GM-CSF Clone 'SPM482 antibody Host Rat
- Known as:
- GM-CSF Clone 'SPM482 (anti-) Host Rat
- Catalog number:
- 'AM11171PU-N
- Product Quantity:
- 1.0 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- GM-CSF Clone 'SPM482 antibody Host Rat
Related genes to: GM-CSF Clone 'SPM482 antibody Host Rat
- Gene:
- CSF2 NIH gene
- Name:
- colony stimulating factor 2
- Previous symbol:
- -
- Synonyms:
- GM-CSF, GMCSF
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2018-12-12
Related products to: GM-CSF Clone 'SPM482 antibody Host Rat
Related articles to: GM-CSF Clone 'SPM482 antibody Host Rat
- () belongs to the genus of the family. In goats, infection can result in respiratory diseases such as pneumonia and bronchopneumonia. In this study, caprine bronchial epithelial cells were infected with , and multi-omics integration analysis was conducted to investigate the immune defense mechanisms triggered by the infection. Enrichment analysis of differentially expressed genes (DEGs) using the KEGG database revealed that immune-related signaling pathways involving TNF and IL-17 were among the top 20 most enriched. Based on the TNF and IL-17 signaling pathways, ten immune pathway-related genes, including , , , , , , , , , and , were selected for RT-qPCR validation. In addition, four miRNAs targeting genes involved in the above pathways, namely chi-miR-148a-5p, miR-1285-z, miR-16-x, and miR-6119-x, were verified by RT-qPCR. The expression trends of chi-miR-148a-5p and miR-1285-z were consistent with microRNA sequencing results. Furthermore, gain- and loss-of-function experiments indicated that chi-miR-148a-5p may target and , while miR-1285-z may target , with predicted as a potential target. This study suggests that chi-miR-148a-5p and miR-1285-z may participate in the TNF and IL-17 signaling pathways by regulating their predicted target genes. Moreover, the TNF and IL-17 signaling pathways are among the most highly enriched immune-related pathways involved in the innate immune response of caprine bronchial epithelial cells. This study provides insights into the molecular mechanisms underlying immune responses in goats infected with . - Source: PubMed
Publication date: 2026/09/12
Chen YimeiGong ZhenxingJing HuiDuan HaoQian HejieLi TengjiaoNiu ShihuaWu LiliWang ZiyingZhang MengqiCheng YiwenMan ChurigaChen QiaolingDu LiChen SiGao HongyanWang Fengyang - Age-related macular degeneration (AMD) is a major cause of irreversible visual impairment, yet identifying effector proteins and tissue-specific mechanisms underlying genome-wide association study (GWAS) loci remains challenging. This study aimed to systematically prioritize candidate causal circulating proteins and delineate their cellular and transcriptional dynamics in AMD. We integrated plasma protein quantitative trait loci (pQTL) summary statistics from the UK Biobank Pharma Proteomics Project (UKB-PPP; N=53,022) with FinnGen AMD GWAS data using proteome-wide association studies (PWAS), summary-data-based Mendelian randomization (SMR) with the HEIDI test, and Bayesian colocalization analysis. Prioritized candidates were mapped across human and murine retinal single-cell/single-nucleus RNA sequencing atlases. Transcriptional responsiveness was validated in an independent clinical microarray dataset (GSE103060) and in human retinal pigment epithelial cells (ARPE-19) via in vitro inflammatory stimulation and RT-qPCR. Target tractability was assessed using pharmacological databases. Multi-stage genetic screening prioritized five candidate proteins stratified into two confidence tiers: three Tier 1 causal drivers supported by colocalization (PP4 > 0.80)-including risk factors CSF2, IL20RB, and WARS1 (also known as WARS)-alongside two Tier 2 candidates supported by SMR and HEIDI, comprising risk factor PILRA and inversely associated metabolic factor ACADSB. Retinal transcriptomic mapping localized specifically to microglia, to inner retinal neurons, and to photoreceptors, RPE, and vascular compartments, while and exhibited low baseline expression. In independent validation cohorts, and were significantly up-regulated in choroidal neovascularization (CNV) membrane-derived RPE from patients with AMD (p<0.01). Exposure of ARPE-19 cells to TNF-α markedly induced mRNA levels of (P=0.0025) and (p<0.0001). Dual normalization against ACTB as a secondary internal reference yielded consistent significant induction. Pathway enrichment highlighted cytokine-driven receptor cascades (JAK-STAT signaling) and mitochondrial substrate catabolism (branched-chain amino acid and fatty acid metabolism). Drug-target profiling identified small molecules and nutraceuticals interacting with ACADSB, CSF2, and WARS1. By combining large-scale plasma proteomic genetics with single-cell mapping and experimental validation, this study identifies a prioritized set of candidate causal proteins linking neuroimmune activation, vascular remodeling, and mitochondrial bioenergetics in AMD, providing candidate entry points for mechanistic and therapeutic exploration. - Source: PubMed
Publication date: 2026/09/11
Wen LeiLi FangranLiu YuanZhang KaMao AiqinLiu LiangjuLv XiaowangGeng LiYu FanFeng LeiKan Hao - Traumatic brain injury (TBI) is a leading cause of death and long-term disability worldwide. Secondary cerebral oedema, driven by neuroinflammation and blood-brain barrier (BBB) disruption, critically determines poor outcomes, yet effective targeted therapies remain absent. This study aimed to identify immune cell subsets associated with post-TBI cerebral oedema and to explore their functional contributions in preclinical models. - Source: PubMed
Hanhan DangKun HeYulian ZhangChuanpeng ZhangYunsheng ZhangZixi WangXu YangPengyu ChenLi ZhangYanbing Yu - This study investigates the therapeutic potential of the synthetic cannabinoid WIN55,212-2 (WIN55) in temporomandibular joint osteoarthritis (TMJOA), focusing on its capacity to attenuate cartilage degradation and modulate inflammatory pathways, thereby providing preclinical evidence to support future clinical translation. - Source: PubMed
Publication date: 2026/09/18
Guo YimanZhang XinchengZhao ShenBian CeZhu MengyaoSu ChengjunZhang YuqingLiu MiaoKurahara Lin-HaiZhang Ning - Air pollution has been associated with the development and exacerbation of atopic dermatitis (AD), but the molecular signatures connecting pollutant-related targets with AD-associated immune dysregulation remain incompletely characterized. - Source: PubMed
Publication date: 2026/09/03
Gao ChangChen LipingHuang TianfengWang Zi