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vivit  (MedChemExpress)


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    MedChemExpress vivit
    Inhibition of the calcineurin A/NFATC2 signalling pathway attenuates the proliferation of human limbal epithelial stem cells (hLESCs) induced by WNT16b. EdU assays (A, B) showed that both 5 <t>μM</t> <t>FK506</t> (A) and 1 μM <t>VIVIT</t> (B) attenuated hLESC proliferation induced by WNT16b ( p = 0.02 and 0.001, respectively), which was further confirmed by a decrease in cell density ( p = 0.002 and 0.005, respectively; C). RT–PCR (D, E) showed that the expression of PPP3CA ( p < 0.001) , PPP3CB ( p = 0.004), PPP3CC ( p < 0.001) and NFATC2 ( p < 0.001) decreased with FK506 treatment (D), whereas VIVIT caused a reduced level of only NFATC2 ( p < 0.001; E). Accordingly, Western blotting (F) revealed that FK506 inhibited the expression of both calcineurin A and NFATC2 ( p = 0.001 and 0.007, respectively), while VIVIT only prohibited the expression of NFATC2 (calcineurin A: p = 0.15, NFATC2: p = 0.004). In addition, the increased expression of ΔNp63α and Ki67 in WNT16b‐treated hLESCs was suppressed by treatment with either FK506 ( p = 0.05 and 0.02, respectively; G) or VIVIT ( p = 0.02 and 0.007, respectively; H). Scale bars: 50 μm (B, H); 100 μm (A, G). * p < 0.05, ** p < 0.01, *** p < 0.001.
    Vivit, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "WNT16b promotes the proliferation and self‐renewal of human limbal epithelial stem/progenitor cells via activating the calcium/calcineurin A/ NFATC2 pathway"

    Article Title: WNT16b promotes the proliferation and self‐renewal of human limbal epithelial stem/progenitor cells via activating the calcium/calcineurin A/ NFATC2 pathway

    Journal: Cell Proliferation

    doi: 10.1111/cpr.13460

    Inhibition of the calcineurin A/NFATC2 signalling pathway attenuates the proliferation of human limbal epithelial stem cells (hLESCs) induced by WNT16b. EdU assays (A, B) showed that both 5 μM FK506 (A) and 1 μM VIVIT (B) attenuated hLESC proliferation induced by WNT16b ( p = 0.02 and 0.001, respectively), which was further confirmed by a decrease in cell density ( p = 0.002 and 0.005, respectively; C). RT–PCR (D, E) showed that the expression of PPP3CA ( p < 0.001) , PPP3CB ( p = 0.004), PPP3CC ( p < 0.001) and NFATC2 ( p < 0.001) decreased with FK506 treatment (D), whereas VIVIT caused a reduced level of only NFATC2 ( p < 0.001; E). Accordingly, Western blotting (F) revealed that FK506 inhibited the expression of both calcineurin A and NFATC2 ( p = 0.001 and 0.007, respectively), while VIVIT only prohibited the expression of NFATC2 (calcineurin A: p = 0.15, NFATC2: p = 0.004). In addition, the increased expression of ΔNp63α and Ki67 in WNT16b‐treated hLESCs was suppressed by treatment with either FK506 ( p = 0.05 and 0.02, respectively; G) or VIVIT ( p = 0.02 and 0.007, respectively; H). Scale bars: 50 μm (B, H); 100 μm (A, G). * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: Inhibition of the calcineurin A/NFATC2 signalling pathway attenuates the proliferation of human limbal epithelial stem cells (hLESCs) induced by WNT16b. EdU assays (A, B) showed that both 5 μM FK506 (A) and 1 μM VIVIT (B) attenuated hLESC proliferation induced by WNT16b ( p = 0.02 and 0.001, respectively), which was further confirmed by a decrease in cell density ( p = 0.002 and 0.005, respectively; C). RT–PCR (D, E) showed that the expression of PPP3CA ( p < 0.001) , PPP3CB ( p = 0.004), PPP3CC ( p < 0.001) and NFATC2 ( p < 0.001) decreased with FK506 treatment (D), whereas VIVIT caused a reduced level of only NFATC2 ( p < 0.001; E). Accordingly, Western blotting (F) revealed that FK506 inhibited the expression of both calcineurin A and NFATC2 ( p = 0.001 and 0.007, respectively), while VIVIT only prohibited the expression of NFATC2 (calcineurin A: p = 0.15, NFATC2: p = 0.004). In addition, the increased expression of ΔNp63α and Ki67 in WNT16b‐treated hLESCs was suppressed by treatment with either FK506 ( p = 0.05 and 0.02, respectively; G) or VIVIT ( p = 0.02 and 0.007, respectively; H). Scale bars: 50 μm (B, H); 100 μm (A, G). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Inhibition, Reverse Transcription Polymerase Chain Reaction, Expressing, Western Blot

