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ly3009120  (Selleck Chemicals)


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    Selleck Chemicals ly3009120
    Kir2.1 activates MEK1/2–ERK1/2–Snail–EMT pathway independent of Raf. A, Human phosphokinase antibody array assay showing 11 elevated phosphorylation kinases (left) with ERK1/2 kinases at the highest level (right). Data are shown as mean. B, The over-Kir2.1 gastric cancer cells showing enhanced phosphorylation of ERK1/2 and sh-Kir2.1 gastric cancer cells showing attenuated phosphorylation of ERK1/2. JNK and p38, the other two members of MAPKs in gastric cancer cells, were unaffected by Kir2.1 expression status. C, Decreased invasion capability of gastric cancer cells after treatment with PD98059 (10 μmol/L), a MEK1/2-specific inhibitor. Data are shown as mean ± SD (n = 5; NS, not significant; ***, P < 0.0001, ANOVA test). D, Increased E-cadherin but decreased vimemtin, Snail, and pERK1/2 in PD98059 (10 μmol/L)-treated gastric cancer cells. E, Attenuation of the invasion capability of control gastric cancer cells by treatment with <t>LY3009120</t> (20 μmol/L), a pan-Raf inhibitor, without effect on over-Kir2.1 gastric cancer cells. Data are shown as mean ± SD (n = 5; ***, P < 0.0001, Student t test). F, Attenuation of the level of pMEK1/2 and pERK1/2 in control gastric cancer cells by LY3009120 (20 μmol/L) treatment, without effect on over-Kir2.1 gastric cancer cells.
    Ly3009120, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 64 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/3-d+cell+capture+structures+array/LY3009120/pmc08111788-126-43-46
    Average 93 stars, based on 64 article reviews
    ly3009120 - by Bioz Stars, 2026-08
    93/100 stars

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    1) Product Images from "Kir2.1 Interaction with Stk38 Promotes Invasion and Metastasis of Human Gastric Cancer by Enhancing MEKK2–MEK1/2–ERK1/2 Signaling"

    Article Title: Kir2.1 Interaction with Stk38 Promotes Invasion and Metastasis of Human Gastric Cancer by Enhancing MEKK2–MEK1/2–ERK1/2 Signaling

    Journal: Cancer research

    doi: 10.1158/0008-5472.CAN-17-3776

    Kir2.1 activates MEK1/2–ERK1/2–Snail–EMT pathway independent of Raf. A, Human phosphokinase antibody array assay showing 11 elevated phosphorylation kinases (left) with ERK1/2 kinases at the highest level (right). Data are shown as mean. B, The over-Kir2.1 gastric cancer cells showing enhanced phosphorylation of ERK1/2 and sh-Kir2.1 gastric cancer cells showing attenuated phosphorylation of ERK1/2. JNK and p38, the other two members of MAPKs in gastric cancer cells, were unaffected by Kir2.1 expression status. C, Decreased invasion capability of gastric cancer cells after treatment with PD98059 (10 μmol/L), a MEK1/2-specific inhibitor. Data are shown as mean ± SD (n = 5; NS, not significant; ***, P < 0.0001, ANOVA test). D, Increased E-cadherin but decreased vimemtin, Snail, and pERK1/2 in PD98059 (10 μmol/L)-treated gastric cancer cells. E, Attenuation of the invasion capability of control gastric cancer cells by treatment with LY3009120 (20 μmol/L), a pan-Raf inhibitor, without effect on over-Kir2.1 gastric cancer cells. Data are shown as mean ± SD (n = 5; ***, P < 0.0001, Student t test). F, Attenuation of the level of pMEK1/2 and pERK1/2 in control gastric cancer cells by LY3009120 (20 μmol/L) treatment, without effect on over-Kir2.1 gastric cancer cells.
    Figure Legend Snippet: Kir2.1 activates MEK1/2–ERK1/2–Snail–EMT pathway independent of Raf. A, Human phosphokinase antibody array assay showing 11 elevated phosphorylation kinases (left) with ERK1/2 kinases at the highest level (right). Data are shown as mean. B, The over-Kir2.1 gastric cancer cells showing enhanced phosphorylation of ERK1/2 and sh-Kir2.1 gastric cancer cells showing attenuated phosphorylation of ERK1/2. JNK and p38, the other two members of MAPKs in gastric cancer cells, were unaffected by Kir2.1 expression status. C, Decreased invasion capability of gastric cancer cells after treatment with PD98059 (10 μmol/L), a MEK1/2-specific inhibitor. Data are shown as mean ± SD (n = 5; NS, not significant; ***, P < 0.0001, ANOVA test). D, Increased E-cadherin but decreased vimemtin, Snail, and pERK1/2 in PD98059 (10 μmol/L)-treated gastric cancer cells. E, Attenuation of the invasion capability of control gastric cancer cells by treatment with LY3009120 (20 μmol/L), a pan-Raf inhibitor, without effect on over-Kir2.1 gastric cancer cells. Data are shown as mean ± SD (n = 5; ***, P < 0.0001, Student t test). F, Attenuation of the level of pMEK1/2 and pERK1/2 in control gastric cancer cells by LY3009120 (20 μmol/L) treatment, without effect on over-Kir2.1 gastric cancer cells.

    Techniques Used: Ab Array, Phospho-proteomics, Expressing, Control



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