Anti-Mouse CD335 (NKp46) FITC 100 ug
- Known as:
- Antibody toMouse CD335 (NKp46) fluorecein 100 ug
- Catalog number:
- 11-3351-82
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Mouse CD335 (NKp46) FITC 100
Related genes to: Anti-Mouse CD335 (NKp46) FITC 100 ug
- Gene:
- NCR1 NIH gene
- Name:
- natural cytotoxicity triggering receptor 1
- Previous symbol:
- LY94
- Synonyms:
- NK-p46, NKP46, CD335
- Chromosome:
- 19q13.42
- Locus Type:
- gene with protein product
- Date approved:
- 1999-04-09
- Date modifiied:
- 2014-11-19
Related products to: Anti-Mouse CD335 (NKp46) FITC 100 ug
Related articles to: Anti-Mouse CD335 (NKp46) FITC 100 ug
- Channelrhodopsins have revolutionized the rapid, contactless modulation of action potentials, driving major advances in both neuroscience and cardiac research. In parallel, the automated patch-clamp (APC) technique has emerged as a powerful platform for drug screening. Here, we present the first biophysical characterization of the Na-selective channelrhodopsin NCR1 2.0 (sharing the rhodopsin part sequences with CCR) and the highly Na/Ca-conductive variant XXM 2.0, using APC combined with integrated optical stimulation. These channels are gaining increasing relevance, as Na- and/or Ca-dependent signaling plays pivotal roles in cancer biology and the development of anti-cancer therapeutics. The combined application of optogenetics and APC offers a transformative approach to drug screening, opening new avenues for biomedical innovation. This vision also includes further optical manipulations such as uncaging of substances and molecular photoswitches in photopharmacology, which form synergistic approaches with APC. - Source: PubMed
Publication date: 2026/07/13
Penttinen ReettaColi ArielHintermaier FlorianMurciano NicolettaHolzhauser StephanGao ShiqiangRotordam Maria GiustinaGeorge MichaelFertig NielsKaestner Lars - T cell receptor-associated transmembrane adaptor 1 (TRAT1) is a well-characterized regulator of T-cell signaling, yet its functional roles in innate lymphocytes remain largely undefined. This study aimed to identify autoimmune hepatitis (AIH)-associated immune targets and perform an exploratory functional characterization of TRAT1 in NK-cell models. - Source: PubMed
Publication date: 2026/07/07
Gao JiapengHuo LixiaZhong JianfengCai JiexunYu JingLi JingwenJiang JunboHong ChuanziYao YunliangFeng Min - Tissue microenvironments shape lymphocyte differentiation to align immune function with local physiological demands. Uterine natural killer (NK) cells are critical for reproductive success, yet the molecular cues in the uterus that instruct their specialized identities remain incompletely understood. Here, we identify a TGF-β-dependent differentiation pathway by which circulating conventional NK cells convert into uterine tissue-resident NK cells during murine pregnancy. Loss of TGF-β receptor II expression in -expressing cells disrupted this conversion, markedly reducing tissue-resident NK cells in the gravid uterus. Impaired TGF-β-driven uterine tissue-resident NK cell differentiation during murine pregnancy led to abnormal spiral artery remodeling and increased fetal resorption rates at mid-gestation, ultimately reducing litter sizes at birth. Collectively, these findings define TGF-β as a pivotal driver of tissue-resident NK cell differentiation in the gravid uterus and establish a mechanistic framework through which the uterine microenvironment programs NK cell identity to meet the physiological demands of gestation. - Source: PubMed
Publication date: 2026/07/08
Barahona Josselyn DYang LipingNelson D MichaelYokoyama Wayne M - Cytomegalovirus (CMV) infection remains a significant cause of morbidity and mortality due to the compromised immune system after hematopoietic stem cell transplantation (HSCT). Natural killer (NK) cells are pivotal in the immune response following HSCT, as these cells regenerate early and play a crucial role in detecting and eliminating infections. In the present study, we analyzed expression and single nucleotide polymorphisms (SNPs) of genes coding for NK cell Natural Cytotoxicity Receptors (NCRs). Expression was studied on the mRNA level and on the protein level, using flow cytometry to examine NCR-positive NK cell populations. Our study revealed significant higher expression of and in HSCT recipients with CMV infection compared to those without complications. Additionally, expression of both receptors correlated with expression of IFN-γ. Changes over time after HSCT were observed in the proportion of NCR1+ NK cells. SNPs genotyping identified associations of rs1433097 and rs11575836 genotypes with increased risk of CMV infection, as well as of rs11575836 with post-HSCT overall survival. These results underscore the crucial role of NCRs in the prevention of infection and the development of post-HSCT complications, highlighting their potential as therapeutic targets to improve transplant outcomes. - Source: PubMed
Publication date: 2026/06/25
Biały SylwiaŁacina PiotrSiemaszko JagodaSzymczak DonataSzeremet AgnieszkaMajcherek MaciejCzyż AnnaSobczyk-Kruszelnicka MałgorzataFidyk WojciechSolarska IwonaNasiłowska-Adamska BarbaraSkowrońska PatrycjaBieniaszewska MariaTomaszewska AgnieszkaBasak Grzegorz WGiebel SebastianWróbel TomaszBogunia-Kubik Katarzyna - The requirement for the T-box transcription factors (TF) T-bet and Eomes in innate lymphoid cells (ILCs) beyond their development is not well understood. Here, we generate an inducible, NKp46-specific T-bet knock-out (KO) model and compare it to corresponding Eomes KO and combined T-bet Eomes double KO mice to define T-box TFs requirement in the homeostasis and function of mature NK cell and other NKp46 ILC. Inducible T-bet deletion reduces stage IV NK cell numbers in the spleen and tissues, while preserving NK cells in the bone marrow and lymph nodes. Liver ILC1 and small intestine lamina propria NKp46 ILC3 are also lost upon T-bet deletion, indicating the requirement for continuous T-bet expression in these ILC types. Combined T-bet and Eomes KO leads to a rapid loss of NK cells, markedly greater than with individual T-bet or Eomes KO. Direct comparison of inducible T-bet and Eomes KO models reveals that Eomes is critical for host protection against murine cytomegalovirus, whereas T-bet is dispensable, despite loss of ILC1. These findings establish the tissue-specific and non-redundant roles for T-box TFs in NKp46 ILCs homeostasis and response to viral infection. - Source: PubMed
Publication date: 2026/06/18
Wong PamelaPaik YeeunChang LilyBurdi AllisonNeal CarlyCubitt Celia CTran JenniferBhattarai BishanMorina LyraMarin Nancy DHwang KimberlySohn HyogonWagner Julia AFoltz Jennifer ASong Wilbur MSchappe TimothyMarsala LynneFoster MarkFoster JuliaBerrien-Elliott Melissa MPiersma Sytse JColonna MarcoYokoyama Wayne MCooper Megan AFehniger Todd A