Human Cellexp Human Recombinant G-CSF proteins
- Known as:
- Human Cellexp Human Recombinant G-CSF proteins
- Catalog number:
- 6453-50
- Product Quantity:
- 50 μg
- Category:
- Proteins
- Supplier:
- Biovis
- Gene target:
- Human Cellexp Recombinant G-CSF proteins
Related genes to: Human Cellexp Human Recombinant G-CSF proteins
- 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: Human Cellexp Human Recombinant G-CSF proteins
Related articles to: Human Cellexp Human Recombinant G-CSF proteins
- 12/15-lipoxygenase (12/15-LOX, ) generates bioactive oxygenated lipids during inflammation, however its homeostatic role(s) in normal healing are unclear. Here, the role of 12/15-LOX in resolving skin wounds was elucidated, focusing on how its lipids act together in physiologically relevant amounts. In mice, wounding caused acute appearance of 12/15-LOX-expressing macrophages and stem cells, coupled to early generation of ~12 monohydroxy-oxylipins and enzymatically oxidized phospholipids (eoxPL). deletion increased collagen deposition, stem cell/fibroblast proliferation, IL6/pSTAT3, pSMAD3, and interferon (IFN)-γ levels. Conversely, CD206 expression, F480+ cells, and MMP9 and MMP2 activities were reduced. skin was deficient in PPARγ/adiponectin activity. Furthermore, while pro-inflammatory genes were upregulated as normal during wounding, many including failed to revert to baseline during healing, indicating disruption of PPARγ's anti-inflammatory brake on NLRP3/inflammasome and TGF-β signaling. Reconstituting wounds with a physiological mixture of -derived primary oxylipins generated by healing wounds restored MMP and dampened collagen deposition. The oxylipin mixture activated the PPARγ response element in vitro, while in vivo, its coactivator, , was significantly upregulated as well as several fatty acid and prostaglandin PPARγ ligands. Additional inflammatory and proliferative gene networks impacted by included , and Tcf3. In summary, 12/15-LOX generates abundant monohydroxy oxylipins that act together via PPARγ. The identification of multiple gene alterations reveals several targets for treating nonhealing wounds. Our studies demonstrate that 12/15-LOX oxylipins act in concert, dampening inflammation in vivo, revealing the need to consider lipid signaling holistically. - Source: PubMed
Publication date: 2025/09/04
Thomas Christopher PTyrrell Victoria JBurston James JJohnson Sam R CAldrovandi MacelerAlvarez-Jarreta JorgeInglis RossaLeonard AdamFice LydiaCostales JeremieVidal-Puig AntonioProtty MajdGuy CarolAndrews RobertSzomolay BarbaraCossins Ben CCardus Figueras AnaCarobbio StefaniaJones Simon AO'Donnell Valerie B - Preeclampsia (PE) is a hypertensive disorder and a major cause of maternal and fetal mortality. We aimed to investigate the molecular properties of early-onset PE, which requires delivery before 34 weeks' gestation by analyzing the molecular cytokine profile of amniotic fluid obtained during cesarean section from pregnant women with early-onset PE, based on the presence or absence of small-for-gestational age (SGA). - Source: PubMed
Publication date: 2025/09/01
Shin SoyoungKim ShinLee GisuBae JingonKang JunhoPark Jaehyun - Avian leukosis viruses (ALVs) are a group of retroviruses with immunosuppressive and tumorigenic effects, causing substantial economic losses to the poultry industry due to the lack of effective commercial vaccines and antiviral drugs. Granulocyte colony-stimulating factor 3 (CSF3) is a cytokine that regulates hematopoiesis and modulates the proliferation and differentiation of immune cells. In our previous study, we unexpectedly observed that CSF3 expression was significantly upregulated upon stimulation with interferon-α (IFN-α) and ALV, suggesting a potential role in ALV infection. In this study, we confirmed that the CSF3 promoter could be activated by ALV and polyinosinic-polycytidylic acid (poly I:C) using a CSF3 promoter-driven reporter construct, and GAS potentially serving as the response element. Phylogenetic analysis showed that avian and mammalian CSF3 genes clustered separately within the phylogenetic tree. Subsequently, we overexpressed and silenced CSF3 in DF-1 cells followed by ALV-J infection. Transcriptome analysis revealed