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dy885b proteome profiler human phospho kinease array kit r d systems  (R&D Systems)


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    R&D Systems dy885b proteome profiler human phospho kinease array kit r d systems
    Dy885b Proteome Profiler Human Phospho Kinease Array Kit R D Systems, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 46 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/dy885b proteome profiler human phospho kinease array kit r d systems/product/R&D Systems
    Average 93 stars, based on 46 article reviews
    dy885b proteome profiler human phospho kinease array kit r d systems - by Bioz Stars, 2026-04
    93/100 stars

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    Image Search Results


    ROC curve for the diagnosis of gestational diabetes mellitus based on serum Gas6 levels GAS6: Growth arrest–specific 6 protein, ROC: Receiver operating characteristic

    Journal: Turkish Journal of Obstetrics and Gynecology

    Article Title: Evaluating midpregnancy Gas6 levels as predictive value for gestational diabetes and birth outcomes

    doi: 10.4274/tjod.galenos.2025.95515

    Figure Lengend Snippet: ROC curve for the diagnosis of gestational diabetes mellitus based on serum Gas6 levels GAS6: Growth arrest–specific 6 protein, ROC: Receiver operating characteristic

    Article Snippet: Gas6 levels were measured using a double antibody sandwich method with a human Gas6 ELISA kit, branded BT Lab Bioassay Technology Laboratory (Cat No. E3257Hu, Shanghai, China).

    Techniques: Biomarker Discovery

    Journal: Turkish Journal of Obstetrics and Gynecology

    Article Title: Evaluating midpregnancy Gas6 levels as predictive value for gestational diabetes and birth outcomes

    doi: 10.4274/tjod.galenos.2025.95515

    Figure Lengend Snippet:

    Article Snippet: Gas6 levels were measured using a double antibody sandwich method with a human Gas6 ELISA kit, branded BT Lab Bioassay Technology Laboratory (Cat No. E3257Hu, Shanghai, China).

    Techniques: Biomarker Discovery

    Rapamycin induces the secretion of chondroprotective and regenerative factors by AD-MSCs. A The list of rapamycin-upregulated genes ( vs vehicle) in AD-MSCs was submitted to KEGG Pathway . Significantly affected pathways (at FDR ≤ 0.05) were plotted as a bubble chart. B The KEGG network of “Hedgehog signaling” and “TGF-β signaling” upregulated genes identified in panel A. C Genes encoding extracellular factors and upregulated or downregulated in AD-MSCs were selected using the Gene Ontology term “Extracellular region ” (GO0005576) and plotted as a Z-score heatmap of normalized counts showing the vehicle- vs. rapamycin-treated groups. D Transcripts Per Million (TPM) of extracellular factors from the “Hedgehog signaling” (SCUBE2 and MEGF8 ) and “TGF-β signaling” ( LTBP2 and FST ) pathways were extracted and plotted as dot-histograms to show their relative expression in the indicated conditions. E TPM of the pro-regenerative factor GAS6 . F GAS6 secreted by AD-MSCs upon exposure to rapamycin or/and IFN-γ. GAS6 level in supernatants was quantified by ELISA and normalized to the relative number of cells; G Diagram summary of all results. p -values: * < 0.05, ** < 0.01, *** < 0.001 (two-way ANOVA)

    Journal: Stem Cell Research & Therapy

    Article Title: Combination of rapamycin and adipose-derived mesenchymal stromal cells enhances therapeutic potential for osteoarthritis

    doi: 10.1186/s13287-024-04090-8

    Figure Lengend Snippet: Rapamycin induces the secretion of chondroprotective and regenerative factors by AD-MSCs. A The list of rapamycin-upregulated genes ( vs vehicle) in AD-MSCs was submitted to KEGG Pathway . Significantly affected pathways (at FDR ≤ 0.05) were plotted as a bubble chart. B The KEGG network of “Hedgehog signaling” and “TGF-β signaling” upregulated genes identified in panel A. C Genes encoding extracellular factors and upregulated or downregulated in AD-MSCs were selected using the Gene Ontology term “Extracellular region ” (GO0005576) and plotted as a Z-score heatmap of normalized counts showing the vehicle- vs. rapamycin-treated groups. D Transcripts Per Million (TPM) of extracellular factors from the “Hedgehog signaling” (SCUBE2 and MEGF8 ) and “TGF-β signaling” ( LTBP2 and FST ) pathways were extracted and plotted as dot-histograms to show their relative expression in the indicated conditions. E TPM of the pro-regenerative factor GAS6 . F GAS6 secreted by AD-MSCs upon exposure to rapamycin or/and IFN-γ. GAS6 level in supernatants was quantified by ELISA and normalized to the relative number of cells; G Diagram summary of all results. p -values: * < 0.05, ** < 0.01, *** < 0.001 (two-way ANOVA)

    Article Snippet: GAS6 secretion by AD-MSCs was assessed using the Human GAS6 ELISA Kit (Invitrogen – BMS2291) following the manufacturer’s instruction, but by initially diluting samples five times in diluent buffer (see Supplementary data for details).

