KITLG _ SCF antibody Host rabbit
- Known as:
- KITLG _ SCF (anti-) Host host: rabbit
- Catalog number:
- 'ARP44354_P050
- Product Quantity:
- 50
- Category:
- -
- Supplier:
- ACR
- Gene target:
- KITLG _ SCF antibody Host rabbit
Related genes to: KITLG _ SCF antibody Host rabbit
- 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: KITLG _ SCF antibody Host rabbit
Related articles to: KITLG _ SCF antibody Host rabbit
- Cryptorchidism, a major reproductive malformation in dogs, is associated with an increased risk of testicular cancer. In this study, we aimed to compare miRNA expression and 3'UTR length variation in the mRNAs of differentially expressed genes (DEGs) between undescended (UD) and descended (D) canine testes without signs of tumorigenesis. In total, expression of 453 miRNA genes was detected, and over 100 miRNA DEGs were identified in the UD vs. D and UD vs. C (control) comparisons. Predicted target sequences for DEG miRNAs were in silico identified in numerous mRNAs, including 12 of 19 a priori selected genes related to testicular cancer. In silico analysis of miRNA and mRNA DEGs revealed that some of target mRNAs showed significant differences in UD and D/C testes and approximately 50% of miRNA-mRNA pairs exhibited an inverse expression pattern, including cancer-related genes (e.g., AR, IGF1R, KIT, KITLG, SALL4, and SPRY4). Analysis of the 3'UTR length of DEG mRNAs identified 962 transcripts with altered 3'UTR length in both the UD vs. D and UD vs. C comparisons. 3'UTR lengthening (e.g., in cancer-related genes such as LATS2, SRPK2, and AKT3) was the most common alteration observed. Our findings provide a new insight into molecular alterations associated with canine cryptorchidism. We suggest that in undescended canine testes without signs of tumorigenesis dysregulated expression of protein-coding genes, including candidate cancer-associated genes, can be associated with altered expression of specific miRNAs, as well as variations in the 3'UTR length of certain target DEG mRNAs. - Source: PubMed
Publication date: 2026/07/06
Nowacka-Woszuk JoannaKajdasz ArkadiuszStachowiak MonikaSzczerbal IzabelaSwitonski Marek - Hepatocellular carcinoma (HCC) is one of the most prevalent malignant tumors of the liver, with increasing incidence and mortality rates globally. This study investigates the role of endothelial cells (ECs) in the progression of HCC, particularly focusing on the process of endothelial-to-mesenchymal transition (EndMT) and its underlying molecular mechanisms. - Source: PubMed
Publication date: 2026/06/17
Wei FuqunYou XiangChen ZhishengChen YipingChen Zhongwu - Penile squamous cell carcinoma (PSCC) can affect men of any age, but we know little about the differences between non-old and old patients with PSCC, which severely limits the precise diagnosis and treatment of PSCC. - Source: PubMed
Publication date: 2026/06/06
Cao JianDu LinQin ZailongMa AiweiBo HaoZhao XuehengLuo YanweiOu ChunlinLiu ZhizhongXie YuZhang WancongTang ShijieTian YuYuan JunbinGong ZhaojianGuo Jie - 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
Publication date: 2026/04/17
Heiss Christina NNovakova LenkaAxelsson MarkusTan KübraPola IlariaTraichel WiebkePesämaa IdaJohnsson MagnusSandgren SofiaMalmeström ClasBenedet Andrea LZetterberg HenrikLycke Jan NFruhwürth StefanieRosenstein Igal