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MedChemExpress solid recombinant human tgf β1 protein

Upregulation of miR-18a-5p in asthma and its role in promoting ASMC proliferation and migration <t>upon</t> <t>TGF-β1</t> stimulation. (A) RT-qPCR revealed that miR-18a-5p levels were significantly higher in sputum from asthma patients compared with healthy controls (n = 10). (B) TGF-β1 stimulation induced a dose-dependent increase in miR-18a-5p expression in ASMCs (n = 3). (C) PDGF-BB stimulation significantly altered miR-18a-5p expression in ASMCs in a concentration-dependent manner (n = 3). (D) miR-18a-5p was effectively overexpressed or silenced in ASMCs following transfection with mimics or inhibitors (n = 3). (E) CCK-8 assay showed altered cell viability under different miR-18a-5p expression levels (n = 3). (F) Transwell assay demonstrated that miR-18a-5p regulates the migratory capacity of ASMCs (n = 3). Data are presented as mean ± SD. **p < 0.01 vs. healthy, 0 ng/mL, or Control group; ##p < 0.01 vs. TGF-β1+in-NC or PDGF-BB 5 ng/mL group; &&p < 0.01 vs. TGF-β1+mi-NC or PDGF-BB 10 ng/mL group.

Solid Recombinant Human Tgf β1 Protein, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/solid+recombinant+human+tgf+%CE%B21+protein/Lefty-A%2FTGF-beta+4%2C+Human/pmc13044553-74-0-8
Average 94 stars, based on 2 article reviews

solid recombinant human tgf β1 protein - by Bioz Stars, 2026-08

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1) Product Images from "miR-18a-5p promotes phenotypic transformation of airway smooth muscle cells by targeting SPRY1 to activate the RAS-MAPK pathway"

Article Title: miR-18a-5p promotes phenotypic transformation of airway smooth muscle cells by targeting SPRY1 to activate the RAS-MAPK pathway

Journal: Frontiers in Genetics

doi: 10.3389/fgene.2026.1760431

Upregulation of miR-18a-5p in asthma and its role in promoting ASMC proliferation and migration upon TGF-β1 stimulation. (A) RT-qPCR revealed that miR-18a-5p levels were significantly higher in sputum from asthma patients compared with healthy controls (n = 10). (B) TGF-β1 stimulation induced a dose-dependent increase in miR-18a-5p expression in ASMCs (n = 3). (C) PDGF-BB stimulation significantly altered miR-18a-5p expression in ASMCs in a concentration-dependent manner (n = 3). (D) miR-18a-5p was effectively overexpressed or silenced in ASMCs following transfection with mimics or inhibitors (n = 3). (E) CCK-8 assay showed altered cell viability under different miR-18a-5p expression levels (n = 3). (F) Transwell assay demonstrated that miR-18a-5p regulates the migratory capacity of ASMCs (n = 3). Data are presented as mean ± SD. **p < 0.01 vs. healthy, 0 ng/mL, or Control group; ##p < 0.01 vs. TGF-β1+in-NC or PDGF-BB 5 ng/mL group; &&p < 0.01 vs. TGF-β1+mi-NC or PDGF-BB 10 ng/mL group.

Figure Legend Snippet: Upregulation of miR-18a-5p in asthma and its role in promoting ASMC proliferation and migration upon TGF-β1 stimulation. (A) RT-qPCR revealed that miR-18a-5p levels were significantly higher in sputum from asthma patients compared with healthy controls (n = 10). (B) TGF-β1 stimulation induced a dose-dependent increase in miR-18a-5p expression in ASMCs (n = 3). (C) PDGF-BB stimulation significantly altered miR-18a-5p expression in ASMCs in a concentration-dependent manner (n = 3). (D) miR-18a-5p was effectively overexpressed or silenced in ASMCs following transfection with mimics or inhibitors (n = 3). (E) CCK-8 assay showed altered cell viability under different miR-18a-5p expression levels (n = 3). (F) Transwell assay demonstrated that miR-18a-5p regulates the migratory capacity of ASMCs (n = 3). Data are presented as mean ± SD. **p < 0.01 vs. healthy, 0 ng/mL, or Control group; ##p < 0.01 vs. TGF-β1+in-NC or PDGF-BB 5 ng/mL group; &&p < 0.01 vs. TGF-β1+mi-NC or PDGF-BB 10 ng/mL group.

