CSF3R Antibody - N-terminal region (ARP33812_P050)
- Known as:
- CSF3R Antibody - N-terminal region (ARP33812_P050)
- Catalog number:
- arp33812_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CSF3R Antibody - N-terminal region (ARP33812_P050)
Related genes to: CSF3R Antibody - N-terminal region (ARP33812_P050)
- 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: CSF3R Antibody - N-terminal region (ARP33812_P050)
Related articles to: CSF3R Antibody - N-terminal region (ARP33812_P050)
- - Source: PubMed
Publication date: 2026/04/10
Mukae JunichiSadato DaichiToya TakashiHirama ChizukoShimabukuro MasashiJinguji AtsushiShimizu HiroakiNajima YuhoHarada HironoriHarada YukaDoki Noriko - Pulmonary hypertension (PH) is characterized by pulmonary vascular remodeling, which ultimately leads to right heart failure. Previous studies have confirmed that DNA variations contribute to the development and progression of PH. This study aims to integrate methylation and transcriptome data to uncover key molecular networks and potential therapeutic targets for PH. - Source: PubMed
Publication date: 2026/04/11
Jin LumingJiang BochenWang XuKong MinChen BingLiu Yun - The Colony-Stimulating Factor 3 Receptor (CSF3R), the receptor for granulocyte colony-stimulating factor (G-CSF), has expanded from a hematopoietic regulator to a multifunctional signalling molecule with significant relevance in gynaecological biology. High-resolution transcriptomic and proteomic studies now identify CSF3R expression in ovarian granulosa cells, endometrial epithelium, cervical tissue, placental trophoblasts, and gynaecologic tumour microenvironments, highlighting its integration into immune, endocrine, and tissue-remodeling networks. Structurally anchored by Box1/Box2 motifs, CSF3R initiates key intracellular pathways JAK-STAT, MAPK/ERK, PI3K-AKT-mTOR, SRC-family kinases, and Nf-κB governing cellular survival, proliferation, angiogenesis, metabolic activity, inflammation, and epithelial-mesenchymal transition. Dysregulated CSF3R signalling contributes to major gynaecological disorders. In polycystic ovary syndrome (PCOS), chronic inflammation and altered CSF3R-STAT3/Nf-κB activity disturb follicular maturation and endocrine-metabolic balance. In endometriosis, CSF3R-associated neutrophil activation, MMP induction, and ERK-driven angiogenesis sustain lesion growth and chronic pelvic inflammation. During implantation, defective CSF3R-mediated STAT3 signalling impairs decidualization, immune tolerance, and trophoblast invasion, contributing to implantation failure and recurrent pregnancy loss. In ovarian and endometrial cancers, CSF3R drives tumour proliferation, EMT, angiogenesis, and recruitment of immunosuppressive myeloid-derived suppressor cells. Therapeutically, targeting G-CSF3R-linked pathways offers emerging opportunities. Approaches include JAK inhibitors, PI3K/mTOR inhibitors, SRC inhibitors, STAT3 antagonists, and investigational anti-G-CSF/anti-CSF3R monoclonal antibodies. G-CSF therapy has also shown benefits in improving endometrial receptivity in select cases of reproductive failure. This review explored CSF3R biology, signalling, disease involvement, and therapeutic potential, positioning G-CSF3R as an emerging, actionable node in reproductive medicine and gynaecologic oncology. - Source: PubMed
Publication date: 2026/04/07
Ansari RashidAwathale Sanjay NGoyal Sameer N - Neutrophils and monocytes are persistently elevated in sickle cell anemia (SCA), yet the intrinsic mechanisms driving pathological myelopoiesis and inflammation remain poorly defined. Through single-cell RNA sequencing and functional assays, we demonstrate that hematopoietic stem and multipotent progenitor cells (HSPCs) in SCA are transcriptionally reprogrammed toward myeloid differentiation. This process is orchestrated by aberrant activation of Type I interferon (IFN-I) signaling, which promotes premature myeloid commitment of hematopoietic stem cells. SCA progenitors further exhibit unexpected responsiveness to granulocyte colony-stimulating factor (G-CSF) through upregulation of CSF3R, resulting in skewed myelopoiesis toward the monocytic lineage. Importantly, hydroxyurea treatment attenuates IFN-I signaling in neutrophils, consistent with its therapeutic role in reducing excessive inflammation and granulopoiesis. Collectively, these findings uncover IFN-I-driven remodeling of hematopoiesis as a fundamental mechanism of leukocytosis and chronic inflammation in SCA, and establish a tractable therapeutic axis to mitigate innate immunity activation in this disease. - Source: PubMed
Publication date: 2026/03/19
Serra MarionAkkaya StevenAglave MarineSalma MohammadBencheikh SaraHermand PatriciaLefevre CarineDuval RomainMerrer JadeLeye FallouMagne JoellePlo IsabelleBlanc LionelSoler EricAzouzi SlimKoehl Berengere - This study integrated multi-omics data analysis to elucidate key molecular alterations associated with monocytes in Parkinson's disease (PD) so as to identify novel biomarkers. - Source: PubMed
Publication date: 2026/03/17
Bao ZhiweiZhi ShaoJie Mao