FLT3 (Ab_591) Antibody
- Known as:
- FLT3 (Ab_591) Antibody
- Catalog number:
- E021187-1
- Product Quantity:
- 50ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- FLT3 (Ab_591) Antibody
Related genes to: FLT3 (Ab_591) Antibody
- Gene:
- FLT3 NIH gene
- Name:
- fms related tyrosine kinase 3
- Previous symbol:
- -
- Synonyms:
- STK1, FLK2, CD135
- Chromosome:
- 13q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-30
- Date modifiied:
- 2019-04-23
Related products to: FLT3 (Ab_591) Antibody
Related articles to: FLT3 (Ab_591) Antibody
- Nucleoside analogues are traditionally developed as antimetabolites that interfere with nucleic acid synthesis after intracellular phosphorylation. In this study, inspired by the 3',4'-unsaturated sugar scaffold of ddhCTP, we designed and synthesized a series of 3',4'-unsaturated nucleoside analogues to explore their antiproliferative potential and possible non-classical cellular effects. Among the synthesized compounds, 17k, a C-nucleoside bearing both a 3',4'-unsaturated sugar moiety and a chlorinated remdesivir-like base, exhibited potent antiproliferative activity against HepG2 cells, with an IC₅₀ value of 2.27 ± 0.36 μM, lower than that of gemcitabine under the same assay conditions. In the nonmalignant GES-1 epithelial cell line, 17k showed an IC₅₀ value of 34.26 ± 3.45 μM, corresponding to a selectivity index of 15.1 relative to HepG2 cells. Closely related compounds 12 and 17j showed no detectable activity, indicating a narrow structure-activity relationship. Exploratory single-concentration kinase profiling at 20 μM showed strong inhibition of several transcription-associated CDK/cyclin complexes (CDK13/CycK, CDK12/CycK, CDK9/CycT1, CDK19/CycC, and CDK8/CycC) and selected receptor tyrosine kinases (KDR/VEGFR2, RET, EPHA1, and FLT3). Compound 17k also suppressed colony formation and wound closure, induced apoptosis, and caused S-phase accumulation in HepG2 cells. These findings identify 17k as a nucleoside analogue with unanticipated antiproliferative activity and suggest that kinase modulation may contribute to its cellular effects. - Source: PubMed
Publication date: 2026/08/14
Wang SongYang JingYang XinyueHuang HaoZou HaiyangZhang YuZhang XushanLuo CongcongZhao BingLiu Feng-WuHerdewijn Piet - Acute myeloid leukemia (AML) remains the most common cause of death in adults with acute leukemia. Tyrosine kinase inhibitors (TKIs) have shown significant clinical efficacy in defined patient subgroups. Real-world outcomes of AML patients undergoing TKI therapy have not been widely reported. - Source: PubMed
Espinoza-Gutarra Manuel RJarret BrookeWang XiaoliangAfghahi AnoshehBae Sejong - Papillary renal neoplasm with reverse polarity (PRNRP) is a rare renal tumor with distinct histomorphologic features and a strong association with KRAS exon 2 mutations, typically at codon 12. We report two cases that expand the molecular spectrum of this entity. The first tumor, a 3.5 cm mass in a 51-year-old female, harbored the classic KRAS codon 12 mutation (p.G12V), whereas the second, a 2.0 cm mass in a 77-year-old female, exhibited a KRAS p.Q61K mutation, rarely reported in PRNRP. Both tumors showed characteristic histology (tubulopapillary architecture, eosinophilic cytoplasm, apical nuclear polarity) and immunoprofile (GATA3+, CK7+, SDHB-retained, FH-retained). Next-generation sequencing using a 505-gene cancer panel also detected additional alterations in FLT3, POLD1, KMT2C, and WHSC1, the significance of which remains uncertain currently but may emerge with more molecular data from additional PRNRP cases. These findings underscore the value of integrated histopathologic and molecular evaluation, highlight KRAS Q61K as a rare variant, and provide a foundation for future genomic studies in this tumor type. - Source: PubMed
Publication date: 2026/07/15
Zhou GangDong XiuhuaLiu Lina - - Source: PubMed
Publication date: 2026/07/07
Menssen Andrew JAshango Amenech BAlonzo Todd AGerbing Robert BPardo LauraHsu Fan-ChiLott Loren LDai FangyanCooper Todd MPollard Jessica ATarlock KatherineAplenc RichardMeshinchi SoheilBrodersen Lisa EidenschinkWells Denise ALoken Michael RHudson Chad A - - Source: PubMed
Levis Mark J