Fab_ IgM (mu) hum biotine
- Known as:
- Fab_ Immunoglobulin M (mu) hum biotine
- Catalog number:
- BI 2407
- Product Quantity:
- 1ml
- Category:
- -
- Supplier:
- P.A.R.I.S
- Gene target:
- Fab_ IgM () hum biotine
Related genes to: Fab_ IgM (mu) hum biotine
- Gene:
- ELDR NIH gene
- Name:
- EGFR long non-coding downstream RNA
- Previous symbol:
- LINC01156
- Synonyms:
- Fabl
- Chromosome:
- 7p11.2
- Locus Type:
- RNA, long non-coding
- Date approved:
- 2014-01-01
- Date modifiied:
- 2017-10-25
Related products to: Fab_ IgM (mu) hum biotine
Related articles to: Fab_ IgM (mu) hum biotine
- To clarify the clinical characteristics and etiologic diversity of pediatric lacrimal duct obstruction in children aged ≥1 year requiring surgical treatment under general anesthesia and to evaluate the outcomes of endoluminal lacrimal duct recanalization (ELDR). - Source: PubMed
Publication date: 2026/07/18
Matsumura NozomiOhno TomokoNakamura JutaroGoto Satoshi - Fluorescent reporters are powerful tools for revealing intercellular heterogeneity among proliferating cells. However, there are few tools to analyze differences among quiescent (G0) cells, though such differences are relevant for development, tissue maintenance, and cancer cell behavior. Quiescence heterogeneity, also known as quiescence depth, typically correlates with time after cell cycle arrest, yet directly measuring cell age is not feasible for all cell types or most tissues. Here, we describe ELDR-Glo, a genetically-encoded fluorescent biosensor that estimates relative cell age, or time since the last cell cycle. The biosensor integrates replication-coupled degradation in S phase with a slow-maturing mCherry and a normalization module. We demonstrate that ELDR-Glo signal correlates with true cell age by both live-cell imaging and in fixed cells. ELDR-Glo distinguishes early and late G0 cells and functions as a relative quiescence depth reporter in situ. The biosensor is compatible with multiplexed immunofluorescence and flow cytometry. ELDR-Glo provides a unique and scalable tool to investigate cell proliferation control. - Source: PubMed
Publication date: 2026/08/13
Johnson Martha SKamath SapnaFleifel DaliaHill TessaMei LiuDas NehaLinares MaryAw WenyihBautch Victoria LCook Jeanette Gowen - Although the outcomes of endoluminal lacrimal duct recanalization (ELDR) for nasolacrimal duct (NLD) obstruction are associated with the obstruction length, NLD obstruction has not been quantified. In this study, we aimed to quantify the obstruction length using a calibrated dacryoendoscope and investigate its relationship with surgical outcomes following endoscopic recanalization of the lacrimal passage. We retrospectively analyzed the eyes of patients who underwent ELDR using a calibrated dacryoendoscope at our institution between January 2023 and February 2025. Patients with dacryocystitis detected during preoperative irrigation testing were excluded. A lacrimal tube was placed for 2 months after recanalization, and we used the calibrated dacryoendoscope to measure the obstruction length. The 3-month postoperative outcomes were determined using irrigation testing, subjective symptoms, and cotton thread testing. A total of 31 eyes of 26 patients (6 eyes of 5 males; 25 eyes of 21 females; mean age, 68.8 ± 10.5 years) were included in this study. The mean obstruction length was 10.8 mm (range: 1-30 mm). The nasolacrimal duct was patent, showed reflux, and was obstructed in 12, 16, and 3 eyes, respectively, at 3 months. The symptoms resolved, improved, and remained unchanged in 18, 11, and 2 eyes, respectively. Trend analysis revealed a significant relationship between the obstruction length and irrigation outcomes. However, no significant association was observed with the symptoms. The obstruction length was significantly correlated with the 3-month postoperative cotton thread test results. The NLD obstruction length was associated with the 3-month postoperative irrigation test results, and longer obstruction was associated with poorer postoperative outcomes. - Source: PubMed
Publication date: 2026/01/20
Ueta YoshikiWatanabe YujiTanaka NobuyaTanaka Anzu - Bladder cancer (BCa) is one of the most prevalent genitourinary malignancies with high recurrence worldwide. A lack of reliable prognostic biomarkers and effective therapeutic targets hinders its treatment. Emerging evidence indicates that long noncoding RNAs (lncRNAs) are involved in human cancers, including BCa. While lncRNAs hold enormous promise, their specific roles and mechanisms in BCa remain largely unexplored. Here, we identify the lncRNA ELDR as a pivotal oncogenic driver in BCa. - Source: PubMed
Publication date: 2025/11/21
Hu XiaoXie TianhangXiao XiaoMei Yuhua - Lysosomal adaptation through the endo-lysosomal damage response (ELDR) enables cancer cells to evade lysosome-targeted therapies. Here, we identified the flavonoid compound V8 as a first-in-class ELDR disruptor that eliminated cancer cells by sabotaging lysosomal resilience. Mechanistically, V8 bound lysosomal HSP70 via hydrogen bonding, destabilizing its interaction with bis(monoacylglycero)phosphate (BMP) and triggering pathological sphingomyelin (SM) accumulation. SM overload allosterically inhibited TRPML1, blocking calcineurin PPP3CB activation and subsequent TFEB dephosphorylation. This dual perturbation: enhanced lysophagy and failed TFEB-driven biogenesis drove catastrophic lysosomal bankruptcy. Crucially, V8 bypassed canonical ELDR activation: unlike lysosomotropic agent LLOMe, it induced global membrane remodeling rather than focal perforations, avoiding Ca²⁺-dependent endosomal sorting complexes required for transport (ESCRT) repair. Genetic validation using HSP70-knockout and point mutation models confirmed target specificity, while SM synthase inhibition rescued TRPML1 activity and mitigated apoptosis. Tumor-selective efficacy arose from malignant cells' heightened SM dependency and lysosomal HSP70 reliance, sparing normal counterparts. Our work established HSP70-BMP-ASM axis disruption as a strategy to subvert lysosomal homeostasis, providing a blueprint for next-generation lysosome-targeting agents that exploit lipid-mediated channelopathy to sensitize cancer cells to lysosomal damage. - Source: PubMed
Publication date: 2025/12/05
Chen HongyuZhu MengyuanZhao ZiyingJiang YuexinWang HaidiLiu YuChen YanLi HuiXun ChenHui Hui