rHu G-CSF
- Known as:
- rHu G-CSF
- Catalog number:
- AK8248-0002
- Product Quantity:
- 2
- 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
- Patients with gastric cancer (GC) and peritoneal metastasis (PM) have poor prognoses due to drug resistance and metastatic relapse. The mechanism underlying PM recurrence remains unclear. - Source: PubMed
Publication date: 2026/07/28
Chen QianZhang LuChen BiyingLi MengjieZhang MuzixianLiu YirouSun MengJiang YuchaoHong MengtingDing YinuoYang YingshuoNi JiaojiaoYing JieerZhou TianhuaZhuo Wei - In numerous demyelinating diseases, brain tissue exhibits excessive inflammatory responses that promote the activation of immune cells, thereby exacerbating cellular damage and amplifying inflammatory cascades. Emerging evidence highlights receptor-interacting protein kinase 1 (RIPK1) is a pivotal regulator of neuroinflammation, and its dysregulation contributes to the pathogenesis of various central nervous system (CNS) disorders. While our previous work established that RIPK1 kinase inhibition promotes remyelination in acute demyelinating models, however, the precise mechanisms of RIPK1 in microglial activation remain unclear. Here, to investigate RIPK1's role in microglial polarization, we employed lipopolysaccharide (LPS)-stimulated BV2 cells and the lysolecithin (LPC)-induced demyelination mouse model. By combining RIPK1 kinase-dead knock-in mice and the pharmacological inhibitor Nec-1s，we performed experiments in both in vitro and in vivo models. We demonstrated that RIPK1 inhibition significantly attenuates M1 microglial polarization and pro-inflammatory cytokine production. Mechanistically, we identified that RIPK1 orchestrates the expression of colony-stimulating factor 3 (Csf3), which subsequently activates the JAK2/STAT3 signaling pathway. Pharmacological inhibition of RIPK1 decreased Csf3 expression, leading to reduced phosphorylation of JAK2/STAT3 and subsequent suppression of M1 polarization. Our findings reveal a novel RIPK1-Csf3-JAK2/STAT3 signaling axis governing microglial polarization and highlight its potential as a therapeutic target for demyelinating diseases. - Source: PubMed
Publication date: 2026/07/26
Yang ShuyingZhou XinZhang JingPan NaLiu MengtingSong Haibo - The porcine reproductive and respiratory syndrome virus (PRRSV) is a highly contagious pathogen. Viral infections often enhance their replication by modulating the structure and expression of host genes. However, it remains unclear whether PRRSV employs a similar mechanism to achieve self-replication. To address this question, the current study combined assay for transposase accessible chromatin sequencing (ATAC-seq) and ribonucleic acid (RNA) sequencing (RNA-seq) to identify accessible chromatin regions and key host genes associated with PRRSV infection. By comparing the PRRSV-infected group with the control group, we initially detected 8664 differentially accessible chromatin regions and 4037 differentially expressed genes. Motif analysis of these differential chromatin regions revealed several potential cis-regulatory elements containing binding sites for transcription factors. Further integration of ATAC-seq and RNA-seq results identified 1352 overlapping genes between the PRRSV-infected and control groups. A significant positive correlation between differential gene expression and chromatin accessibility signals suggests that chromatin remodeling may drive transcriptional changes during infection. Protein-protein interaction (PPI) network analysis highlighted candidate genes potentially associated with PRRSV infection in hosts, such as IL1B, CCL20, CXCL10, CSF3, etc. Given their potential association with the infection mechanism, these genes could serve as candidate targets for the future development of prophylactic vaccines and therapeutic strategies. Additionally, several signaling pathways that may regulate immune and inflammatory responses were significantly enriched in our ATAC-seq and RNA-seq analyses. These findings provide valuable insights into the molecular mechanisms underlying PRRSV infection and pave the way for developing more effective preventive and treatment measures. - Source: PubMed
Publication date: 2026/07/23
Liu HouchunXu ZhongChen HongboPeng XianwenShi LiangyuWang ChengZhou AoMei ShuqiWu Junjing - Dysregulated innate immunity contributes to clonal cytopenias and myeloid neoplasms, but its extent across disease stages and clinical relevance remain incompletely defined. We analyzed plasma ASC/NLRP3 double-positive (DP) specks, ASC single-positive (SP) specks, and 45 cytokines in 223 patients with idiopathic cytopenias of undetermined significance (ICUS)/clonal cytopenias of undetermined significance (CCUS), myelodysplastic syndromes (MDS), and chronic myelomonocytic leukemia (CMML) and 39 matched non-inflammatory controls using adjusted regression, survival modeling, and paired longitudinal analyses. Inflammasome activation and cytokine perturbations were evident across the disease spectrum. DP-ASC specks were elevated in MDS and CMML, whereas SP-ASC specks were increased across all groups, indicating activation of ASC-containing inflammasomes beyond NLRP3. Cytokines followed a graded ICUS → MDS → CMML pattern, with widespread upregulation of interleukins and chemokines (including IL-7, IL-8, IL-11/CXCL11, and CCL7) alongside suppression of stem and progenitor support factors such as CSF3, FLT3LG, TRAIL, and TWEAK. At baseline, elevated IL-15 and MMP1 predicted progression to acute myeloid Leukaemia, while higher IL-10, CXCL8, and IL-18 were associated with reduced survival; ASC specks were not independently prognostic. Longitudinal increases in selected cytokines distinguished progressors (area under the curve 0.82; 95% CI: 0.49-1.0). Cytokine patterns correlated with mutation categories, with the isolated SF3B1 mutation associated with higher DP-ASC specks. These findings define early and progressive inflammasome engagement and nominate dynamic cytokine panels and the inflammasome-IL-1 axis as actionable biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/07/07
Ibbotson AliceCrouch SimonFerrari JacquelineYoung ThomasMorgan Ann WGallì AnnaPozzi SaraSarchi MartinaCamilotto VirginiaBoldini MartinaElena ChiaraMalcovati LucaSavic Sinisa - Heart failure (HF) and body mass index (BMI) share substantial genetic architecture, which may lead genetically informed target discovery to preferentially identify adiposity-related pathways. We sought to identify circulating proteins associated with HF beyond this shared genetic component. - Source: PubMed
Publication date: 2026/06/22
Su Chen-YangLu Tianyuan