Ask about this productRelated genes to: FLT3 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 antibody
Related articles to: FLT3 antibody
- - Source: PubMed
Publication date: 2026/06/23
Liu YuyuBai GuanchenZhao XingliSuo XiaohuiBai YanliangZheng FangZhao WeihuaPeng HonglingWang DongmeiZhao LiyunLiu JieLi LingZhou ZepingMi YingchangLiu Kaiqi - Despite advances in antiretroviral therapy (ART), HIV-1 cure efforts remain hindered by viral reservoirs in long-lived myeloid cells and immune-privileged tissues that are less accessible and therefore unlikely to be assessed in human clinical trials. Consequently, there is a critical need for robust research platforms such as immune cell humanized mice to bridge preclinical and clinical HIV research. However, previously described humanized mouse models have demonstrated incomplete hematopoietic development, particularly showing low levels of NK or myeloid cells. Herein, we present the novel humanized FLT3 mouse model that develops NK cells, myeloid progenitors, monocytes, and both functional conventional (cDCs) and plasmacytoid dendritic cells (pDCs) to support HIV-1 infection. Human cord blood derived CD34 hematopoietic stem cells (HSC) were engrafted in the FLT3 (Hu-FLT3) and NSG (Hu-NSG) mouse strains for comparison. Our data showed that while Hu-NSG and Hu-FLT3 mice have comparable human lymphocyte levels, the proportion of myeloid cells (including monocytes, pDCs and cDCs) in Hu-FLT3 mice (16.2 %) was three-fold higher than in Hu-NSG mice (5.6 %) and the proportion of NK cells was six-fold higher (12.8 % and 1.9 %, respectively). Both strains successfully supported HIV-1 infection, maintain viral replication for 17 weeks in untreated mice, and proviral DNA was detectable in peripheral blood, bone marrow and spleen. While ART effectively reduced viral load to undetectable levels in four weeks in both strains, we observed viral rebound after treatment discontinuation within 3 weeks, reaching the same levels of viral load pre-ART and mimicking what is observed in people living with HIV (PLWH).Human immune cells and HIV-1 RNA were higher in tissues of Hu-FLT3 mice compared to Hu-NSG mice, mirroring features reported in human tissue reservoirs. Our findings demonstrated that Hu-FLT3 mice support enhanced development of human innate immune cells in blood and tissues, which are associated with higher levels of HIV-1 replication compared to Hu-NSG mice. This study establishes a novel, robust and accessible platform to investigate potential HIV cure and persistence-targeting interventions with translational relevance to human therapeutic development thanks to the improved and more complete human immune repertoire in Hu-FLT3. - Source: PubMed
Publication date: 2026/06/08
Resa-Infante PatriciaPiñol PatriciaLaguía FernandoCampos-Gonzalez GerardCobos ÀlexUrrea VictorDel Carmen Garcia-Guerrero MariaRosales-Salgado YaizaCid MarinaDíaz-Pedroza JorgeShultz Leonard DYin VootBrehm Michael ASoper BrianSalgado MaríaMartinez-Picado Javier - The With-No-Lysine (WNK) kinase family plays critical roles in cellular signaling, yet its significance in acute myeloid leukemia (AML) remains unclear. - Source: PubMed
Publication date: 2026/06/05
Chen FangliWang YuanqinFu ZhenChang LiJiang XueweiZhang ZhizhiLi ChongyangLiu LigenYang Li - Myelofibrosis (MF) is a rare, clonal disorder of pluripotent hematopoietic stem and progenitor cells. It is characterized by abnormal proliferation of hematopoiesis, associated with pathologically increased fibrosis in the bone marrow, which is primarily caused by activation of the JAK2 signaling pathway. Myelofibrosis (MF) may occur de novo as primary myelofibrosis (PMF), or secondarily as a consequence of polycythemia vera (PV) or essential thrombocythemia (ET), termed post-PV-MF and post-ET-MF, respectively. The latter two are collectively referred to as secondary myelofibrosis. The most recent updates of the diagnostic criteria by the WHO and ICC were published in 2022. These revisions defined prefibrotic primary