CD135 _ FLT3
- Known as:
- CD135 _ FLT3
- Catalog number:
- BM2462
- Product Quantity:
- 0.2 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD135 _ FLT3
Related genes to: CD135 _ FLT3
- 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: CD135 _ FLT3
AC220 AC220 is a uniquely potent and selective FLT3 inhibitor with IC50 of 0.56 +_- 0.3 nM and >10 mM for MC4-11 and A375, respectively. For research use only.anti-Flt3 CD135 (1A11)anti-Flt3 CD135 (1A11) type: Primary antibodies host: Mouseanti-Flt3 CD135 (3H1)anti-Flt3 CD135 (3H1) type: Primary antibodies host: Mouseanti-FLT3 CD135 (BV10A4H2)anti-FLT3 CD135 (BV10A4H2) type: Primary antibodies host: Mouseanti-FLT3 CD135 (Internal)anti-FLT3 (Ab-591)anti-FLT3 (Ab-591)anti-FLT3 (Ab-591)anti-FLT3 (Ab-591), Rabbit polyclonal to FLT3, Isotype IgG, Host Rabbitanti-FLT3 (Ab-591), Rabbit polyclonal to FLT3, Isotype IgG, Host RabbitAnti-FLT3 (BV10A4H2), Mouse Monoclonal to FLT3, Isotype IgG1, Host Mouseanti-FLT3 (Phospho-Tyr591) Related articles to: CD135 _ FLT3
- 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 - The aim of this study was to generate lentiviral vectors carrying an array of AP-1 motifs driving luciferase gene expression as reporters of Mitogen Activated Protein Kinase (MAPK) activity. We created a series of vectors based on LeGO-iG that were used to generate stably transduced leukaemia cell lines. A vector termed LEGO-AP1 × 6-GM55 containing an array of 6 AP-1 sites linked to the minimal CSF2 promoter was sufficient to support high levels of MAPK-inducible luciferase activity in leukaemic cell lines that was suppressed by MAPK inhibitors. The inclusion of a putative chromatin priming element encompassing RUNX and ETS motifs increased the activity of these vectors. The additional inclusion of the full-length mouse CSF2 promoter, or the human DUSP5 promoter further increased the MAPK-dependent activity of these vectors in leukaemic cells. These vectors support moderate levels of constitutive activity in cells carrying mutations that activate the RAS/RAF/MEK MAPK signalling pathway, and high-level activity after direct activation of MAPK signalling. They also respond to T cell receptor activation via MAPK and Ca2+ signalling pathways. This resource will now make it easier to track receptor or oncogene-inducible MAPK activity in cultured cells, and potentially in tumours, in close to real time. TEASER ABSTRACT: Here we developed a series of lentiviral luciferase reporter vectors activated by RAS/RAF/MAPK signalling to AP-1. These vectors are activated in response to signalling driven by most of the signalling mutations detected in cancer cells or by receptors that control cell growth, differentiation and activation. These vectors have been optimised based on pathways known to activate gene expression in acute myeloid leukaemia or in activated T cells. The regulatory elements tested in these vectors includes an array of 6 AP-1 sites, the CSF2 promoter, the DUSP5 promoter and a chromatin priming element that binds RUNX and ETS factors. - Source: PubMed
Publication date: 2026/08/13
Coleman Danial J LAmes LukeAain HurooulGamble JoannaKoscielniak KingaZhang ZijinLau CherisseJoyce AbigailCockerill Peter N - Relapse remains the leading cause of treatment failure after allogeneic hematopoietic cell transplantation (HCT) for acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS), and outcomes after relapse are poor. This review summarizes and critically appraises current evidence for post-HCT maintenance therapy aimed at relapse prevention. - Source: PubMed
Publication date: 2026/08/13
Desai NiharPasic Ivan