Anti-Mouse CD262 (DR5) PE 100 ug
- Known as:
- Antibody toMouse CD262 (DR5) PE 100 ug
- Catalog number:
- 12-5883-82
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD262 (DR5) 100
Related genes to: Anti-Mouse CD262 (DR5) PE 100 ug
- Gene:
- CFAP44 NIH gene
- Name:
- cilia and flagella associated protein 44
- Previous symbol:
- WDR52
- Synonyms:
- FLJ11142
- Chromosome:
- 3q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-01
- Date modifiied:
- 2019-02-18
- Gene:
- CFAP44-AS1 NIH gene
- Name:
- CFAP44 antisense RNA 1
- Previous symbol:
- WDR52-AS1
- Synonyms:
- -
- Chromosome:
- 3q13.2
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2011-07-25
- Date modifiied:
- 2014-11-18
- Gene:
- HSD17B10 NIH gene
- Name:
- hydroxysteroid 17-beta dehydrogenase 10
- Previous symbol:
- HADH2, MRXS10
- Synonyms:
- ERAB, MHBD, 17b-HSD10, ABAD, SDR5C1, MRPP2, CAMR
- Chromosome:
- Xp11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-25
- Date modifiied:
- 2019-04-23
- Gene:
- IFT80 NIH gene
- Name:
- intraflagellar transport 80
- Previous symbol:
- WDR56
- Synonyms:
- KIAA1374
- Chromosome:
- 3q25.33
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-25
- Date modifiied:
- 2014-11-19
- Gene:
- POC1A NIH gene
- Name:
- POC1 centriolar protein A
- Previous symbol:
- WDR51A
- Synonyms:
- DKFZP434C245
- Chromosome:
- 3p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-02-01
- Date modifiied:
- 2014-11-18
Related products to: Anti-Mouse CD262 (DR5) PE 100 ug
Related articles to: Anti-Mouse CD262 (DR5) PE 100 ug
- Progression from differentiated thyroid cancer to anaplastic thyroid cancer (ATC) involves profound epithelial plasticity and remodeling of the tumor microenvironment (TME), but how BRAF and RAS driver mutations shape these processes remains unclear. Here, we integrated single-nucleus RNA-seq, spatial transcriptomics, and bulk RNA-seq across BRAF- and RAS-driven thyroid tumors to delineate mutation-specific progression trajectories. BRAF-driven tumors exhibited a gradual dedifferentiation trajectory with immune pathway activation, whereas RAS-driven tumors displayed abrupt transitions characterized by aneuploidy, epithelial-mesenchymal transition, hypoxia, and extracellular matrix remodeling. Cancer-associated fibroblasts (CAFs) emerged as key regulators, with mutation-specific ligand-receptor interactions: integrin-based signaling predominated in BRAF-mutant ATCs, while PLAU-PLAUR, TNFSF10-TNFRSF10B, and AREG-EGFR were additionally enriched in RAS-driven ATCs. These CAF-epithelial circuits were spatially validated and associated with poor prognosis. Together, our findings reveal mutation-dependent epithelial and TME dynamics associated with thyroid cancer dedifferentiation and highlight the potential importance of molecular-tailored approaches in the management of advanced thyroid cancer. - Source: PubMed
Publication date: 2026/07/16
Joo Eun HyeSong Young ShinLee Han SaiJung GyeongseoChung Eun-JaeKim Su-JinKim Yoo HyungCho Sun WookChoi HongyoonWon Jae-KyungPark Woong-YangPark Young Joo - Colorectal cancer (CRC) is one of the global health issues. Current treatments still present major challenges such as off-target cytotoxicity and the emergence of drug resistance, the development of potent and innovative therapeutics is urgently needed. Here, we synthesized copper‑aluminum (CuAl) layered double hydroxides (LDH) using a hydrothermal method and loaded them with the 5-fluorouracil (5-FU) (CuAl-5FU) to improve their anticancer efficacy. The LDHs were 2D-sheeted and rosette-like in shape. The hydrodynamic diameter of CuAl and CuAl-5FU was 568 and 661 nm, respectively. Zeta potential values of CuAl-5FU ranged from +31.39 to +34.93 mV across pH 3 to 9, indicating good colloidal stability. The drug loading and encapsulation efficiency were 18.19% and 36.37%, respectively. Dose-dependent cytotoxicity was seen in HCT-116 and HT-29 CRC cells. Comparatively, CuAl-5FU LDH exhibited greater anticancer activity compared to LDH alone and free 5-FU drug in both monolayer and tumor spheroid models. Mechanistic studies revealed that CuAl-5FU significantly induced reactive oxygen species (ROS) production, mitochondrial membrane depolarization, and promoted apoptosis by upregulating the pro-apoptotic Bax protein and PARP cleavage in both CRC cells. Transcriptomic analysis and qPCR validation revealed the downregulation of oncogenic MAPK signaling and modulation of key genes related to proliferation (JUN, DUSP1, FOSB, EGR1, and FOS), apoptosis (TP53I3, ZMAT3, GADD45A, BBC3, MDM2, TNFRSF10B, E2F1, and ORC1), and cell cycle arrest (CDKN1A and CDC25A). Notably, we identified altered expression of several chemoresistance-related genes (AVPI1, HROB, DDIAS, PTGES, and LAMA3), suggesting the early emergence of adaptive responses in CRC cells. To validate this observation, CuAl-5FU-resistant HCT-116 G3 and HT-29 G2 cell lines were established