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anti pmlc2  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti pmlc2
    Anti Pmlc2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 95 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pmlc2+ser19/pm41933938-251-34-36?v=Cell+Signaling+Technology+Inc
    Average 95 stars, based on 95 article reviews
    anti pmlc2 - by Bioz Stars, 2026-07
    95/100 stars

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    (A) Top: representative western blot showing the effect of SMAD3 siRNA (siSMAD3) on total SMAD3 protein level and on TGFβ-induced SMAD3 phosphorylation in healthy control (HC) and systemic sclerosis (SSc) fibroblasts, compared to scrambled siRNA (siSCR). Bottom: Densitometric quantification of SMAD3 in control (siSCR) and siSMAD3-treated HC and SSc fibroblasts (n=3 individual donors per group). (B) Quantification of cilium length in HC and SSc fibroblasts treated with siSCR or siSMAD3 and stimulated for 24 h with TGFβ. n=3 individual donors per group. (C) Top: representative western blots showing <t>pMLC2,</t> ppMLC2, and total MLC2, in response to treatments TGFβ with or without KD025 in three HC donor and three SSc donor fibroblast lines. Bottom: Densitometric quantification of pMLC2 normalised to MLC2 in the same condition. (D) Cilium length in HC and SSc fibroblasts treated with the ROCK2 inhibitor KD205 ± TGFβ. Mean cilia length was measured in three HC donor and three SSc donor fibroblast lines treated as indicated. All data panels were analysed by ANOVA (ns, non-significant; * P<0.05; ****P<0.0001).
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    (A) Top: representative western blot showing the effect of SMAD3 siRNA (siSMAD3) on total SMAD3 protein level and on TGFβ-induced SMAD3 phosphorylation in healthy control (HC) and systemic sclerosis (SSc) fibroblasts, compared to scrambled siRNA (siSCR). Bottom: Densitometric quantification of SMAD3 in control (siSCR) and siSMAD3-treated HC and SSc fibroblasts (n=3 individual donors per group). (B) Quantification of cilium length in HC and SSc fibroblasts treated with siSCR or siSMAD3 and stimulated for 24 h with TGFβ. n=3 individual donors per group. (C) Top: representative western blots showing <t>pMLC2,</t> ppMLC2, and total MLC2, in response to treatments TGFβ with or without KD025 in three HC donor and three SSc donor fibroblast lines. Bottom: Densitometric quantification of pMLC2 normalised to MLC2 in the same condition. (D) Cilium length in HC and SSc fibroblasts treated with the ROCK2 inhibitor KD205 ± TGFβ. Mean cilia length was measured in three HC donor and three SSc donor fibroblast lines treated as indicated. All data panels were analysed by ANOVA (ns, non-significant; * P<0.05; ****P<0.0001).
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    (A) Top: representative western blot showing the effect of SMAD3 siRNA (siSMAD3) on total SMAD3 protein level and on TGFβ-induced SMAD3 phosphorylation in healthy control (HC) and systemic sclerosis (SSc) fibroblasts, compared to scrambled siRNA (siSCR). Bottom: Densitometric quantification of SMAD3 in control (siSCR) and siSMAD3-treated HC and SSc fibroblasts (n=3 individual donors per group). (B) Quantification of cilium length in HC and SSc fibroblasts treated with siSCR or siSMAD3 and stimulated for 24 h with TGFβ. n=3 individual donors per group. (C) Top: representative western blots showing <t>pMLC2,</t> ppMLC2, and total MLC2, in response to treatments TGFβ with or without KD025 in three HC donor and three SSc donor fibroblast lines. Bottom: Densitometric quantification of pMLC2 normalised to MLC2 in the same condition. (D) Cilium length in HC and SSc fibroblasts treated with the ROCK2 inhibitor KD205 ± TGFβ. Mean cilia length was measured in three HC donor and three SSc donor fibroblast lines treated as indicated. All data panels were analysed by ANOVA (ns, non-significant; * P<0.05; ****P<0.0001).
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    (A) Top: representative western blot showing the effect of SMAD3 siRNA (siSMAD3) on total SMAD3 protein level and on TGFβ-induced SMAD3 phosphorylation in healthy control (HC) and systemic sclerosis (SSc) fibroblasts, compared to scrambled siRNA (siSCR). Bottom: Densitometric quantification of SMAD3 in control (siSCR) and siSMAD3-treated HC and SSc fibroblasts (n=3 individual donors per group). (B) Quantification of cilium length in HC and SSc fibroblasts treated with siSCR or siSMAD3 and stimulated for 24 h with TGFβ. n=3 individual donors per group. (C) Top: representative western blots showing <t>pMLC2,</t> ppMLC2, and total MLC2, in response to treatments TGFβ with or without KD025 in three HC donor and three SSc donor fibroblast lines. Bottom: Densitometric quantification of pMLC2 normalised to MLC2 in the same condition. (D) Cilium length in HC and SSc fibroblasts treated with the ROCK2 inhibitor KD205 ± TGFβ. Mean cilia length was measured in three HC donor and three SSc donor fibroblast lines treated as indicated. All data panels were analysed by ANOVA (ns, non-significant; * P<0.05; ****P<0.0001).
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    (A) Top: representative western blot showing the effect of SMAD3 siRNA (siSMAD3) on total SMAD3 protein level and on TGFβ-induced SMAD3 phosphorylation in healthy control (HC) and systemic sclerosis (SSc) fibroblasts, compared to scrambled siRNA (siSCR). Bottom: Densitometric quantification of SMAD3 in control (siSCR) and siSMAD3-treated HC and SSc fibroblasts (n=3 individual donors per group). (B) Quantification of cilium length in HC and SSc fibroblasts treated with siSCR or siSMAD3 and stimulated for 24 h with TGFβ. n=3 individual donors per group. (C) Top: representative western blots showing pMLC2, ppMLC2, and total MLC2, in response to treatments TGFβ with or without KD025 in three HC donor and three SSc donor fibroblast lines. Bottom: Densitometric quantification of pMLC2 normalised to MLC2 in the same condition. (D) Cilium length in HC and SSc fibroblasts treated with the ROCK2 inhibitor KD205 ± TGFβ. Mean cilia length was measured in three HC donor and three SSc donor fibroblast lines treated as indicated. All data panels were analysed by ANOVA (ns, non-significant; * P<0.05; ****P<0.0001).