Techniques Used: Migration, Quantitative RT-PCR, Expressing, Concentration Assay, Transfection, CCK-8 Assay, Transwell Assay, Control

miR-18a-5p regulates migration-associated proteins in TGF-β1-stimulated ASMCs. Representative Western blot images and quantitative analysis showed the expression levels of Integrin β1, p-FAK, total FAK, p-Paxillin, total Paxillin, and MMP9. α-Tubulin was used as a loading control. Data are presented as mean ± SD (n = 3). ***p < 0.001 vs. Control group; ###p < 0.001 vs. TGF-β1+in-NC group; &&&p < 0.001 vs. TGF-β1+mi-NC group.

Figure Legend Snippet: miR-18a-5p regulates migration-associated proteins in TGF-β1-stimulated ASMCs. Representative Western blot images and quantitative analysis showed the expression levels of Integrin β1, p-FAK, total FAK, p-Paxillin, total Paxillin, and MMP9. α-Tubulin was used as a loading control. Data are presented as mean ± SD (n = 3). ***p < 0.001 vs. Control group; ###p < 0.001 vs. TGF-β1+in-NC group; &&&p < 0.001 vs. TGF-β1+mi-NC group.

Techniques Used: Migration, Western Blot, Expressing, Control

miR-18a-5p modulates the expression of structural proteins in TGF-β1-induced ASMCs. (A,B) Immunofluorescence staining of α-SMA and Collagen I in ASMCs subjected to different treatments. (C) Representative Western blot images of OPN, α-SMA, Calponin, Collagen I, and Collagen III in ASMCs following different interventions. (D) Quantitative analysis of protein expression levels based on Western blot results. Data are presented as mean ± SD (n = 3). **p < 0.01 vs. Control group; ##p < 0.01 vs. TGF-β1+in-NC group; &&p < 0.01 vs. TGF-β1+mi-NC group.

Figure Legend Snippet: miR-18a-5p modulates the expression of structural proteins in TGF-β1-induced ASMCs. (A,B) Immunofluorescence staining of α-SMA and Collagen I in ASMCs subjected to different treatments. (C) Representative Western blot images of OPN, α-SMA, Calponin, Collagen I, and Collagen III in ASMCs following different interventions. (D) Quantitative analysis of protein expression levels based on Western blot results. Data are presented as mean ± SD (n = 3). **p < 0.01 vs. Control group; ##p < 0.01 vs. TGF-β1+in-NC group; &&p < 0.01 vs. TGF-β1+mi-NC group.

Techniques Used: Expressing, Immunofluorescence, Staining, Western Blot, Control

miR-18a-5p enhances RAS-MAPK pathway activation in TGF-β1-induced ASMCs. (A) Representative Western blot images of KRAS, MEK1/2, p-MEK1/2, ERK1/2, and p-ERK1/2 protein levels in ASMCs subjected to different treatments. (B) Quantitative analysis of protein expression based on Western blot results. Data are presented as mean ± SD (n = 3). **p < 0.01 vs. Control group; ##p < 0.01 vs. TGF-β1+in-NC group; &&p < 0.01 vs. TGF-β1+mi-NC group.

