GCSF
- Known as:
- GCSF
- Catalog number:
- ANT-184
- Product Quantity:
- 500µg
- Category:
- -
- Supplier:
- Prospecbio
- Gene target:
- GCSF
Related genes to: GCSF
- 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: GCSF
Related articles to: GCSF
- Colony-stimulating factor 3 (CSF3), additionally called granulocyte colony-stimulating factor (G-CSF), is the major cytokine regulating neutrophil production and also impacting their function. The actions of this cytokine are mediated through its unique receptor, the colony-stimulating factor 3 receptor (CSF3R). Several classes of pathogenic mutations in the gene have been identified that have distinct biological properties and clinical impacts. This review provides an overview of CSF3R, the various pathogenic CSF3R mutations/variants and their biological effects. It also details the diseases to which they contribute, notably including chronic neutrophilic leukemia (CNL) and other myeloproliferative neoplasms (MPNs), myelodysplastic neoplasms (MDS), combined MDS/MPN disorders such as atypical chronic myeloid leukemia (aCML) and chronic myelomonocytic leukemia (CMML), as well as acute myeloid leukemia (AML) and lymphoid malignancies. - Source: PubMed
Publication date: 2025/10/20
Liongue CliffordRatnayake TarindhiWard Alister C - Discovering mechanisms of regeneration holds great promise for advancing regenerative medicine. Non-histone modifications by epigenetic factors participate in important biological processes. Through in vivo CRISPR screening combined with partial hepatectomy (PHx-CRISPR), we identified the histone H3K9 methyltransferase SETDB1 as an enhancer of regeneration. Loss of SETDB1 delays regeneration, and overexpressing SETDB1 accelerates liver regeneration across various liver injury models. SETDB1 promotes liver regeneration by positively regulating the expression of granulocyte colony-stimulating factor (CSF3) in hepatocytes. SETDB1 facilitates the expression of CSF3 in hepatocytes by methylating and activating AKT, establishing CSF3 as a critical downstream effector in the SETDB1-AKT liver regeneration pathway. Notably, increasing SETDB1 levels in humanized mouse liver suppresses drug-induced liver damage. Our findings reveal an unexpected role for non-histone modification by SETDB1 in regulating cytokine signaling during liver regeneration and offer insights into targeted therapies for regenerative medicine and tissue repair. - Source: PubMed
Publication date: 2025/06/17
Huang Xiao-YanYang DongLiu Yin-ZheZhang En-XiangYang QiaoKang WangZhang Xiao-OuShi JunweiSong Chun-Qing - Triple-negative breast cancer (TNBC) is characterized by a pronounced hypoxic tumor microenvironment, with cancer-associated fibroblasts (CAFs) serving as the predominant cellular component and playing crucial roles in regulating tumor progression. However, the mechanism by which CAFs affect the biological behavior of tumor cells in hypoxic environment remain elusive. This study employed a bead-based multiplex immunoassay to analyze a panel of cytokines/chemokines and identified colony stimulating factor 3 (CSF3) as a significantly elevated component in the secretome of hypoxic CAFs. We found that CSF3 promoted the invasive behavior of TNBC cells by activating the downstream signaling pathway of its receptor, CSF3R. RNA sequencing analysis further revealed that phosphoglucomutase 2-like 1 (PGM2L1) is a downstream target of the CSF3/CSF3R signaling, enhancing the glycolysis pathway and providing energy to support the malignant phenotype of breast cancer. In vivo, we further confirmed that CSF3 promotes TNBC progression by targeting PGM2L1. These findings suggest that targeting CSF3/CSF3R may represent a potential therapeutic approach for TNBC. - Source: PubMed
Publication date: 2025/04/04
Qin WenqiChen BingLi XinZhao WenjingWang LijuanZhang NingWang XiaolongLuo DanLiang YiranLi YamingChen XiChen TongYang Qifeng - Colony-stimulating factor 3 (CSF3) and its receptor (CSF3R) are known to promote gastric cancer (GC) growth and metastasis. However, their effects on the immune microenvironment remain unclear. Our analysis indicated a potential link between CSF3R expression and the immunosuppressive receptor leukocyte immunoglobulin-like receptor B2 (LILRB2) in GC. We hypothesized that CSF3/CSF3R may regulate LILRB2 and its ligands, angiopoietin-like protein 2 (ANGPTL2) and human leukocyte antigen-G (HLA-G), contributing to immunosuppression. - Source: PubMed
Wang LongWu QiZhang Zong-WenZhang HuiJin HuiZhou Xin-LiangLiu Jia-YinLi DanLiu YanFan Zhi-Song - Colony-stimulating factor 3 (CSF3) is a key factor in neutrophil production and function, and recombinant forms have been used clinically for decades to treat congenital and acquired neutropenia. Although biallelic inactivation of its receptor CSF3R is a well-established cause of severe congenital neutropenia (SCN), no corresponding Mendelian disease has been ascribed to date to CSF3. Here, we describe three patients from two families each segregating a different biallelic inactivating variant in CSF3 with SCN. Complete deficiency of CSF3 as a result of nonsense-mediated decay (NMD) could be demonstrated on RT-PCR using skin fibroblasts-derived RNA. The phenotype observed in this cohort mirrors that documented in mouse and zebrafish models of CSF3 deficiency. Our results suggest that CSF3 deficiency in humans causes a novel autosomal recessive form of SCN. - Source: PubMed
Publication date: 2023/08/23
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