KRTHB1 Mouse Monoclonal Antibody
- Known as:
- KRTHB1 Mouse Monoclonal Antibody
- Catalog number:
- BIN-003887-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- KRTHB1 Mouse Monoclonal Antibody
Related genes to: KRTHB1 Mouse Monoclonal Antibody
- Gene:
- KRT81 NIH gene
- Name:
- keratin 81
- Previous symbol:
- KRTHB1
- Synonyms:
- Hb-1
- Chromosome:
- 12q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-21
- Date modifiied:
- 2016-10-05
Related products to: KRTHB1 Mouse Monoclonal Antibody
Related articles to: KRTHB1 Mouse Monoclonal Antibody
- Lenvatinib resistance is a major clinical obstacle in the treatment of radioiodine-refractory papillary thyroid cancer (PTC). Clarification of the molecular mechanisms of this resistance is of utmost importance to devise effective therapeutic strategies. We investigated the role of Keratin 15 (KRT15) in lenvatinib resistance through comprehensive in vitro and in vivo studies. Tumor and normal thyroid tissues were analyzed for KRT15 expression and correlation with patient survival. Metabolic profiling was performed to investigate KRT15-dependent alterations in lipid metabolism, namely fatty acid oxidation (FAO). Mechanistic investigations explored the interaction between KRT15, Keratin 81 (KRT81), and Diacylglycerol Kinase B (DGKB). The therapeutic potential of targeting this pathway was evaluated using shRNA-mediated knockdown and pharmacological inhibition. KRT15 overexpression was associated with unfavorable clinical prognosis in thyroid cancer patients. We identified that KRT15 interacts with KRT81 to constitute a regulatory complex, which induces DGKB upregulation. The KRT15-KRT81-DGKB axis controls metabolic reprogramming by upregulating key FAO enzymes (CPT1A and ACOX1), resulting in increased cellular energetics and survival against therapeutic stress. Inhibition of this pathway successfully restored lenvatinib sensitivity in resistant cells. This study illustrates a novel mechanism of cytoskeletal proteins involvement in metabolic adaptation of drug-resistant thyroid cancer cells. The KRT15-KRT81-DGKB pathway is a promising therapeutic target, particularly in combination with lenvatinib, for refractory thyroid cancer patients. - Source: PubMed
Publication date: 2026/04/16
Wang YunjunZhang YuZhao DanWu YiLiao TianWang YuXiang JunChen QiSun Tuanqi - The hairy ear () mutation in heterozygous mice (/+) results in elongated and additional ear hairs, along with altered pinna morphology compared to wild-type (+/+) mice. Previous studies suggest that disruption of the gene cluster caused by the inversion influences the hair growth cycle. - Source: PubMed
Publication date: 2026/01/31
Ahn ByeongyongChoi HojunYum JooriKim DayoungLewin HarrisPark Chankyu - Lung cancer is a highly heterogeneous disease, and the tumor microenvironment (TME) characteristics are closely related to disease progression and treatment outcomes. We elucidated the cell type-specific transcriptome landscape of cancer cells and the effect of the TME on lung adenocarcinoma (LUAD). - Source: PubMed
Publication date: 2025/12/03
Cao ZimengBai XuefengLi JingCai JinruCao GangXiao YuncaiZhou Wei - Metastasis to distant organs represents the most fatal prognostic factor for colorectal cancer (CRC). The distant metastasis of tumor cells results from the collaborative effort of multiple subcellular structures, with dynamic cytoskeletal remodeling underlying this entire process. Here, we found that knockdown of KRT81 expression (shKRT81) inhibited the proliferation, invasion, and migration, while ectopic overexpression of KRT81 enhanced the CRC cells migration. Furthermore, we identified a potential downstream effector of KRT81, ezrin, a member of the ezrin/radixin/moesin (ERM) protein family that regulates cell morphology and motility. Phenotypically, the shKRT81 attenuated ezrin protein expression and reduced the number and length of filopodia in CRC cells, which were restored when KRT81 was re-overexpressed. Mechanistically, KRT81 formed a complex with ezrin, and recruitment of ezrin to the membrane and phosphorylation at the Thr567 residue were significantly abolished in shKRT81 cells. Interestingly, we found that Myosin 1B (MYO1B) might provide the driving force for the recruitment of ezrin. Notably, combinatorial inhibition (shKRT81 + ezrin-specific inhibitor) exerted significantly greater suppression of CRC cell migration and invasion than either intervention alone. Consistently, KRT81 expression was increased in CRC, and relatively high expression of KRT81 was associated with a poor prognosis. In summary, we identified a novel regulatory axis that involves KRT81, MYO1B, and ezrin, which regulates filopodia formation and migration behavior in CRC. Therefore, KRT81 may serve as a therapeutic target for CRC. - Source: PubMed
Publication date: 2025/12/17
Huang MinghanXie WenqingWu MeihuaOu ZhimeiLi CaibinJi ShuhuiLiu WanjunZhi MinChen Daici - Genetic polymorphisms in microRNA binding sites (mir-SNPs) may affect rheumatic diseases risk. We genotyped two mir-SNPs in the 3' UTR of (rs16917496) and (rs3660) in ankylosing spondylitis (AS) patients to assess their association with AS risk. DNAs were extracted from blood samples for polymerase chain reaction analysis. Western blot was used to detect protein expression. Plasma reactive oxygen species (ROS) levels were measured by fluorescent probe technology. We found that CC genotype had an increased chance of developing AS than the TT + CT genotype carrier (odds ratio, 5.378; 95% confidence interval, 1.130-25.593; = 0.019). Moreover, the CC genotype displayed a lower expression of SET8 than the TT genotype. Additionally, increased ROS generation in AS patients was observed compared with controls (23859.055 ± 12283.038 vs. 14758.330 ± 5854.946, < 0.001). Furthermore, the AS-susceptible CC genotype was associated with high ROS levels (35062.000 ± 17748.785 vs. 22629.463 ± 11002.181, = 0.033). Our study revealed that the SNP rs16917496 located in the miR-502 binding site in the 3' UTR of could be used as a biomarker to predict AS risk. Importantly, SNP rs16917496 could participate in the pathogenesis of AS by regulating the expression of SET8, thereby promoting oxidative stress levels. - Source: PubMed
Publication date: 2025/11/12
Zhang ShashaZhao YufeiWang SongSha ZiyueZhang XiaoyunPeng ChenxingZhang Jingjing