    Techniques: Expressing, Enzyme-linked Immunosorbent Assay

    Inhibition of EMT and fibroblast activation via Gas6/Axl signaling events. Where indicated, the Axl inhibitor BGB324 (BGB, 5 mg/kg, i.o. ), COX-2 inhibitor NS-398 (NS, 5 mg/kg, i.o. ), EP1/EP2 inhibitor AH-6809 (AH, 5 mg/kg, i.p. ), or DP2 inhibitor BAY-u3405 (BAY, 30 mg/kg, i.p. ) was co-administered with rGas6 1 day before BLM treatment and then administered once/day (AH) or once every 2 days (BGB, NS, and BAY). Mice were euthanized 14 days following BLM treatment. ( a , b ) qRT-PCR of EMT markers and EMT-regulating transcription factors in primary ATII cells. ( c , d ) qRT-PCR of activated fibroblast markers and invasive myofibroblast-related molecules in primary lung fibroblasts. ( e ) Left: The cells were visualized by phase-contrast microscopy to analyze their invasive ability in Matrigel-coated Transwell assays. Scale bar: 100 µm. Right: The invaded fibroblasts were quantified by counting the number of cells adhering to the bottom surface of the upper chamber. * P < 0.05, ** P < 0.01, *** P < 0.001 compared with BLM + Sal or for BLM + Gas6 vs. BLM + rGas6 + the inhibitor. Data were obtained from five replicates per condition with cells pooled from three mice per replicate (means ± S.E.M.)

    Journal: Cell Biology and Toxicology

    Article Title: Administration of Gas6 attenuates lung fibrosis via inhibition of the epithelial-mesenchymal transition and fibroblast activation

    doi: 10.1007/s10565-024-09858-5

    Figure Lengend Snippet: Inhibition of EMT and fibroblast activation via Gas6/Axl signaling events. Where indicated, the Axl inhibitor BGB324 (BGB, 5 mg/kg, i.o. ), COX-2 inhibitor NS-398 (NS, 5 mg/kg, i.o. ), EP1/EP2 inhibitor AH-6809 (AH, 5 mg/kg, i.p. ), or DP2 inhibitor BAY-u3405 (BAY, 30 mg/kg, i.p. ) was co-administered with rGas6 1 day before BLM treatment and then administered once/day (AH) or once every 2 days (BGB, NS, and BAY). Mice were euthanized 14 days following BLM treatment. ( a , b ) qRT-PCR of EMT markers and EMT-regulating transcription factors in primary ATII cells. ( c , d ) qRT-PCR of activated fibroblast markers and invasive myofibroblast-related molecules in primary lung fibroblasts. ( e ) Left: The cells were visualized by phase-contrast microscopy to analyze their invasive ability in Matrigel-coated Transwell assays. Scale bar: 100 µm. Right: The invaded fibroblasts were quantified by counting the number of cells adhering to the bottom surface of the upper chamber. * P < 0.05, ** P < 0.01, *** P < 0.001 compared with BLM + Sal or for BLM + Gas6 vs. BLM + rGas6 + the inhibitor. Data were obtained from five replicates per condition with cells pooled from three mice per replicate (means ± S.E.M.)

    Article Snippet: Furthermore, active transforming growth factor-β1 (TGF-β1) (BioLegend, San Diego, California, US), hepatocyte growth factor (HGF), and Gas6 (R&D Systems) were evaluated using ELISA kits in accordance with the manufacturer's instructions.

    Techniques: Inhibition, Activation Assay, Quantitative RT-PCR, Microscopy

    Effect of Gas6 deficiency on EMT and fibroblast activation. WT and GAS6 −/− mice were intratracheally instilled with BLM (5 U/kg). Mice were euthanized 14 days after BLM treatment. ( a – c ) qRT-PCR of EMT markers and EMT-regulating transcription factors in primary ATII cells ( a , b ) and lung tissue ( c ). ( d ) qRT-PCR of activated fibroblast markers and invasive myofibroblast phenotype-regulating molecules in primary fibroblasts. ( e ) Left: Immunoblot analysis of the indicated proteins in lung tissue. Right: Densitometric analysis of each band normalized to that of β-actin. ( f , g ) PGE 2 and PGD 2 levels in BAL fluid (BALF) and conditioned media of ATII cells and alveolar macrophages (AM) were measured using an enzyme immunoassay. * P < 0.05, ** P < 0.01, *** P < 0.001 compared with Sal control or for WT + BLM vs. GAS6 −/− + BLM. Data were obtained from three ( f and g middle, right ) or five replicates ( a , b , d ) per condition with cells pooled from two mice per replicate (means ± S.E.M.). Values represent the means ± S.E.M. of results from three ( e right , f and g left ) or five mice ( c ) per group

