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cnn1 calponin 1 alexafluor 555  (Bioss)


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    Structured Review

    Bioss cnn1 calponin 1 alexafluor 555
    Cnn1 Calponin 1 Alexafluor 555, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cnn1 calponin 1 alexafluor 555/product/Bioss
    Average 94 stars, based on 1 article reviews
    cnn1 calponin 1 alexafluor 555 - by Bioz Stars, 2026-04
    94/100 stars

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    Cnn1 Calponin 1 Alexafluor 555, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher gene exp cnn1 hs00959434 m1
    FKBP51 and dexamethasone induce a switch in leiomyoma cells from a smooth muscle to myofibroblast phenotype. (A) RNA-sequencing analysis of cultured leiomyoma cells (n = 4) shows lower expression levels of extracellular matrix genes including LAMA2 , LAMB1 , and FN1 , and higher expression levels of smooth muscle expressed genes <t>CNN1</t> , MYH9 , MYH10, and ACTA2 following dexamethasone (DEX) treatment in FKBP5 siRNA (FKsi) vs control siRNA (Csi) transfected cells. (B) Confirmation of significantly lower expression levels of LAMA2 and FN1 , and higher expression levels of CNN1 in FKsi-Dex vs Csi-Dex by qPCR analysis. Bars represent mean ± standard error of the mean; n = 4. RNA sequencing raw data available in the NCBI GEO repository, accession number GSE292403 .
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    Proteintech cnn1
    Inhibition of MELK delays the phenotypic switch of HPASMCs from a contractile to a synthetic phenotype. HPASMCs were treated with vehicle or OTS167 (10 nM, 48 h) under basal conditions or PDGF-BB stimulation (20 ng/mL, 48 h). (A–C) Relative mRNA expression of ACTA2 (A) , TAGLN (B) , and <t>CNN1</t> (C) measured by qRT-PCR. OTS167 treatment significantly attenuated the PDGF-BB–induced downregulation of these contractile markers. (D) Representative immunoblots showing protein expression of ACTA2, CNN1, and SM22α in HPASMCs, with α-tubulin as a loading control. (E–G) Quantification of TAGLN (E) , ACTA2 (F) , and CNN1 (G) protein levels normalized to α-tubulin. OTS167 treatment preserved the expression of contractile markers under both basal and PDGF-BB-stimulated conditions. Data are presented as mean ± SD, n = 6 per group. Two-way ANOVA followed by Tukey’s post hoc test was used. P < 0.05 was considered statistically significant.
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    Proteintech manuscript cnn1 13938 1 ap
    Inhibition of MELK delays the phenotypic switch of HPASMCs from a contractile to a synthetic phenotype. HPASMCs were treated with vehicle or OTS167 (10 nM, 48 h) under basal conditions or PDGF-BB stimulation (20 ng/mL, 48 h). (A–C) Relative mRNA expression of ACTA2 (A) , TAGLN (B) , and <t>CNN1</t> (C) measured by qRT-PCR. OTS167 treatment significantly attenuated the PDGF-BB–induced downregulation of these contractile markers. (D) Representative immunoblots showing protein expression of ACTA2, CNN1, and SM22α in HPASMCs, with α-tubulin as a loading control. (E–G) Quantification of TAGLN (E) , ACTA2 (F) , and CNN1 (G) protein levels normalized to α-tubulin. OTS167 treatment preserved the expression of contractile markers under both basal and PDGF-BB-stimulated conditions. Data are presented as mean ± SD, n = 6 per group. Two-way ANOVA followed by Tukey’s post hoc test was used. P < 0.05 was considered statistically significant.
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    Boster Bio anti cnn1
    Inhibition of MELK delays the phenotypic switch of HPASMCs from a contractile to a synthetic phenotype. HPASMCs were treated with vehicle or OTS167 (10 nM, 48 h) under basal conditions or PDGF-BB stimulation (20 ng/mL, 48 h). (A–C) Relative mRNA expression of ACTA2 (A) , TAGLN (B) , and <t>CNN1</t> (C) measured by qRT-PCR. OTS167 treatment significantly attenuated the PDGF-BB–induced downregulation of these contractile markers. (D) Representative immunoblots showing protein expression of ACTA2, CNN1, and SM22α in HPASMCs, with α-tubulin as a loading control. (E–G) Quantification of TAGLN (E) , ACTA2 (F) , and CNN1 (G) protein levels normalized to α-tubulin. OTS167 treatment preserved the expression of contractile markers under both basal and PDGF-BB-stimulated conditions. Data are presented as mean ± SD, n = 6 per group. Two-way ANOVA followed by Tukey’s post hoc test was used. P < 0.05 was considered statistically significant.
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    Inhibition of MELK delays the phenotypic switch of HPASMCs from a contractile to a synthetic phenotype. HPASMCs were treated with vehicle or OTS167 (10 nM, 48 h) under basal conditions or PDGF-BB stimulation (20 ng/mL, 48 h). (A–C) Relative mRNA expression of ACTA2 (A) , TAGLN (B) , and <t>CNN1</t> (C) measured by qRT-PCR. OTS167 treatment significantly attenuated the PDGF-BB–induced downregulation of these contractile markers. (D) Representative immunoblots showing protein expression of ACTA2, CNN1, and SM22α in HPASMCs, with α-tubulin as a loading control. (E–G) Quantification of TAGLN (E) , ACTA2 (F) , and CNN1 (G) protein levels normalized to α-tubulin. OTS167 treatment preserved the expression of contractile markers under both basal and PDGF-BB-stimulated conditions. Data are presented as mean ± SD, n = 6 per group. Two-way ANOVA followed by Tukey’s post hoc test was used. P < 0.05 was considered statistically significant.
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    Proteintech anti cnn1
    Inhibition of MELK delays the phenotypic switch of HPASMCs from a contractile to a synthetic phenotype. HPASMCs were treated with vehicle or OTS167 (10 nM, 48 h) under basal conditions or PDGF-BB stimulation (20 ng/mL, 48 h). (A–C) Relative mRNA expression of ACTA2 (A) , TAGLN (B) , and <t>CNN1</t> (C) measured by qRT-PCR. OTS167 treatment significantly attenuated the PDGF-BB–induced downregulation of these contractile markers. (D) Representative immunoblots showing protein expression of ACTA2, CNN1, and SM22α in HPASMCs, with α-tubulin as a loading control. (E–G) Quantification of TAGLN (E) , ACTA2 (F) , and CNN1 (G) protein levels normalized to α-tubulin. OTS167 treatment preserved the expression of contractile markers under both basal and PDGF-BB-stimulated conditions. Data are presented as mean ± SD, n = 6 per group. Two-way ANOVA followed by Tukey’s post hoc test was used. P < 0.05 was considered statistically significant.
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    Image Search Results