Figure Legend Snippet: miR-18a-5p enhances RAS-MAPK pathway activation in TGF-β1-induced ASMCs. (A) Representative Western blot images of KRAS, MEK1/2, p-MEK1/2, ERK1/2, and p-ERK1/2 protein levels in ASMCs subjected to different treatments. (B) Quantitative analysis of protein expression based on Western blot results. Data are presented as mean ± SD (n = 3). **p < 0.01 vs. Control group; ##p < 0.01 vs. TGF-β1+in-NC group; &&p < 0.01 vs. TGF-β1+mi-NC group.

Techniques Used: Activation Assay, Western Blot, Expressing, Control

miR-18a-5p targets and negatively regulates SPRY1 (A) RT-qPCR analysis of SPRY1 expression in sputum samples from asthma patients and healthy controls (n = 10). (B) Correlation analysis of the relationship between miR-18a-5p and SPRY1 expression levels. (C) RT-qPCR analysis of SPRY1 mRNA expression in ASMCs under different treatment conditions (n = 3). (D) Western blot analysis of SPRY1 protein expression in ASMCs following different interventions (n = 3). (E) Bioinformatic prediction of the putative binding site between miR-18a-5p and the SPRY1 3′UTR. (F) Dual-luciferase reporter assay confirming the direct interaction between miR-18a-5p and SPRY1 (n = 3). Data are presented as mean ± SD. **p < 0.01, ***p < 0.001 vs. healthy, Control or WT + NC-mimics group; ##p < 0.01 vs. TGF-β1+in-NC group; &&p < 0.01 vs. TGF-β1+mi-NC group.

Figure Legend Snippet: miR-18a-5p targets and negatively regulates SPRY1 (A) RT-qPCR analysis of SPRY1 expression in sputum samples from asthma patients and healthy controls (n = 10). (B) Correlation analysis of the relationship between miR-18a-5p and SPRY1 expression levels. (C) RT-qPCR analysis of SPRY1 mRNA expression in ASMCs under different treatment conditions (n = 3). (D) Western blot analysis of SPRY1 protein expression in ASMCs following different interventions (n = 3). (E) Bioinformatic prediction of the putative binding site between miR-18a-5p and the SPRY1 3′UTR. (F) Dual-luciferase reporter assay confirming the direct interaction between miR-18a-5p and SPRY1 (n = 3). Data are presented as mean ± SD. **p < 0.01, ***p < 0.001 vs. healthy, Control or WT + NC-mimics group; ##p < 0.01 vs. TGF-β1+in-NC group; &&p < 0.01 vs. TGF-β1+mi-NC group.

Techniques Used: Quantitative RT-PCR, Expressing, Western Blot, Binding Assay, Luciferase, Reporter Assay, Control

miR-18a-5p promotes TGF-β1-induced phenotypic transformation of ASMCs by targeting SPRY1 and activating the RAS-MAPK signaling pathway. (A) Western blot analysis of SPRY1 protein expression in ASMCs under different treatment conditions. (B) Western blot analysis of KRAS, MEK1/2, p-MEK1/2, ERK1/2, and p-ERK1/2 in ASMCs following different interventions. (C) CCK-8 assay evaluating ASMC viability under various treatment conditions. (D) Transwell assay assessing the migration capacity of ASMCs after different treatments. (E) Western blot analysis of OPN, α-SMA, Calponin, Collagen I, and Collagen III protein levels in ASMCs under different conditions. Data are presented as mean ± SD (n = 3). **p < 0.01 vs. si-NC or TGF-β1 group; ##p < 0.01 vs. TGF-β1+in-miR group; &&p < 0.01 vs. TGF-β1+si-SPRY1 group.

Figure Legend Snippet: miR-18a-5p promotes TGF-β1-induced phenotypic transformation of ASMCs by targeting SPRY1 and activating the RAS-MAPK signaling pathway. (A) Western blot analysis of SPRY1 protein expression in ASMCs under different treatment conditions. (B) Western blot analysis of KRAS, MEK1/2, p-MEK1/2, ERK1/2, and p-ERK1/2 in ASMCs following different interventions. (C) CCK-8 assay evaluating ASMC viability under various treatment conditions. (D) Transwell assay assessing the migration capacity of ASMCs after different treatments. (E) Western blot analysis of OPN, α-SMA, Calponin, Collagen I, and Collagen III protein levels in ASMCs under different conditions. Data are presented as mean ± SD (n = 3). **p < 0.01 vs. si-NC or TGF-β1 group; ##p < 0.01 vs. TGF-β1+in-miR group; &&p < 0.01 vs. TGF-β1+si-SPRY1 group.