    Journal: Cell Biology and Toxicology

    Article Title: Administration of Gas6 attenuates lung fibrosis via inhibition of the epithelial-mesenchymal transition and fibroblast activation

    doi: 10.1007/s10565-024-09858-5

    Figure Lengend Snippet: Effect of Gas6 deficiency on EMT and fibroblast activation. WT and GAS6 −/− mice were intratracheally instilled with BLM (5 U/kg). Mice were euthanized 14 days after BLM treatment. ( a – c ) qRT-PCR of EMT markers and EMT-regulating transcription factors in primary ATII cells ( a , b ) and lung tissue ( c ). ( d ) qRT-PCR of activated fibroblast markers and invasive myofibroblast phenotype-regulating molecules in primary fibroblasts. ( e ) Left: Immunoblot analysis of the indicated proteins in lung tissue. Right: Densitometric analysis of each band normalized to that of β-actin. ( f , g ) PGE 2 and PGD 2 levels in BAL fluid (BALF) and conditioned media of ATII cells and alveolar macrophages (AM) were measured using an enzyme immunoassay. * P < 0.05, ** P < 0.01, *** P < 0.001 compared with Sal control or for WT + BLM vs. GAS6 −/− + BLM. Data were obtained from three ( f and g middle, right ) or five replicates ( a , b , d ) per condition with cells pooled from two mice per replicate (means ± S.E.M.). Values represent the means ± S.E.M. of results from three ( e right , f and g left ) or five mice ( c ) per group

    Article Snippet: Furthermore, active transforming growth factor-β1 (TGF-β1) (BioLegend, San Diego, California, US), hepatocyte growth factor (HGF), and Gas6 (R&D Systems) were evaluated using ELISA kits in accordance with the manufacturer's instructions.

    Techniques: Activation Assay, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Control

    Effect of Gas6 deficiency on collagen deposition in lung fibrosis. WT and GAS6 −/− mice were intratracheally instilled with BLM (5 U/kg). Mice were euthanized 14 days after BLM treatment. ( a ) Collagen deposition in the whole lung was determined by measuring hydroxyproline content. ( b ) Lung sections were visualized with Masson’s trichrome staining on day 14. Representative results from three mice per group are shown (scale bar: 50 μm). ( c ) Ashcroft scoring of the lung sections. * P < 0.05, ** P < 0.01, *** P < 0.001 compared with Sal control or for WT + BLM vs. GAS6 −/− + BLM. Values represent the means ± S.E.M. of results from three ( c ) or five mice ( a ) per group

    Journal: Cell Biology and Toxicology

    Article Title: Administration of Gas6 attenuates lung fibrosis via inhibition of the epithelial-mesenchymal transition and fibroblast activation

    doi: 10.1007/s10565-024-09858-5

    Figure Lengend Snippet: Effect of Gas6 deficiency on collagen deposition in lung fibrosis. WT and GAS6 −/− mice were intratracheally instilled with BLM (5 U/kg). Mice were euthanized 14 days after BLM treatment. ( a ) Collagen deposition in the whole lung was determined by measuring hydroxyproline content. ( b ) Lung sections were visualized with Masson’s trichrome staining on day 14. Representative results from three mice per group are shown (scale bar: 50 μm). ( c ) Ashcroft scoring of the lung sections. * P < 0.05, ** P < 0.01, *** P < 0.001 compared with Sal control or for WT + BLM vs. GAS6 −/− + BLM. Values represent the means ± S.E.M. of results from three ( c ) or five mice ( a ) per group

    Article Snippet: Furthermore, active transforming growth factor-β1 (TGF-β1) (BioLegend, San Diego, California, US), hepatocyte growth factor (HGF), and Gas6 (R&D Systems) were evaluated using ELISA kits in accordance with the manufacturer's instructions.

    Techniques: Staining, Control

    A schematic diagram summarizing the role of Gas6/Axl signaling events for the prevention of lung fibrosis. rGas6 inhibits EMT and apoptosis in ATII cells and concomitantly suppresses fibroblast activation, consequently preventing the development of BLM-induced lung fibrosis. This occurs through the activation of Axl signaling pathway, including COX-2-derived PGE 2 and PGD 2 production in ATII cells and alveolar macrophages

    Journal: Cell Biology and Toxicology

    Article Title: Administration of Gas6 attenuates lung fibrosis via inhibition of the epithelial-mesenchymal transition and fibroblast activation

    doi: 10.1007/s10565-024-09858-5

    Figure Lengend Snippet: A schematic diagram summarizing the role of Gas6/Axl signaling events for the prevention of lung fibrosis. rGas6 inhibits EMT and apoptosis in ATII cells and concomitantly suppresses fibroblast activation, consequently preventing the development of BLM-induced lung fibrosis. This occurs through the activation of Axl signaling pathway, including COX-2-derived PGE 2 and PGD 2 production in ATII cells and alveolar macrophages

    Article Snippet: Furthermore, active transforming growth factor-β1 (TGF-β1) (BioLegend, San Diego, California, US), hepatocyte growth factor (HGF), and Gas6 (R&D Systems) were evaluated using ELISA kits in accordance with the manufacturer's instructions.

    Techniques: Activation Assay, Derivative Assay