human mertk peptide (R&D Systems)
Structured Review

Human Mertk Peptide, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 14 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+mertk/Human+C-Peptide+Antibody/pmc13032267-67-15-18
Average 94 stars, based on 14 article reviews
Images
1) Product Images from "RGX-019-MMAE inhibits leukemia progression by targeting MER proto-oncogene tyrosine kinase (MERTK) in acute myeloid leukemia"
Article Title: RGX-019-MMAE inhibits leukemia progression by targeting MER proto-oncogene tyrosine kinase (MERTK) in acute myeloid leukemia
Journal: Journal of Experimental & Clinical Cancer Research : CR
doi: 10.1186/s13046-026-03657-y
Figure Legend Snippet: The antibody-drug conjugate RGX-019-MMAE induced cytotoxic activity in MERTK-expressing AML cell lines. A MERTK expression in the indicated AML cell lines; leukemic cells (1 × 10 6 ) were stained with anti-MERTK-APC antibody, and the expression was measured by flow cytometry. Data are plotted as mean values with error bars representing standard error. B - F Bar graph showing the percentage of relative luminescence in Kasumi 1 ( B ), OCI-AML3 ( C ), MOLM-13 ( D ), MOLM-14 ( E ), and MV4-11 ( F ) cells treated with the indicated concentrations of RGX-019-MMAE and monoclonal antibody RGX-019. Data are plotted as mean values with error bars representing standard error (Student unpaired t -test). * p ≤0.05, ** p ≤0.01, *** p ≤0.001, **** p ≤0.0001. UT = untreated
Techniques Used: Activity Assay, Expressing, Staining, Flow Cytometry
Figure Legend Snippet: The antibody-drug conjugate RGX-019-MMAE induced cytotoxic activity in MERTK-expressing AML primary cells. A - D Bar graphs show the percentage of relative luminescence in primary AML cells, RGX946 ( A ), RGX694 ( B ), RGX702 ( C ), and RGX470 ( D ) treated with the indicated concentrations of RGX-019-MMAE or the monoclonal antibody RGX-019. Data are plotted as mean values with error bars representing standard error (Student unpaired t -test). E Representative figures of colony-forming units for normal peripheral blood mononuclear cells in response to DMSO and indicated concentrations of RGX-019-MMAE and RGX-019. Data are plotted as mean values with error bars representing standard error (Student unpaired t -test) * p ≤0.05, ** p ≤0.01, *** p ≤0.001, **** p ≤0.0001
Techniques Used: Activity Assay, Expressing
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Article Title: Inflammatory crosstalk impairs phagocytic receptors and aggravates atherosclerosis in clonal hematopoiesis in mice Article Snippet: Then the 549 membranes were blocked with 5% non-fat milk in TBST and immunostained with primary 550 antibodies, anti-p-Syk (cell signaling technology 2710s, 1:1000), anti-Syk (cell signaling 551 technology 13198, 1:1000), anti-p-AKT (cell signaling technology 4060s, 1:1000) anti-552 AKT (cell signaling technology 4685, 1:1000), anti-cleaved Gasdermin D (cell signaling 553 technology 10137S, 1:1000), anti-p-β-Catenin (cell signaling technology 5651, 1:1000), 554 anti-β-Catenin (cell signaling technology 8480S, 1:1000), anti-PDGFB (abcam 555 ab23914,1:1000), anti-Histone H3 (cell signaling technology 4499, 1:1000), anti-MERTK 556 27 ( Article Title: Inflammatory crosstalk impairs phagocytic receptors and aggravates atherosclerosis in clonal hematopoiesis in mice Article Snippet: Then, the membranes were blocked with 5% nonfat milk in TBST and immunostained with the primary antibodies anti–p-Syk (Cell Signaling Technology, 2710s, 1:1,000), anti-Syk (Cell Signaling Technology, 13198, 1:1,000), anti–p-AKT (Cell Signaling Technology, 4060s, 1:1,000), anti-AKT (Cell Signaling Technology, 4685, 1:1,000), anti–cleaved gasdermin D (Cell Signaling Technology, 10137S, 1:1,000), anti–p–β-catenin (Cell Signaling Technology, 5651, 1:1,000), anti–β-catenin (Cell Signaling Technology, 8480S, 1:1,000), anti-PDGFB (Abcam, ab23914,1:1,000), anti–histone H3 (Cell Signaling Technology, 4499, 1:1,000), Bioprocessing:Article Title: Cardiac Macrophages Promote Polarization of Macrophages toward M2 Phenotype to Improve Myocardial Remodeling via NGAL after Myocardial Infarction. 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