Anti-Mouse CD309 (FLK1) PE 200 ug
- Known as:
- Antibody toMouse CD309 (FLK1) PE 200 ug
- Catalog number:
- 12-5821-83
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD309 (FLK1) 200
Related genes to: Anti-Mouse CD309 (FLK1) PE 200 ug
- Gene:
- KDR NIH gene
- Name:
- kinase insert domain receptor
- Previous symbol:
- -
- Synonyms:
- FLK1, VEGFR, VEGFR2, CD309
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 1991-07-10
- Date modifiied:
- 2019-04-23
Related products to: Anti-Mouse CD309 (FLK1) PE 200 ug
Related articles to: Anti-Mouse CD309 (FLK1) PE 200 ug
- Gastric cancer is a major global health issue, especially in advanced stages with metastasis. However, anti-angiogenic treatments such as ramucirumab target vascular endothelial growth factor, yet the exact mechanisms behind hematogenous metastasis remain unclear. This study analyzed RNA sequencing data from TCGA to identify angiogenesis-related genes in metastatic gastric cancer. - Source: PubMed
Publication date: 2026/08/31
Yoo JaeunKim Hyun MyongJeong KyoungyunYoo Yie-RiShin Ji-YeonLee SeunghoLee SeungbokLee Hye SeungPark Kyoung UnKong Seong-HoPark Do JoongLee Hyuk-JoonYang Han-Kwang - Atopic dermatitis (AD) is a multifactorial inflammatory skin disease characterized by chronic inflammation, immune dysregulation, and compromised skin barrier function. Thespesia populnea is found to be a rich source of polyphenols and flavonoids and it provides various therapeutic applications in dermatology. The pharmacological action of phytocompounds present in the flower part of Thespesia populnea in treating the skin inflammation is largely unknown. In the present study, we have employed a network pharmacology and molecular docking approach to explore the therapeutic potential of Thespesia populnea in treating AD and to understand the molecular mechanism of action of phytocompounds present in the flower part of Thespesia populnea. The phytochemical data of Thespesia populnea were extracted from the IMPPAT database, which includes 16 phytocompounds: gossypol, kaempferol, quercetin, lupenone, lupeol, quercetin-3-glucoside, beta-sitosterol, etc. Based on the SEA database search, 226 targets were identified to have binding affinity with the phytocompounds present in Thespesia populnea flowers. A total of 1538 AD-associated targets were retrieved and out of which 71 were identified to be ligand-associated AD targets and were further used for network construction. The AD network revealed the multi-targeted mechanism of phytocompounds present in Thespesia populnea against AD targets responsible for its anti-dermatitic activity. The top 15 potential protein targets in the network were found to be AKT1, NFKB1, MMP9, STAT3, EGFR, BCL2, PPARG, ESR1, MMP2, IL2, TLR2, GSK3B, KDR, CREB1, and ALOX5. Based on virtual screening and SwissADME prediction, eight docking complexes with high binding affinity and favorable pharmacokinetic properties were selected for AutoDock analysis. Among the selected docking complexes, beta-sitosterol and glycogen synthase kinase-3 beta (GSK3B) complex were found to possess the maximum binding energy of -8.3 kcal/mol with interacting amino acids GLU B:290, PRO A:212, PRO B:286, and TYR B:288. Other potent interactions that signify the anti-dermatitic potential of Thespesia populnea include kaempferol-GSK3B, lupeol-GSK3B, beta-sitosterol-GSK3B, herbacetin-ALOX5, gossypetin-ALOX5, quercetin-ALOX5, lupenone-ALOX5, and lupeol-ALOX5. The GSK3B complex and arachidonate 5-lipoxygenase were found to be the key anti-dermatitic targets for the phytocompounds present in Thespesia populnea flowers. The network pharmacological study revealed the mechanism of action of the phytocompounds present in Thespesia populnea flowers against potential dermatitis targets and molecular docking analysis highlighted the potent interactions responsible for its anti-dermatitic property. The present study offers valuable insights into the anti-dermatitic property of Thespesia populnea flowers (Supporting information). - Source: PubMed
Publication date: 2026/09/02
