as a key driver and potential therapeutic axis in lung adenocarcinoma (LUAD). We utilized spatial transcriptomics sequencing (ST-seq) and LUAD-associated single-cell RNA sequencing (scRNA-seq) to explore crucial AA-related biomarkers in LUAD. - Source: PubMed
Publication date: 2026/05/19
Sun ChongqiZhang YuchenPan YunXia GuixiYang GuangrongHuang ChunkaiLi JunMa Pei - Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors globally, with liver cirrhosis (LC) recognized as a significant precursor. Xenobiotic metabolism plays a pivotal role in liver diseases, where the liver's primary function as a detoxifying organ directly influences health and tumor development. Therefore, exploring the function of genes associated with xenobiotic metabolism in patients with HCC and LC is crucial for advancing diagnosis and treatment strategies. - Source: PubMed
Publication date: 2026/05/13
Xu HaoLi YanpengZhao RuiMa ShaoweiHu NingYu ShuoLv Xuefeng - Conventional allele specific PCR (AS-PCR) genotyping using gel electrophoresis and ethidium bromide (EtBr) is costly, particularly in developing countries. It also poses health risks to working personnel as it requires specialized equipment and toxic dyes like EtBr. Hence, the present study developed a simple and cost-effective colorimetric genotyping method using gold nanoparticles solution (AuNPs) and unmodified primers. Specifically, 15 μl of AuNPs solution was found sufficient for detecting an amplicon in 5 μl of PCR product. In this approach, the amplified PCR products appear red while the non-amplified PCR products appear blue with a PCR mastermix without a dye. Transmission Electron Microscopy (TEM) revealed the sequestration of AuNPs in amplified PCR products and the aggregation of AuNPs in non-amplified PCR products, resulting in red and blue colors, respectively. The method was tested on genotyping of six SNPs from six genes (Akr1c3, Plg, Myf5, Sec14l2, Tpm1, and Lama2) in buffaloes, and the results were perfectly matched with those obtained using agarose gel electrophoresis analysis. Therefore, the AS-PCR combined with AuNPs provides an easy visual detection method for the amplified and non-amplified PCR products of single-nucleotide polymorphisms (SNPs). In addition, the presented method has the potential to replace agarose gel electrophoresis, the use of EtBr, and UV-transilluminator. - Source: PubMed
Publication date: 2026/05/02
Verma Surya KantKumar Lal KrishanMitra Murli DharKumar JitendraSingh PrashantMohiddin RoshanNayan VarijSingh DheerOnteru Suneel Kumar - Developing targeted antitumor agents with minimal systemic toxicity is highly desirable. Exatecan, a potent camptothecin derivative, is clinically restricted due to its toxicity and limited efficacy. Targeting the tumor-enriched enzyme AKR1C3 enables selective drug activation. We designed two novel AKR1C3-responsive Exatecan conjugates, EP-1 and EP-2, with a fluorescence-quenched module for real-time "turn-on" tracking of drug release. The conjugates exhibited potent cytotoxicity in AKR1C3-high cancer cells (IC: 7.7 ± 0.2 nM for EP-1, 4.6 ± 0.4 nM for EP-2), similar to Exatecan, but markedly reduced toxicity in AKR1C3-low and normal cells, and overcame sorafenib resistance. Cellular and zebrafish imaging confirmed a targeted release. In a mouse model, EP-2 displayed potent efficacy with significantly reduced systemic toxicity (MTD > 60 mg/kg) compared to Exatecan. These results nominate EP-2 as an ideal candidate for selective and safe tumor therapy, providing a new paradigm for biomarker-driven antitumor drug design. - Source: PubMed
Publication date: 2026/05/02
Kang NingfangLiu ShuainanLi XiaoyuLuo RuxiangChen WenyanRan ChongzhaoWang PengYang Jing - Ferroptosis, an iron-dependent form of programmed cell death driven by lipid peroxidation, represents a new potential therapeutic target in cancer. However, emerging evidence indicates that hepatocellular carcinoma (HCC) frequently exhibits resistance to ferroptosis induction, while the underlying molecular mechanism is poorly understood. Here, we found that aldo-keto reductase family 1 member C3 (AKR1C3), a protein highly expressed in ferroptosis-resistant HCC cells, negatively regulates ferroptosis in an enzyme-independent manner. Mechanistically, AKR1C3 promotes ubiquitin-proteasomal degradation of the transferrin receptor (TFRC), which is indispensable for cellular iron uptake. AKR1C3 knockdown restores TFRC expression, increases the level of labile iron pool, and sensitizes HCC cells to ferroptosis. Furthermore, AKR1C3 acts as a scaffolding protein to promote the degradation of TFRC and reduce iron uptake by promoting nuclear export of Beta-transducin repeats-containing proteins (β-TrCP) and its binding to TFRC. Notably, AKR1C3 is upregulated in NRF2-driven sorafenib-resistant HCC, and its inhibition reversed ferroptosis and sorafenib resistance. Our work uncovers AKR1C3 suppresses ferroptosis in HCC by promoting β-TrCP-mediated TFRC degradation, positioning AKR1C3 as a promising therapeutic target to enhance ferroptosis-based anticancer strategies. - Source: PubMed
Publication date: 2026/05/02
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