Techniques Used: Transformation Assay, Western Blot, Expressing, CCK-8 Assay, Transwell Assay, Migration

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Journal: Frontiers in Genetics

Article Title: miR-18a-5p promotes phenotypic transformation of airway smooth muscle cells by targeting SPRY1 to activate the RAS-MAPK pathway

doi: 10.3389/fgene.2026.1760431

Figure Lengend Snippet: Upregulation of miR-18a-5p in asthma and its role in promoting ASMC proliferation and migration upon TGF-β1 stimulation. (A) RT-qPCR revealed that miR-18a-5p levels were significantly higher in sputum from asthma patients compared with healthy controls (n = 10). (B) TGF-β1 stimulation induced a dose-dependent increase in miR-18a-5p expression in ASMCs (n = 3). (C) PDGF-BB stimulation significantly altered miR-18a-5p expression in ASMCs in a concentration-dependent manner (n = 3). (D) miR-18a-5p was effectively overexpressed or silenced in ASMCs following transfection with mimics or inhibitors (n = 3). (E) CCK-8 assay showed altered cell viability under different miR-18a-5p expression levels (n = 3). (F) Transwell assay demonstrated that miR-18a-5p regulates the migratory capacity of ASMCs (n = 3). Data are presented as mean ± SD. **p < 0.01 vs. healthy, 0 ng/mL, or Control group; ##p < 0.01 vs. TGF-β1+in-NC or PDGF-BB 5 ng/mL group; &&p < 0.01 vs. TGF-β1+mi-NC or PDGF-BB 10 ng/mL group.

Article Snippet: Solid recombinant human TGF-β1 protein was purchased from MedChemExpress (United States).

Techniques: Migration, Quantitative RT-PCR, Expressing, Concentration Assay, Transfection, CCK-8 Assay, Transwell Assay, Control

Journal: Frontiers in Genetics

Article Title: miR-18a-5p promotes phenotypic transformation of airway smooth muscle cells by targeting SPRY1 to activate the RAS-MAPK pathway

doi: 10.3389/fgene.2026.1760431

Figure Lengend Snippet: miR-18a-5p regulates migration-associated proteins in TGF-β1-stimulated ASMCs. Representative Western blot images and quantitative analysis showed the expression levels of Integrin β1, p-FAK, total FAK, p-Paxillin, total Paxillin, and MMP9. α-Tubulin was used as a loading control. Data are presented as mean ± SD (n = 3). ***p < 0.001 vs. Control group; ###p < 0.001 vs. TGF-β1+in-NC group; &&&p < 0.001 vs. TGF-β1+mi-NC group.

Article Snippet: Solid recombinant human TGF-β1 protein was purchased from MedChemExpress (United States).

Techniques: Migration, Western Blot, Expressing, Control

Journal: Frontiers in Genetics

Article Title: miR-18a-5p promotes phenotypic transformation of airway smooth muscle cells by targeting SPRY1 to activate the RAS-MAPK pathway

doi: 10.3389/fgene.2026.1760431

Figure Lengend Snippet: miR-18a-5p modulates the expression of structural proteins in TGF-β1-induced ASMCs. (A,B) Immunofluorescence staining of α-SMA and Collagen I in ASMCs subjected to different treatments. (C) Representative Western blot images of OPN, α-SMA, Calponin, Collagen I, and Collagen III in ASMCs following different interventions. (D) Quantitative analysis of protein expression levels based on Western blot results. Data are presented as mean ± SD (n = 3). **p < 0.01 vs. Control group; ##p < 0.01 vs. TGF-β1+in-NC group; &&p < 0.01 vs. TGF-β1+mi-NC group.