that CSF3 overexpression significantly upregulated genes involved in antiviral and inflammatory responses, particularly those in the TLR, RIG-I, JAK/STAT, and NF-κB signaling pathways. Our results demonstrated that CSF3 induced the expression of IFNs and antiviral genes (IRF7, Mx, MDA5, OASL, and ACSL1). Furthermore, CSF3 improved the phosphorylation level of IκBα, leading to the production of pro-inflammatory cytokines and activation of the NF-κB pathway, ultimately suppressing ALV-J envelope glycoprotein expression. Notably, the pro-inflammatory and antiviral effects of CSF3 were abolished upon treatment with a STAT3 inhibitor, suggesting that CSF3 exerts its antiviral function through STAT3 phosphorylation. A similar effect of CSF3 was observed in primary fibroblasts derived from chicken embryos. Collectively, our findings indicate that CSF3 may function as an atypical interferon-stimulated gene (ISG), enhancing the immune response against ALV-J by activating the NF-κB signaling pathway and interferon-mediated antiviral mechanisms. These results not only reveal the antiviral role of CSF3 but also provide new insights into the host's innate immune response to ALV. Furthermore, they highlight the potential of CSF3 as a candidate resistance gene for breeding programs or as a vaccine adjuvant for disease prevention. - Source: PubMed
Publication date: 2025/08/06
Xia JunliangChen WeidingXu ChengxunWang MeihuiziMo GuodongZhang Xiquan - Sarcoidosis patients exhibit an elevated risk of developing lung cancer (LC), suggesting shared genetic and molecular mechanisms between these conditions. This study aimed to identify common differentially expressed genes (DEGs) in sarcoidosis and LC and to evaluate the therapeutic potential of a repurposable drug targeting these shared genes. Gene expression datasets (GSE157671 and GSE229253) were analyzed to identify overlapping DEGs, with validation performed using additional GEO datasets and the GEPIA tool. Functional enrichment and protein-protein interaction (PPI) analyses were conducted using Enrichr and STRING, while associated miRNAs and transcription factors were identified via miRNet. Twelve DEGs-SALL4, WNT10A, RASAL1, CAMK2B, GADD45B, KLF4, OLR1, CSF3, WIF1, RAMP3, AGER, and PRKAG3-were consistently dysregulated in both diseases. These genes were significantly associated with epithelial cell enrichment and the Wnt signaling pathway. Drug-gene interaction analysis using DGIdb prioritized metformin as a candidate drug targeting PRKAG3. Its structural integrity was confirmed via X-ray diffraction (XRD) and Rietveld refinement. In vitro validation using MTT assays revealed that metformin selectively reduced viability in A549 (adenocarcinoma human alveolar basal epithelial cells) and HeLa (a widely used epithelial cancer cell line), with minimal cytotoxicity in WI38 normal lung fibroblasts. Colony formation assays further demonstrated dose-dependent, long-term growth inhibition in cancer cells, corroborated by observable morphological alterations. Overall, this study highlights shared pathogenic signatures between sarcoidosis and LC and proposes metformin as a promising therapeutic candidate. These findings support the rationale for drug repurposing and the development of targeted therapies for patients with overlapping disease profiles or those at increased risk of LC progression from sarcoidosis. - Source: PubMed
Publication date: 2025/08/12
Dasgupta SanjuktaGhosh MoupiyaChakrabarty SubhenduChakrabarti GopalDas Amlan - Oxaliplatin, in combination with 5-fluorouracil and leucovorin, is a standard treatment for colorectal cancer and shows high efficacy. However, oxaliplatin induces side effects, such as chemotherapy-induced peripheral neuropathy and myelosuppression, which may lead to dose reduction, temporary drug withdrawal, or discontinuation. Lecithinized superoxide dismutase (PC-SOD) is a drug delivery system formulation with improved blood stability and tissue affinity for SOD. A phase II clinical trial of PC-SOD for chemotherapy-induced peripheral neuropathy has been conducted, and its efficacy has been confirmed for certain parameters. - Source: PubMed
Publication date: 2025/07/22
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