rHu G-CSF
- Known as:
- rHu G-CSF
- Catalog number:
- AK8248-0010
- Product Quantity:
- 10
- Category:
- -
- Supplier:
- Akro
- Gene target:
- rHu G-CSF
Related genes to: rHu G-CSF
- Gene:
- CSF3 NIH gene
- Name:
- colony stimulating factor 3
- Previous symbol:
- GCSF, G-CSF, C17orf33
- Synonyms:
- MGC45931
- Chromosome:
- 17q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
- 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: rHu G-CSF
Related articles to: rHu G-CSF
- Plasma proteomic profiling of 92 individuals with Post-Acute Sequelae of SARS-CoV-2 infection (PASC), assessed a mean of 34 months after acute infection, revealed a distinct inflammatory signature. Using proximity extension assay technology, 358 proteins were quantified, identifying 26 differentially expressed proteins (DEPs) in PASC: 23 upregulated and 3 downregulated. The most upregulated proteins were Oncostatin M (OSM) and IL-1 receptor antagonist (IL1RN). Additional increases were observed in IL-6, IL-12B, IL-2, CCL22, CSF3, CSF1, and HLA-DRA, as well as proteins involved in tissue remodeling and angiogenesis such as ANGPTL2 and TGFA. Random forest analysis confirmed IL1RN, OSM, ANGPTL2, HLA-DRA, and CLEC4A as strong discriminators between patients and controls. Gene set enrichment analysis demonstrated activation of multiple immune pathways, including Inflammatory Response, TNF-α/NF-κB signaling, IL-6/JAK/STAT3, IL-2/STAT5, and Allograft Rejection, indicating persistent activation of innate and adaptive immunity. STRING network analysis highlighted a tightly connected cytokine-driven inflammatory module. Plasma spike protein levels did not differ between patients and controls, suggesting that PASC-related inflammation may persist independently of ongoing viral replication. Overall, the findings indicate a consistent low-grade inflammatory state in PASC without evidence for distinct biological subtypes. - Source: PubMed
Publication date: 2026/02/23
Fineschi SerenaKlar JoakimSchuster JensBergquist JonasDahl Niklas - The Orchidaceae family is renowned for its remarkable floral diversity, showing a wide range of colors primarily influenced by pigments especially anthocyanins. is a terrestrial orchid characterized by vibrant flower colors, making it an ideal resource for studying anthocyanin biosynthesis in orchids. In this study, we systematically identified and characterized the structural genes involved in anthocyanin biosynthesis in and compared their roles between and its close relative . Pigment analysis revealed that anthocyanins were the predominant pigments in the red-colored tepals of , exhibiting significantly higher levels in dark red (DR) and red (R) accessions compared to lighter color accessions. Transcriptome sequencing identified 20 structural genes, including , , , , , and . Phylogenetic analysis indicated close evolutionary relationships with other species. Notably, and exhibited high expression levels in red tepals, while and were up-regulated in . This suggests species-specific regulatory mechanisms governing pigment production. Subcellular localization assays confirmed cytoplasmic distribution for , chloroplast localization for , and cell membrane association for , implicating diverse functional roles related to anthocyanin transportation and biosynthesis. These findings highlight the functional divergence of structural genes in anthocyanin biosynthesis between and , and have specifically identified as key genes of red coloration in flowers. This study provides foundational insights into the molecular mechanisms underlying flower color variation among orchids, offering potential targets for future genetic manipulation aimed at enhancing ornamental breeding practices. - Source: PubMed
Publication date: 2026/02/13
Zhao KunkunXie JunyiZheng YihongYang XiaodongWang YunzhuZhang Xue - C-type lectin-like receptor 2 (CLEC2) is a transmembrane receptor highly expressed on platelets which regulates platelet aggregation and immune response. Yet, the function of CLEC2 in lung epithelium and its contribution to acute lung injury (ALI) is unclear. In this study, lung epithelial-specific CLEC2 knockout mouse (Clec1b AT2-KO) was generated and performed for ALI models. In both lipopolysaccharide (LPS)- and acid-induced lung injury models, the ALI signs of Clec1b AT2-KO mice were further exacerbated. The therapeutic application of epithelial-restricted CLEC2 overexpression using adeno-associated virus (AAV) or CLEC2 activation using its endogenous ligand podoplanin (PDPN) serves as a lung epithelial protective agent in the setting of ALI. Transcriptomic analyses reveal that CLEC2-regulated genes are highly enriched in chemotaxis, cytokine, and extracellular matrix (ECM) components. Lung injury was partially attenuated in Ccl5-/-, Csf3-/- and Cxcl1-/- mice pretreated with AAV-si-CLEC2, followed by LPS challenge. Loss of CLEC2 leads to ECM degradation, which could be reversed by exogenous transforming growth factor (TGF)-β. Furthermore, interferon regulatory factor 1 (IRF1) was identified as the key molecule that regulates CLEC2-related cytokine/chemokine production and ECM degradation. These findings suggest that epithelial CLEC2 protects against ALI by modulating spleen tyrosine kinase (Syk)/IRF1-mediated cytokine/chemokine production and TGF-β-mediated ECM remodeling. - Source: PubMed
Publication date: 2026/01/23
Jiang TianWu LinfengWang YingYang XuHuang RenhuiRen ChanghaoZhang QiHu YunfanZhang ShaoyuanYang XinyuYin JunWang LanTan Lijie - Respiratory tract infections (RTIs) remain a major global cause of morbidity, yet the causal role of circulating plasma proteins in RTI susceptibility is unclear. We aimed to systematically identify plasma proteins that causally influence the risk of upper and lower respiratory tract infections (URTIs, LRTIs) using a proteome-wide Mendelian randomization (MR) framework. - Source: PubMed
Publication date: 2026/02/11
Yuan YuhuaLiu BinChen ShuhuiWang ManliZhao ShuyueMao Yingying - is a high-priority, emerging fungal pathogen frequently isolated from urine in healthcare settings. These isolates are often associated with indwelling urinary catheters, a primary risk factor for catheter-associated urinary tract infections (CAUTIs). Despite its clinical prevalence, the mechanisms of colonization and pathogenesis within the bladder remain poorly understood. In this study, we screened isolates from diverse clades using an biofilm model and murine models of uncomplicated UTI and CAUTI. While biofilm formation varied among isolates, the presence of a catheter significantly enhanced fungal burden in the bladder. Notably, one strain (B11103) caused rapid systemic dissemination and mortality. To address this, we evaluated a liquid-infused silicone (LIS)-catheter coating, which has previously shown efficacy against other uropathogens. The LIS-coating significantly reduced attachment and, crucially, mitigated fungal burden on both the catheter and bladder tissue across all tested strains. For the hyper-virulent B11103 strain, LIS-catheters also significantly reduced dissemination to the kidneys and bloodstream. Furthermore, cytokine analysis revealed that CAUTI upregulates IL-6, CSF3, and CXCL1; notably, this damaging inflammatory response was dampened by the LIS-catheter. These findings demonstrate that catheterization potentiates pathogenicity and identify LIS-catheters as a promising, antimicrobial-sparing strategy to prevent colonization, systemic spread, and inflammation during CAUTI. - Source: PubMed
Publication date: 2026/02/05
La Bella Alyssa AnnAkegbe HopeHowell CaitlinSantiago-Tirado Felipe HFlores-Mireles Ana L