myelofibrosis (pre-PMF) as a distinct subentity alongside "classic" overtly fibrotic PMF and secondary myelofibrosis. A hallmark of pre-PMF is an initial isolated thrombocytosis, whereas in overt MF, anemia is frequently present already at diagnosis. Splenomegaly is also more commonly detected at diagnosis in overt fibrotic MF than in pre-PMF. The prognosis of MF is determined by patient age, the presence of constitutional symptoms, as well as hematologic and genetic parameters. Increasingly, cytogenetic and molecular genetic markers play a decisive role. The most common causes of death in MF include transformation to acute myeloid leukemia, infections, and cardiovascular complications. The only potentially curative treatment is allogeneic stem cell transplantation (alloSCT), which is generally indicated in transplant-eligible patients with unfavorable prognosis, that is, those classified as high- or very-high risk according to the MIPSS70+ v2.0. For symptomatic treatment of MF, a variety of therapeutic options are available. In recent years, oral therapy with the JAK1/2 inhibitor ruxolitinib has become the standard of care. Since 2021, the JAK2/FLT3 inhibitor fedratinib has also been approved in the EU (note: in Switzerland, fedratinib will no longer be available as of February 28, 2025, as Swissmedic did not extend its time-limited approval). Since 2024, the JAK1/2 and ACVR1/ALK2 inhibitor momelotinib has been approved for MF treatment in the EU (irrespective of risk category) and in Switzerland (restricted to intermediate- or high-risk disease) for patients with moderate or severe anemia and/or after prior treatment with ruxolitinib. Compared to the other two JAK inhibitors, momelotinib is particularly effective in patients with clinically symptomatic moderate to severe anemia. Results from studies investigating additional JAK inhibitors, combination therapies, and novel agents have also demonstrated significant efficacy and point toward future therapeutic developments, although these approaches are not yet available for routine clinical practice. - Source: PubMed
Publication date: 2026/06/21
Griesshammer MartinAl-Ali Haifa KathrinBaerlocher Gabriela MDöhner KonstanzeKoschmieder SteffenKröger NicolausPetrides Petro EWolf DominikHeidel Florian H - Pathogen-derived RNAs function as pathogen-associated molecular patterns (PAMPs) that activate innate immune responses through pattern recognition receptors (PRRs). While viral RNA is well established as a trigger of antiviral immunity, the identity of bacterial RNA species that function as immunostimulatory ligands and the host PRRs that recognize them remain poorly defined. Here, we identify bacterial-specific transfer-messenger RNA (tmRNA), a conserved RNA involved in ribosome rescue during bacterial trans-translation, as a previously unrecognized RNA PAMP. tmRNA robustly induced the production of IL-6, TNF-α, and IFN-α in murine Flt3 ligand-derived dendritic cells. Genetic analyses revealed that this response was dependent on the TLR7-MyD88 signaling pathway. Systemic administration of tmRNA in mice induced transient cytokinemia and inflammatory changes in the liver and lung, both of which were abolished in TLR7-deficient mice, demonstrating a critical role for TLR7 signaling in tmRNA-induced inflammation in vivo. In contrast, tmRNA failed to induce cytokine production in the human plasmacytoid dendritic cell line CAL-1 despite preserved responsiveness to the TLR7/8 agonist R848, suggesting that bacterial RNA sensing mechanisms may differ between murine and human immune cells. Together, these findings identify tmRNA as a bacterial RNA ligand capable of activating antiviral RNA-sensing pathways in murine immune cells; however, the relevance of these findings to human immune cells remains a limitation of the present study. - Source: PubMed
Matsumiya TomohDing JiangliIkegami SakuraIzumiyama KokoroShiba YukoYamanouchi KanakoKurita DaisukeKawaguchi ShogoKubota KoseiTanaka Makoto TimonMiki YasuoHimeno HyoutaImaizumi Tadaatsu