and their chemoresistant phenotypes were characterized. Indeed, the chemoresistance-associated genes were upregulated, together with significantly higher IC values and clonogenic survival fractions than their respective parental cells. Collectively, these findings suggest that CuAl-5FU improves anticancer activity in CRC cells by modulating multiple genes involved in ROS production, mitochondrial membrane depolarization, apoptosis, and cell cycle regulation. Nevertheless, chemoresistance developed rapidly following repeated treatment, highlighting a potential limitation of this therapeutic approach. Overall, this study provides a new potential strategy for CRC treatment while emphasizing the importance of elucidating the molecular mechanisms underlying acquired chemoresistance. Future studies should also optimize the physicochemical properties of the CuAl-5FU LDH, particularly the large particle size (∼661 nm) by optimizing the hydrothermal synthesis conditions and incorporating surface modifications to further improve the tumor penetration and drug delivery. - Source: PubMed
Publication date: 2026/07/10
Yin YingShi JiayanLu DingyiWang YueranXiang XuemianLiu RuohanHu ZhantuBahadur AliArtoadi Muhammad IdrusZheng ChenxiaoShameli KamyarZhang XiaodongTeow Sin-Yeang - Reduced left atrial (LA) strain is associated with cerebral small vessel disease (CSVD). In memory clinic patients without atrial fibrillation, LA reservoir strain and LA conduit strain were significantly associated with white matter hyperintensity volume and cerebral microinfarcts. From plasma proteomic profiling of 1,441 proteins, we identified 23 proteins significantly associated with LA reservoir strain, 425 with LA conduit strain, 199 with white matter hyperintensity volume, and 247 with cerebral microinfarcts. Among them, 13 proteins were commonly associated with both LA strain and CSVD, with 8 proteins showing evidence of significant mediation effects for the association between LA strain and CSVD. The mediators included tumor necrosis factor receptor superfamily member (TNFRSF)-11A, TNFRSF1B, TNFRSF10B, cystatin-C, nectin-4, insulin-like growth factor-binding protein, CD27, and brorin. Partial correlation network analysis also supported TNFRSF11A and insulin-like growth factor-binding protein as highly interconnected proteins in this study population. These plasma proteins may offer pathobiological clues linking LA dysfunction to CSVD. - Source: PubMed
Publication date: 2026/07/01
Tan Eugene S JSim Ming AnnChoi HyungwonChan Siew PangCai Vera YuanGong LingliVenketasubramanian NarayanaswamyTan Boon-YeowHilal SaimaLai Mitchell K PLing Lieng-HsiRichards A MarkChen Christopher - Copyright: © 2026 Khursheed et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Breast cancer is considered to be one of the most widespread malignancies, however, its molecular processes are not fully comprehended. Another important epigenetic process that regulates the expression of genes in cancer is promoter methylation. TRAIL-R2 is also a key mediator of apoptosis but its clinical implications and epigenetic regulation in breast cancer are not clearly understood. In this research, the level of the promoter of the gene TRAIL-R2 in the matched tumor and normal breast tissues was analyzed using methylation-specific PCR and the level of the mRNA and protein products in the matched tumor and normal breast tissues were measured using quantitative real-time PCR and western blotting. Methylation of TRAIL-R2 promoter was significantly enhanced in tumor tissues and was negatively correlated with the levels of mRNA and protein. We found that hypermethylation was much more common in invasive ductal carcinoma patients and in patients with a history of use of oral contraceptives. A decreased expression of mRNA of TRAIL-R2 was significantly related to advanced TNM stage (III–IV) and the absence of progesterone receptor, and low protein expression was significantly related to postmenopausal status. These results suggest that aggressive clinicopathological phenotypes are associated with TRAIL-R2 silencing via promoter hypermethylation that may be relevant as a prognostic biomarker and therapeutic target in breast cancer. - Source: PubMed
Khursheed NuzhatAndrabi Syed IshfaThakur NatashaQadir QuratulAshraf SuhailFarooq AmbreenaRashid SafeenaJabeen FarhatKhan Waseen YounisKhursheed Allah-U-DeenZargar Mohmmad AfzalAsiaf AsiaGanie Showkat Ahmad - Dry age-related macular degeneration (AMD) is characterized by progressive degeneration of the retinal pigment epithelium-choroid interface, accompanied by immune dysregulation. However, the cellular interactions and regulatory mechanisms driving macrophage activation in this process remain incompletely understood. - Source: PubMed
Publication date: 2026/06/16
Chen YujieLiu ChulingChen JinghanHuang YiminPan GuipingWang PanHu YishanChen LinZhang YuxiWang Yan