Only in Titles

Search results for: ELISA Human , Stem Cell Factor Receptor (CD117)

paperclip

#33389076   2021/01/03 To Up

A new monoclonal antibody that blocks dimerisation and inhibits c-kit mutation-driven tumour growth.

Imatinib, a small-molecule tyrosine kinase inhibitor, has shown good clinical activity by inhibiting adenosine triphosphate (ATP) binding to the receptor. Unfortunately, majority of patients eventually develop drug resistance, which limits the long-term benefits of the tyrosine kinase inhibitors and poses a significant challenge in the clinical management of GIST. The aim of our study was to explore the feasibility of blocking KIT dimerisation upstream of the phosphorylation in imatinib-resistant GIST.
Chenguang Bai, Yi Xu, Cen Qiu

1620 related Products with: A new monoclonal antibody that blocks dimerisation and inhibits c-kit mutation-driven tumour growth.

1 mg1 mg1 mg1 mg100ul100ul100 ul1 mg1 mg100ul50ug100ul

Related Pathways

paperclip

#32831979   2020/08/08 To Up

Extracorporeal Shock Waves Increase Markers of Cellular Proliferation in Bronchial Epithelium and in Primary Bronchial Fibroblasts of COPD Patients.

Chronic obstructive pulmonary disease (COPD) is due to structural changes and narrowing of small airways and parenchymal destruction (loss of the alveolar attachment as a result of pulmonary emphysema), which all lead to airflow limitation. Extracorporeal shock waves (ESW) increase cell proliferation and differentiation of connective tissue fibroblasts. To date no studies are available on ESW treatment of human bronchial fibroblasts and epithelial cells from COPD and control subjects. We obtained primary bronchial fibroblasts from bronchial biopsies of 3 patients with mild/moderate COPD and 3 control smokers with normal lung function. 16HBE cells were also studied. Cells were treated with a piezoelectric shock wave generator at low energy (0.3 mJ/mm, 500 pulses). After treatment, viability was evaluated and cells were recultured and followed up for 4, 24, 48, and 72 h. Cell growth (WST-1 test) was assessed, and proliferation markers were analyzed by qRT-PCR in cell lysates and by ELISA tests in cell supernatants and cell lysates. After ESW treatment, we observed a significant increase of cell proliferation in all cell types. C-Kit (CD117) mRNA was significantly increased in 16HBE cells at 4 h. Protein levels were significantly increased for c-Kit (CD117) at 4 h in 16HBE ( < 0.0001) and at 24 h in COPD-fibroblasts ( = 0.037); for PCNA at 4 h in 16HBE ( = 0.046); for Thy1 (CD90) at 24 and 72 h in CS-fibroblasts ( = 0.031 and  = 0.041); for TGF1 at 72 h in CS-fibroblasts ( = 0.038); for procollagen-1 at 4 h in COPD-fibroblasts ( = 0.020); and for NF-B-p65 at 4 and 24 h in 16HBE ( = 0.015 and  = 0.0002). In the peripheral lung tissue of a representative COPD patient, alveolar type II epithelial cells (TTF-1+) coexpressing c-Kit (CD117) and PCNA were occasionally observed. These data show an increase of cell proliferation induced by a low dosage of extracorporeal shock waves in 16HBE cells and primary bronchial fibroblasts of COPD and control smoking subjects.
Antonino Di Stefano, Roberto Frairia, Fabio L M Ricciardolo, Isabella Gnemmi, Antonella Marino Gammazza, Alessio Piraino, Francesco Cappello, Bruno Balbi, Maria Graziella Catalano

2936 related Products with: Extracorporeal Shock Waves Increase Markers of Cellular Proliferation in Bronchial Epithelium and in Primary Bronchial Fibroblasts of COPD Patients.

100ug96 assays100 ml.25 ml.96 tests96 assays100 μg100 μg

Related Pathways

paperclip

#31434494   2019/08/22 To Up

SCF (Stem Cell Factor) and cKIT Modulate Pathological Ocular Neovascularization.

Aberrant neovascularization is a leading cause of blindness in several eye diseases, including age-related macular degeneration and proliferative diabetic retinopathy. The identification of key regulators of pathological ocular neovascularization has been a subject of extensive research and great therapeutic interest. Here, we explored the previously unrecognized role of cKIT and its ligand, SCF (stem cell factor), in the pathological ocular neovascularization process. Approach and Results: Compared with normoxia, hypoxia, a crucial driver of neovascularization, caused cKIT to be highly upregulated in endothelial cells, which significantly enhanced the angiogenic response of endothelial cells to SCF. In murine models of pathological ocular neovascularization, such as oxygen-induced retinopathy and laser-induced choroidal neovascularization models, cKIT and SCF expression was significantly increased in ocular tissues, and blockade of cKIT and SCF using mutant mice and anti-SCF neutralizing IgG substantially suppressed pathological ocular neovascularization. Mechanistically, SCF/cKIT signaling induced neovascularization through phosphorylation of glycogen synthase kinase-3β and enhancement of the nuclear translocation of β-catenin and the transcription of β-catenin target genes related to angiogenesis. Inhibition of β-catenin-mediated transcription using chemical inhibitors blocked SCF-induced in vitro angiogenesis in hypoxia, and injection of a β-catenin agonist into mutant mice with oxygen-induced retinopathy significantly enhanced pathological neovascularization in the retina. Conclusions; Our data reveal that SCF and cKIT are promising novel therapeutic targets for treating vision-threatening ocular neovascular diseases.
Koung Li Kim, Songyi Seo, Jee Taek Kim, Jaeteak Kim, Won Kim, Yeongju Yeo, Jong-Hyuk Sung, Sang Gyu Park, Wonhee Suh

2386 related Products with: SCF (Stem Cell Factor) and cKIT Modulate Pathological Ocular Neovascularization.