    FKBP51 and dexamethasone induce a switch in leiomyoma cells from a smooth muscle to myofibroblast phenotype. (A) RNA-sequencing analysis of cultured leiomyoma cells (n = 4) shows lower expression levels of extracellular matrix genes including LAMA2 , LAMB1 , and FN1 , and higher expression levels of smooth muscle expressed genes CNN1 , MYH9 , MYH10, and ACTA2 following dexamethasone (DEX) treatment in FKBP5 siRNA (FKsi) vs control siRNA (Csi) transfected cells. (B) Confirmation of significantly lower expression levels of LAMA2 and FN1 , and higher expression levels of CNN1 in FKsi-Dex vs Csi-Dex by qPCR analysis. Bars represent mean ± standard error of the mean; n = 4. RNA sequencing raw data available in the NCBI GEO repository, accession number GSE292403 .

    Journal: The Journal of Clinical Endocrinology and Metabolism

    Article Title: Increased HSD11β1 Expression in Human Leiomyomatous Uteri: Implication for Enhanced Glucocorticoid Signaling

    doi: 10.1210/clinem/dgaf255

    Figure Lengend Snippet: FKBP51 and dexamethasone induce a switch in leiomyoma cells from a smooth muscle to myofibroblast phenotype. (A) RNA-sequencing analysis of cultured leiomyoma cells (n = 4) shows lower expression levels of extracellular matrix genes including LAMA2 , LAMB1 , and FN1 , and higher expression levels of smooth muscle expressed genes CNN1 , MYH9 , MYH10, and ACTA2 following dexamethasone (DEX) treatment in FKBP5 siRNA (FKsi) vs control siRNA (Csi) transfected cells. (B) Confirmation of significantly lower expression levels of LAMA2 and FN1 , and higher expression levels of CNN1 in FKsi-Dex vs Csi-Dex by qPCR analysis. Bars represent mean ± standard error of the mean; n = 4. RNA sequencing raw data available in the NCBI GEO repository, accession number GSE292403 .

