Human GCSFR _CD114 Protein Vector: HEK293
- Known as:
- Human GCSFR _CD114 Protein Vector: HEK293
- Catalog number:
- 10108-H03H
- Product Quantity:
- 200μg
- Category:
- -
- Supplier:
- Provo
- Gene target:
- Human GCSFR _CD114 Protein Vector: HEK293
Related genes to: Human GCSFR _CD114 Protein Vector: HEK293
- Gene:
- CSF3R NIH gene
- Name:
- colony stimulating factor 3 receptor
- Previous symbol:
- CD114
- Synonyms:
- GCSFR
- Chromosome:
- 1p34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-12-10
- Date modifiied:
- 2019-04-23
Related products to: Human GCSFR _CD114 Protein Vector: HEK293
Related articles to: Human GCSFR _CD114 Protein Vector: HEK293
- Colony Stimulating Factor 3 Receptor (CSF3R) mutations are the molecular hallmark of chronic neutrophilic leukemia (CNL). A subset of these patients (~25%) have two mutations in CSF3R on the same allele. These "compound" CSF3R mutations include both an activating point mutation and a cytoplasmic truncating mutation. While compound mutations are prevalent, we have a limited understanding of their molecular characteristics. In this study, we interrogated the mechanisms driving the evolution of compound mutations. We found that CSF3R compound mutations induce a hyperproliferative leukemia compared to single mutations. Compound mutations also markedly enhance activation of STAT5 and ERK1/2 downstream of CSF3R. Utilizing a proteomics approach, we identified enrichment of MYC and mTOR pathways in compound mutant-cells. The most differentially expressed protein in this dataset was the kinase PIM1. We find that in CSF3R compound mutant-cells with high STAT activity there is increased transcription of PIM kinases. We further validated that PIM1 transcript levels are high in a human CSF3R mutant-cohort. High PIM levels drive stabilization of MYC protein, and the downstream activation of MYC-driven leukemogenic transcriptional programs. Indeed, inhibitors of PIM reverse MYC stabilization. Finally, we show promising therapeutic potential for PIM-inhibition in CSF3R mutant-disease using both human cell lines and CNL patient samples. Together, these findings uncover a novel and targetable vulnerability in CSF3R compound mutant-CNL, thus opening a new avenue of treatment for patients with this devastating disease. - Source: PubMed
Publication date: 2026/09/09
Maniaci Breanna NPorter Jacob EdwardCarlson Hanqian LPotter GraceNguyen Thai TPang AmaraTyner Jeffrey WEmili AndrewBraun Theodore PMaxson Julia E - Cyclic GMP-AMP synthase (cGAS) is a cytosolic DNA sensor that detects aberrant DNA and activates the STING-dependent innate immune response. Although cGAS is predominantly localized in the nucleus under physiological conditions, its nuclear function remains incompletely understood. Here, we identify nuclear cGAS as a transcriptional repressor that restrains inflammatory gene expression independently of STING signaling. Using macrophages challenged with lipopolysaccharide (LPS), we found that cGAS selectively suppresses the transcription of primary response genes, including and . Mechanistically, this activity requires nucleosome binding but not cGAS enzymatic signaling. Upon inflammatory stimulation, the transcription factor PU.1 recruits cGAS to target promoters, where the carboxyl-terminal domain of cGAS interacts with histone deacetylase 1 (HDAC1). This complex promotes deacetylation of H3K27ac and restricts transcriptional activation of inflammatory genes. Genome-wide chromatin accessibility and occupancy analyses revealed that cGAS-dependent transcriptional repression occurs at a distinct subset of PU.1-associated inflammatory loci. Functionally, macrophage-specific deficiency phenocopied the exaggerated inflammatory responses observed in -deficient mice during endotoxemia, whereas the pathogenic effects of loss were abolished in the absence of . Moreover, increased mortality and neutrophil infiltration in deficient mice were rescued by deletion of . Together, these findings uncover a previously unrecognized transcriptional function of nuclear cGAS and identify nuclear cGAS as an intrinsic brake that restrains excessive inflammatory responses. - Source: PubMed
Publication date: 2026/09/28
Gao ShangzeLi HongpengYan ShuaitingHou ShengpingYin Hang - Southwestern local chicken breeds in China have long been recognized for their strong adaptability and disease resistance, shaped by unique selective pressures during domestication. In this study, we combined Fst and π ratio analyses to detect selection signatures from RAD-seq data of four southwestern local breeds, Red Junglefowl, and 17 other Chinese local breeds. We identified 460 candidate genes under strong selection potentially associated with domestication, affecting behaviors, physiology, reproduction, immunity, and adaptability. Importantly, 34 genes showed strong and unique selection signals when comparing southwestern breeds with other local breeds. Among these, , , and represent candidate genes that have been previously associated with immune processes, while , , and represent candidate genes potentially related to disease resistance. Furthermore, , and represent candidate genes potentially associated with environmental adaptability. Notably, , the only gene detected across all comparison groups, may reflect morphological adaptation related to feeding efficiency. Our findings provide valuable insights into the genetic basis of unique adaptations in southwestern local chicken breeds and highlight potential targets for breeding and conservation. - Source: PubMed
Publication date: 2026/09/09
Wang MengyuZou MingyangZhou ChenghaoHan Wei - The underlying mechanisms of exosomes in chronic lung allograft dysfunction (CLAD) remain poorly understood. The primary challenge lies in the substantial functional heterogeneity of exosomes in CLAD. In this study, lung transplantation was initially performed, followed by the generation of a chronic rejection (CR) model in rats to simulate CLAD in humans. Exosomes from lung graft tissues were extracted, purified, and subjected to proximity barcoding assay-based single-vesicle membrane proteomic profiling. Additionally, bulk proteomic and metabolomic profiling of the graft tissues was conducted. Exosomes were categorized into 14 clusters. Compared with the syngeneic group, the CR group had significantly lower levels of clusters 7 (Nphs1), 13 (Aqp1), and 14 (Csf3r), and higher levels of clusters 2 (Lrp2 Mrc1) and 4 (Nt5e). The abundance of cluster 12 (Ilk) exosomes was strongly correlated with pleural thickness (r = -0.90, P < 0.001). Cluster 12 exosomes exhibited the greatest number of related differentially expressed proteins and metabolites. The proteins correlated with cluster 12 were enriched in the "complement and coagulation cascades", whereas the metabolites were enriched in the "glycerophospholipid metabolism". Further verification in patients with restrictive allograft syndrome revealed the same decrease in abundance of cluster 12 exosomes as that observed in the rat model. Finally, the core molecular network of cluster 12 that contributes to pleural thickening in CLAD was constructed. In this study, the heterogeneous composition of exosomes in lung grafts was mapped to expand the understanding of their effects and to drive their application in CLAD. - Source: PubMed
Publication date: 2026/09/17
Tian DongZheng XiangyunYu ZengweiWang DapengChen WeiyangLiu YalingLiu ZehuiXia BoyangJin XiaohanYan HaojiWu YeZhao YongshengZhang ChuanfenPu QiangChen JingyuSato MasaakiLiu Lunxu - Non-small cell lung cancer (NSCLC) is one of the frequently occurring cancers characterized by molecular heterogeneity and multiple immune cell infiltration patterns, which are associated with treatment sensitivity and resistance. However, the specific microenvironmental cells and their mechanisms that lead to treatment resistance in patients need to be explored in greater depth. - Source: PubMed
Publication date: 2026/09/08
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