    Journal: bioRxiv

    Article Title: Aurora A kinase activation contributes to the fibrotic phenotype in Systemic Sclerosis through primary cilia shortening

    doi: 10.64898/2026.03.13.711548

    Figure Lengend Snippet: (A) Top: representative western blot showing the effect of SMAD3 siRNA (siSMAD3) on total SMAD3 protein level and on TGFβ-induced SMAD3 phosphorylation in healthy control (HC) and systemic sclerosis (SSc) fibroblasts, compared to scrambled siRNA (siSCR). Bottom: Densitometric quantification of SMAD3 in control (siSCR) and siSMAD3-treated HC and SSc fibroblasts (n=3 individual donors per group). (B) Quantification of cilium length in HC and SSc fibroblasts treated with siSCR or siSMAD3 and stimulated for 24 h with TGFβ. n=3 individual donors per group. (C) Top: representative western blots showing pMLC2, ppMLC2, and total MLC2, in response to treatments TGFβ with or without KD025 in three HC donor and three SSc donor fibroblast lines. Bottom: Densitometric quantification of pMLC2 normalised to MLC2 in the same condition. (D) Cilium length in HC and SSc fibroblasts treated with the ROCK2 inhibitor KD205 ± TGFβ. Mean cilia length was measured in three HC donor and three SSc donor fibroblast lines treated as indicated. All data panels were analysed by ANOVA (ns, non-significant; * P<0.05; ****P<0.0001).

    Article Snippet: Proteins were transferred onto Hybond nitrocellulose membranes (Amersham) and probed with antibodies specific for αSMA (Abcam ab7817), β-Actin (Sigma A5441), CAV1 (Santa Cruz sc894), p53 (Santa Cruz sc126), acetylated-α-Tubulin (Cell Signaling 5335), MLC2 (Cell Signaling 8505), pMLC2 (Ser19) (Cell Signaling 3674), ppMLC2 (Ser19, Thr18) (Cell Signaling 3674), SMAD3 (Cell Signalling 9523), pSMAD3 (Abcam ab52903).

    Techniques: Western Blot, Phospho-proteomics, Control