    Article Snippet: The full name and Taq-Man Probe Assay IDs for each target gene include: FK506-binding protein 5 ( FKBP5 )- Hs01561006_m1; Hydroxysteroid 11-β dehydrogenase 1 ( HSD11B1) - Hs01547870_m1; IL-1 receptor type 1 ( IL1R1 )- Hs00991002_m1; TSC22 domain family member 3 ( TSC22D3 )- Hs00608272_m1; alcohol dehydrogenase 1B, β polypeptide ( ADH1B )- Hs00605175_m1; Gremlin 1, DAN family BMP antagonist ( GREM1 )- Hs00171951_m1; IGF-binding protein 5 ( IGFBP5 )- Hs00181213_m1; adhesion molecule with Ig-like domain 2 ( AMIGO2 )- Hs05001325_s1; laminin subunit alpha 2 ( LAMA2 )- Hs00166308_m1; fibronectin 1 ( FN1 )- Hs00365052_m1; calponin 1 ( CNN1 )- Hs00959434_m1; actin β ( ACTB )- Hs99999903_m1; and glyceraldehyde-3-phosphate dehydrogenase ( GAPDH )- Hs99999905_m1.

    Techniques: RNA Sequencing, Cell Culture, Expressing, Control, Transfection

    Inhibition of MELK delays the phenotypic switch of HPASMCs from a contractile to a synthetic phenotype. HPASMCs were treated with vehicle or OTS167 (10 nM, 48 h) under basal conditions or PDGF-BB stimulation (20 ng/mL, 48 h). (A–C) Relative mRNA expression of ACTA2 (A) , TAGLN (B) , and CNN1 (C) measured by qRT-PCR. OTS167 treatment significantly attenuated the PDGF-BB–induced downregulation of these contractile markers. (D) Representative immunoblots showing protein expression of ACTA2, CNN1, and SM22α in HPASMCs, with α-tubulin as a loading control. (E–G) Quantification of TAGLN (E) , ACTA2 (F) , and CNN1 (G) protein levels normalized to α-tubulin. OTS167 treatment preserved the expression of contractile markers under both basal and PDGF-BB-stimulated conditions. Data are presented as mean ± SD, n = 6 per group. Two-way ANOVA followed by Tukey’s post hoc test was used. P < 0.05 was considered statistically significant.

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Melk facilitates pulmonary artery smooth muscle cell proliferation and migration in pulmonary hypertension via modulation of YAP/TAZ signaling

    doi: 10.3389/fcell.2025.1693346

    Figure Lengend Snippet: Inhibition of MELK delays the phenotypic switch of HPASMCs from a contractile to a synthetic phenotype. HPASMCs were treated with vehicle or OTS167 (10 nM, 48 h) under basal conditions or PDGF-BB stimulation (20 ng/mL, 48 h). (A–C) Relative mRNA expression of ACTA2 (A) , TAGLN (B) , and CNN1 (C) measured by qRT-PCR. OTS167 treatment significantly attenuated the PDGF-BB–induced downregulation of these contractile markers. (D) Representative immunoblots showing protein expression of ACTA2, CNN1, and SM22α in HPASMCs, with α-tubulin as a loading control. (E–G) Quantification of TAGLN (E) , ACTA2 (F) , and CNN1 (G) protein levels normalized to α-tubulin. OTS167 treatment preserved the expression of contractile markers under both basal and PDGF-BB-stimulated conditions. Data are presented as mean ± SD, n = 6 per group. Two-way ANOVA followed by Tukey’s post hoc test was used. P < 0.05 was considered statistically significant.

    Article Snippet: The primary antibodies used were as follows: Melk (1:2000 dilution; 11403-1-AP), ACTA2 (1:20,000, 67735-1-Ig), CNN1 (1:2000 dilution; 24855-1-AP), SM22α (1:5000 dilution; 10493-1-AP), YAP1 (1:2000, 13584-1-AP), TAZ (1:2000 dilution; 66500-1-Ig), Alpha Tubulin (1:20000 dilution; 66031-1-Ig) (ProteinTech), PCNA (1:1000 dilution; ab29), Cyclin D1(1:1000 dilution; ab16663), GAPDH (1:500, ab8245) (Abcam), Phospho-YAP (Ser127) (1:1000 dilution; # 13008) (Cell Signaling Technology).

    Techniques: Inhibition, Expressing, Quantitative RT-PCR, Western Blot, Control