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    Article Title: Temporal vascular pattern remodeling mediated by the FHL2/sFRP2 signaling pathway in tenocytes affects tendon repair and regeneration
    Article Snippet: .. Next, HUVECs were divided into the following groups for further assessments: NC group (negative control, untreated), 7 pM-sFRP2 treatment group, 7 pM-sFRP2 + U73122 (1 μM, phospholipase C inhibitor, HY-13419, MedChemExpress) group, 7 pM-sFRP2 + Ceapin-A7 (30 μM, selective ATF6α signaling blocker, HY-108434, MedChemExpress) group and 7 pM-sFRP2 + Fz7-21 (30 μM, FZD7 receptor peptide antagonist, HY-P1454, MedChemExpress) group. ..



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    a Cell viability of HUVECs treated with gradient concentrations of <t>sFRP2</t> protein (CCK8). The 5–10 pM concentration showed the most significant effect. b Cell viability (CCK8) of HUVECs treated with sFRP2 + U73122 (phospholipase C inhibitor) or Ceapin-A7 (selective ATF6α signaling blocker) <t>or</t> <t>Fz7-21</t> <t>(FZD7</t> receptor peptide antagonist). c , d Flow cytometry analysis (panel c ) of apoptosis in HUVECs treated with sFRP2 (7 pM) + U73122 (1 μM)/Ceapin-A7 (30 μM)/Fz7-21 (30 μM), with the percentage of cells exhibiting early apoptosis (LR) and late apoptosis (UR); the relevant statistical results displayed in panel d . e , f Flow cytometry analysis (panel e ) of cell cycle in HUVECs treated with sFRP2 (7 pM) + U73122 (1 μM)/Ceapin-A7 (30 μM)/Fz7-21 (30 μM), with the percentages of cells in the G0/G1, S and G2/M phases; the relevant statistical results displayed in panel f . g , h Scratch wound healing assay (panel g ); %Cell migration rate = (initial width at 0 h − width at specific time point)/initial width at 0 h, *** P < 0.05 versus the sFRP2-treated group; the relevant statistical results displayed in panel h . i – m Tube formation assay (panel i ) with the number of branches (statistical results in panel j ), total branching length (statistical results in panel k ), number of junctions (statistical results in panel l ) and number of meshes (statistical results in panel m ), *** P < 0.05 versus the sFRP2-treated group. n Tenocyte-HUVECs coculture models. o , p WB (panel o ) assessing the expression levels of sFRP2 in tenocytes transfected with siSFRP2 , ** P < 0.05 versus NC, ns: P > 0.05; the relevant statistical results displayed in panel p . q Tube formation assay of HUVECs after coculturing with tenocytes (Calcein-AM staining) (Supplementary Data File ). r The number of branches, total branching length, number of junctions and number of meshes, *** P < 0.05 versus IL-1β-stimulated normal tenocyte-HUVECs coculture group, # P < 0.05 between any two groups.
    Pm Sfrp2 Fz7 21, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p1454/Fz7-21/pmc12686517-168-47-57
    Average 93 stars, based on 1 article reviews
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    vivit  (MedChemExpress)
    93
    MedChemExpress vivit
    Inhibition of the calcineurin A/NFATC2 signalling pathway attenuates the proliferation of human limbal epithelial stem cells (hLESCs) induced by WNT16b. EdU assays (A, B) showed that both 5 <t>μM</t> <t>FK506</t> (A) and 1 μM <t>VIVIT</t> (B) attenuated hLESC proliferation induced by WNT16b ( p = 0.02 and 0.001, respectively), which was further confirmed by a decrease in cell density ( p = 0.002 and 0.005, respectively; C). RT–PCR (D, E) showed that the expression of PPP3CA ( p < 0.001) , PPP3CB ( p = 0.004), PPP3CC ( p < 0.001) and NFATC2 ( p < 0.001) decreased with FK506 treatment (D), whereas VIVIT caused a reduced level of only NFATC2 ( p < 0.001; E). Accordingly, Western blotting (F) revealed that FK506 inhibited the expression of both calcineurin A and NFATC2 ( p = 0.001 and 0.007, respectively), while VIVIT only prohibited the expression of NFATC2 (calcineurin A: p = 0.15, NFATC2: p = 0.004). In addition, the increased expression of ΔNp63α and Ki67 in WNT16b‐treated hLESCs was suppressed by treatment with either FK506 ( p = 0.05 and 0.02, respectively; G) or VIVIT ( p = 0.02 and 0.007, respectively; H). Scale bars: 50 μm (B, H); 100 μm (A, G). * p < 0.05, ** p < 0.01, *** p < 0.001.
    Vivit, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-p1454/Fz7-21/pmc10542615-123-16-19
    Average 93 stars, based on 1 article reviews
    vivit - by Bioz Stars, 2026-10
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    a Cell viability of HUVECs treated with gradient concentrations of sFRP2 protein (CCK8). The 5–10 pM concentration showed the most significant effect. b Cell viability (CCK8) of HUVECs treated with sFRP2 + U73122 (phospholipase C inhibitor) or Ceapin-A7 (selective ATF6α signaling blocker) or Fz7-21 (FZD7 receptor peptide antagonist). c , d Flow cytometry analysis (panel c ) of apoptosis in HUVECs treated with sFRP2 (7 pM) + U73122 (1 μM)/Ceapin-A7 (30 μM)/Fz7-21 (30 μM), with the percentage of cells exhibiting early apoptosis (LR) and late apoptosis (UR); the relevant statistical results displayed in panel d . e , f Flow cytometry analysis (panel e ) of cell cycle in HUVECs treated with sFRP2 (7 pM) + U73122 (1 μM)/Ceapin-A7 (30 μM)/Fz7-21 (30 μM), with the percentages of cells in the G0/G1, S and G2/M phases; the relevant statistical results displayed in panel f . g , h Scratch wound healing assay (panel g ); %Cell migration rate = (initial width at 0 h − width at specific time point)/initial width at 0 h, *** P < 0.05 versus the sFRP2-treated group; the relevant statistical results displayed in panel h . i – m Tube formation assay (panel i ) with the number of branches (statistical results in panel j ), total branching length (statistical results in panel k ), number of junctions (statistical results in panel l ) and number of meshes (statistical results in panel m ), *** P < 0.05 versus the sFRP2-treated group. n Tenocyte-HUVECs coculture models. o , p WB (panel o ) assessing the expression levels of sFRP2 in tenocytes transfected with siSFRP2 , ** P < 0.05 versus NC, ns: P > 0.05; the relevant statistical results displayed in panel p . q Tube formation assay of HUVECs after coculturing with tenocytes (Calcein-AM staining) (Supplementary Data File ). r The number of branches, total branching length, number of junctions and number of meshes, *** P < 0.05 versus IL-1β-stimulated normal tenocyte-HUVECs coculture group, # P < 0.05 between any two groups.