Thangavel PoongodiAngamuthu KandavelmaniSundaramurthy Gayathri Devi - Preeclampsia is characterized by endothelial dysfunction and angiogenic imbalance driven, in part, by excess soluble fms-like tyrosine kinase-1 (sFLT-1). Building on previous findings demonstrating vascular modulatory effects of cardiac and quercetin glycosides from Dacryodes edulis seeds during L-NAME-induced vascular perturbation, we investigated whether pear seed glycosides (PSG) modulate sFLT-1-mediated endothelial injury in preeclampsia. Endothelial, preclinical, biophysical, pharmacodynamic, and exploratory clinical approaches were integrated to evaluate PSG activity. TGFβ-stimulated HUVECs, an L-NAME-induced rat model of preeclampsia, orthogonal binding assays (SPR/BLI and MST), ligand competition assays, and a multicenter double-blind phase 1-2a exploratory clinical trial were employed. PSG reduced endothelial migration and suppressed αSMA, TNFα, and fibronectin expression in stimulated HUVECs. In preeclamptic rats, PSG attenuated systolic and diastolic blood pressure elevation, reduced inflammatory and cardiovascular injury markers, restored VEGF and placental growth factor (PlGF), and reduced circulating sFLT-1 and the sFLT-1/PlGF ratio. Bioactivity-guided fractionation identified glycosides as the principal active fraction and improved mean birth weight from 2.7 g in untreated preeclamptic dams to 3.5 g, approaching normotensive controls (3.7 g). Orthogonal SPR/BLI and MST assays demonstrated concentration-dependent PSG-sFLT-1 interactions, while competitive ELISA and BLI assays showed inhibition of sFLT-1-mediated sequestration of VEGF and PlGF. PSG additionally restored VEGFR2/KDR, AKT, and ERK signaling in sFLT-1-exposed endothelial cells. In the exploratory clinical trial, 83 participants were randomized following screening of 125 women, with approximately 80% completing follow-up. PSG administration alongside standard care did not reveal major treatment-emergent safety concerns. These findings support further investigation of PSG as a candidate adjunctive strategy targeting angiogenic dysfunction in preeclampsia. - Source: PubMed
Publication date: 2026/09/01
Amadi Peter UOsuoha Justice OOgbolosingha Atieme JGill Govind SJarad Suha JOdika Prince CEfiong Esienanwan EAhmed Sayem AAgomuo Emmanuel NAgbagwara QueendarlynAmadi Chiamaka WAmadi Joy AEkweogu Celestine NGu Hong-MeiZhang Da-Wei - Aedes albopictus is a major global vector of arboviruses. Pyriproxyfen, an insect growth regulator, is increasingly used for mosquito control, but the potential for resistance and cross-resistance with pyrethroids poses a serious threat. Through 13 generations of laboratory selection, we established a highly pyriproxyfen-resistant Ae. albopictus strain (Lab-R, RR50 = 10.12). This strain developed moderate to high cross-resistance to the permethrin, deltamethrin, and beta-cypermethrin (RR50 = 8.11-10.30). Resistance was associated with significant fitness costs, including prolonged larval development, reduced female longevity, and lower fecundity and egg hatching. Crucially, resistance of Lab-R was driven by enhanced metabolic enzyme activity (P450s, GSTs, Car Es), with no target-site mutations detected in the CHS-1 or kdr genes. Synergist assays confirmed that enzyme inhibitors largely restored insecticide susceptibility. These findings demonstrate that metabolic resistance mediates cross-resistance between pyriproxyfen and pyrethroids in Ae. albopictus, carrying substantial fitness trade-offs. For vector control programs, this warns against the overreliance on rotational or sequential use of pyriproxyfen and pyrethroids as the sole rotation strategy, emphasizes the need for routine monitoring of metabolic resistance, and supports the potential use of synergists such as PBO to restore efficacy where resistance has emerged. - Source: PubMed
Publication date: 2026/08/31
Kong XuexueWang DanZhou JingzhuChen DijunLu XiaoyiLei TingHu YongLiang Wenqin - Bispecific antibody-drug conjugates (BsADCs) represent a promising therapeutic strategy to overcome single-target resistance. Here, we developed a dual-targeting BsADC that simultaneously recognizes CD44v6 and VEGFR2. - Source: PubMed
Publication date: 2026/08/05
Wu MenghuaiFeng XuezheHuang WenqiangWu YeCui Juanjuan