Mouse SCF / KITLG Protein
- Known as:
- Mouse SCF / KITLG Protein
- Catalog number:
- SCF-M5228
- Product Quantity:
- 50ug
- Category:
- -
- Supplier:
- acrobyosystems
- Gene target:
- Mouse SCF / KITLG Protein
Related genes to: Mouse SCF / KITLG Protein
- Gene:
- KITLG NIH gene
- Name:
- KIT ligand
- Previous symbol:
- MGF
- Synonyms:
- SCF, SF, Kitl, KL-1, FPH2, SLF, DFNA69
- Chromosome:
- 12q21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-04
- Date modifiied:
- 2019-04-23
Related products to: Mouse SCF / KITLG Protein
Related articles to: Mouse SCF / KITLG Protein
- Blood deficiency syndrome (BDS) is a systemic disorder characterized by hematopoietic dysfunction and immune dysregulation. Given the limitations of current therapies, such as single efficacy and adverse effects, there is an urgent need for multitarget therapeutic agents with systemic regulatory effects. In this study, a mouse model of BDS was established through chronic benzene inhalation. Using an integrated transcriptomics and proteomics approach, we systematically investigated the therapeutic mechanism of Danggui Buxue Decoction (DBD). The results demonstrated that DBD significantly restored body weight, thymic and splenic indices, and bone marrow microstructure in model mice but also improved peripheral blood parameters such as the red blood cell count and mean corpuscular volume. Furthermore, DBD coordinately modulated serum hematopoietic factor and inflammatory cytokine levels. Mechanistically, DBD exerts its therapeutic effects through dual pathways. On the one hand, it promotes hematopoietic repair by upregulating transferrin receptor (TFRC) to support iron-dependent erythropoiesis, modulating KITLG/FLT3LG to maintain stem cell pool stability, and reprogramming integrin expression (e.g., upregulating ITGA4 and downregulating ITGA1) to facilitate stem cell homing and suppress fibrosis. On the other hand, it reshapes the immune microenvironment by enhancing MHC class II antigen presentation (e.g., H2Aa, H2-Ab1, H2-DMb1, and H2-Eb1) and immune cell activation (e.g., CD22, CD37, CD20, and CD8a), thereby reestablishing immune homeostasis. This study provides a systematic molecular basis for the multitarget and holistic regulatory properties of DBD, supporting its clinical application and suggesting potential therapeutic targets for BDS-related disorders. - Source: PubMed
Publication date: 2026/05/22
Liu HongdaRen JunlingHu YuYang YuSun HuiFang HengYan GuangliHan YingWang Xijun - Progressive multiple sclerosis is characterized by gradual neurological decline, often occurring independently of relapses or MRI activity-a phenomenon known as progression independent of relapse and MRI activity (PIRMA). Despite the effectiveness of disease-modifying therapies in controlling inflammatory activity, identifying individuals at risk of PIRMA remains an unmet clinical need. The objective of this exploratory study was to identify biomarkers and underlying molecular pathways associated with multiple sclerosis progression and especially PIRMA. Using the NUcleic acid Linked Immuno-Sandwich Assay (NULISA) inflammatory panel, we quantified 250 immune-related proteins in CSF and plasma from 49 controls, 49 patients with early active relapsing-remitting multiple sclerosis (RRMS) and 33 patients with inactive progressive multiple sclerosis (iPMS). Longitudinal clinical data were used to define PIRMA and conversion to secondary progressive multiple sclerosis (SPMS). We identified distinct proteomic signatures in CSF of both RRMS and iPMS patients compared with controls, with no significant differences in plasma. Both were associated with elevated markers of adaptive immunity, while iPMS showed a shift towards innate immune markers. Among RRMS patients, low baseline CSF concentrations of KIT ligand (KITLG) predicted both conversion to SPMS and future PIRMA events. Receiver operating characteristic analysis demonstrated KITLG's potential as a prognostic biomarker. Additionally, plasma concentrations of interleukin 1 beta and 36 gamma were elevated in RRMS patients who later developed SPMS. A model selection analysis identified a two-protein logistic regression model including interleukin 1 beta and interleukin 36 gamma as the best-performing combination (area under the curve = 0.990). Our findings reveal distinct immunological profiles across multiple sclerosis subtypes and identify KITLG as a promising biomarker for predicting disease progression and PIRMA. These results highlight potential targets for therapeutic intervention and demonstrate the utility of NULISA in uncovering novel molecular signatures in multiple sclerosis. - Source: PubMed
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