    Journal: Experimental & Molecular Medicine

    Article Title: Temporal vascular pattern remodeling mediated by the FHL2/sFRP2 signaling pathway in tenocytes affects tendon repair and regeneration

    doi: 10.1038/s12276-025-01574-2

    Figure Lengend Snippet: a Cell viability of HUVECs treated with gradient concentrations of sFRP2 protein (CCK8). The 5–10 pM concentration showed the most significant effect. b Cell viability (CCK8) of HUVECs treated with sFRP2 + U73122 (phospholipase C inhibitor) or Ceapin-A7 (selective ATF6α signaling blocker) or Fz7-21 (FZD7 receptor peptide antagonist). c , d Flow cytometry analysis (panel c ) of apoptosis in HUVECs treated with sFRP2 (7 pM) + U73122 (1 μM)/Ceapin-A7 (30 μM)/Fz7-21 (30 μM), with the percentage of cells exhibiting early apoptosis (LR) and late apoptosis (UR); the relevant statistical results displayed in panel d . e , f Flow cytometry analysis (panel e ) of cell cycle in HUVECs treated with sFRP2 (7 pM) + U73122 (1 μM)/Ceapin-A7 (30 μM)/Fz7-21 (30 μM), with the percentages of cells in the G0/G1, S and G2/M phases; the relevant statistical results displayed in panel f . g , h Scratch wound healing assay (panel g ); %Cell migration rate = (initial width at 0 h − width at specific time point)/initial width at 0 h, *** P < 0.05 versus the sFRP2-treated group; the relevant statistical results displayed in panel h . i – m Tube formation assay (panel i ) with the number of branches (statistical results in panel j ), total branching length (statistical results in panel k ), number of junctions (statistical results in panel l ) and number of meshes (statistical results in panel m ), *** P < 0.05 versus the sFRP2-treated group. n Tenocyte-HUVECs coculture models. o , p WB (panel o ) assessing the expression levels of sFRP2 in tenocytes transfected with siSFRP2 , ** P < 0.05 versus NC, ns: P > 0.05; the relevant statistical results displayed in panel p . q Tube formation assay of HUVECs after coculturing with tenocytes (Calcein-AM staining) (Supplementary Data File ). r The number of branches, total branching length, number of junctions and number of meshes, *** P < 0.05 versus IL-1β-stimulated normal tenocyte-HUVECs coculture group, # P < 0.05 between any two groups.

    Article Snippet: Next, HUVECs were divided into the following groups for further assessments: NC group (negative control, untreated), 7 pM-sFRP2 treatment group, 7 pM-sFRP2 + U73122 (1 μM, phospholipase C inhibitor, HY-13419, MedChemExpress) group, 7 pM-sFRP2 + Ceapin-A7 (30 μM, selective ATF6α signaling blocker, HY-108434, MedChemExpress) group and 7 pM-sFRP2 + Fz7-21 (30 μM, FZD7 receptor peptide antagonist, HY-P1454, MedChemExpress) group.

    Techniques: Concentration Assay, Flow Cytometry, Wound Healing Assay, Migration, Tube Formation Assay, Expressing, Transfection, Staining

    Inhibition of the calcineurin A/NFATC2 signalling pathway attenuates the proliferation of human limbal epithelial stem cells (hLESCs) induced by WNT16b. EdU assays (A, B) showed that both 5 μM FK506 (A) and 1 μM VIVIT (B) attenuated hLESC proliferation induced by WNT16b ( p = 0.02 and 0.001, respectively), which was further confirmed by a decrease in cell density ( p = 0.002 and 0.005, respectively; C). RT–PCR (D, E) showed that the expression of PPP3CA ( p < 0.001) , PPP3CB ( p = 0.004), PPP3CC ( p < 0.001) and NFATC2 ( p < 0.001) decreased with FK506 treatment (D), whereas VIVIT caused a reduced level of only NFATC2 ( p < 0.001; E). Accordingly, Western blotting (F) revealed that FK506 inhibited the expression of both calcineurin A and NFATC2 ( p = 0.001 and 0.007, respectively), while VIVIT only prohibited the expression of NFATC2 (calcineurin A: p = 0.15, NFATC2: p = 0.004). In addition, the increased expression of ΔNp63α and Ki67 in WNT16b‐treated hLESCs was suppressed by treatment with either FK506 ( p = 0.05 and 0.02, respectively; G) or VIVIT ( p = 0.02 and 0.007, respectively; H). Scale bars: 50 μm (B, H); 100 μm (A, G). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: Cell Proliferation

    Article Title: WNT16b promotes the proliferation and self‐renewal of human limbal epithelial stem/progenitor cells via activating the calcium/calcineurin A/ NFATC2 pathway

    doi: 10.1111/cpr.13460

    Figure Lengend Snippet: Inhibition of the calcineurin A/NFATC2 signalling pathway attenuates the proliferation of human limbal epithelial stem cells (hLESCs) induced by WNT16b. EdU assays (A, B) showed that both 5 μM FK506 (A) and 1 μM VIVIT (B) attenuated hLESC proliferation induced by WNT16b ( p = 0.02 and 0.001, respectively), which was further confirmed by a decrease in cell density ( p = 0.002 and 0.005, respectively; C). RT–PCR (D, E) showed that the expression of PPP3CA ( p < 0.001) , PPP3CB ( p = 0.004), PPP3CC ( p < 0.001) and NFATC2 ( p < 0.001) decreased with FK506 treatment (D), whereas VIVIT caused a reduced level of only NFATC2 ( p < 0.001; E). Accordingly, Western blotting (F) revealed that FK506 inhibited the expression of both calcineurin A and NFATC2 ( p = 0.001 and 0.007, respectively), while VIVIT only prohibited the expression of NFATC2 (calcineurin A: p = 0.15, NFATC2: p = 0.004). In addition, the increased expression of ΔNp63α and Ki67 in WNT16b‐treated hLESCs was suppressed by treatment with either FK506 ( p = 0.05 and 0.02, respectively; G) or VIVIT ( p = 0.02 and 0.007, respectively; H). Scale bars: 50 μm (B, H); 100 μm (A, G). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: The specific inhibitors used in inhibitory experiments were added also on Day 3 such as FK506, VIVIT and Fz7‐21 (MedChemExpress, final concentrations shown in the Results Section).

    Techniques: Inhibition, Reverse Transcription Polymerase Chain Reaction, Expressing, Western Blot