Article Snippet: Solid recombinant human TGF-β1 protein was purchased from MedChemExpress (United States).

Techniques: Expressing, Immunofluorescence, Staining, Western Blot, Control

Journal: Frontiers in Genetics

Article Title: miR-18a-5p promotes phenotypic transformation of airway smooth muscle cells by targeting SPRY1 to activate the RAS-MAPK pathway

doi: 10.3389/fgene.2026.1760431

Figure Lengend Snippet: miR-18a-5p enhances RAS-MAPK pathway activation in TGF-β1-induced ASMCs. (A) Representative Western blot images of KRAS, MEK1/2, p-MEK1/2, ERK1/2, and p-ERK1/2 protein levels in ASMCs subjected to different treatments. (B) Quantitative analysis of protein expression based on Western blot results. Data are presented as mean ± SD (n = 3). **p < 0.01 vs. Control group; ##p < 0.01 vs. TGF-β1+in-NC group; &&p < 0.01 vs. TGF-β1+mi-NC group.

Article Snippet: Solid recombinant human TGF-β1 protein was purchased from MedChemExpress (United States).

Techniques: Activation Assay, Western Blot, Expressing, Control

Journal: Frontiers in Genetics

Article Title: miR-18a-5p promotes phenotypic transformation of airway smooth muscle cells by targeting SPRY1 to activate the RAS-MAPK pathway

doi: 10.3389/fgene.2026.1760431

Figure Lengend Snippet: miR-18a-5p targets and negatively regulates SPRY1 (A) RT-qPCR analysis of SPRY1 expression in sputum samples from asthma patients and healthy controls (n = 10). (B) Correlation analysis of the relationship between miR-18a-5p and SPRY1 expression levels. (C) RT-qPCR analysis of SPRY1 mRNA expression in ASMCs under different treatment conditions (n = 3). (D) Western blot analysis of SPRY1 protein expression in ASMCs following different interventions (n = 3). (E) Bioinformatic prediction of the putative binding site between miR-18a-5p and the SPRY1 3′UTR. (F) Dual-luciferase reporter assay confirming the direct interaction between miR-18a-5p and SPRY1 (n = 3). Data are presented as mean ± SD. **p < 0.01, ***p < 0.001 vs. healthy, Control or WT + NC-mimics group; ##p < 0.01 vs. TGF-β1+in-NC group; &&p < 0.01 vs. TGF-β1+mi-NC group.

Article Snippet: Solid recombinant human TGF-β1 protein was purchased from MedChemExpress (United States).

Techniques: Quantitative RT-PCR, Expressing, Western Blot, Binding Assay, Luciferase, Reporter Assay, Control

Journal: Frontiers in Genetics

Article Title: miR-18a-5p promotes phenotypic transformation of airway smooth muscle cells by targeting SPRY1 to activate the RAS-MAPK pathway

doi: 10.3389/fgene.2026.1760431

Figure Lengend Snippet: miR-18a-5p promotes TGF-β1-induced phenotypic transformation of ASMCs by targeting SPRY1 and activating the RAS-MAPK signaling pathway. (A) Western blot analysis of SPRY1 protein expression in ASMCs under different treatment conditions. (B) Western blot analysis of KRAS, MEK1/2, p-MEK1/2, ERK1/2, and p-ERK1/2 in ASMCs following different interventions. (C) CCK-8 assay evaluating ASMC viability under various treatment conditions. (D) Transwell assay assessing the migration capacity of ASMCs after different treatments. (E) Western blot analysis of OPN, α-SMA, Calponin, Collagen I, and Collagen III protein levels in ASMCs under different conditions. Data are presented as mean ± SD (n = 3). **p < 0.01 vs. si-NC or TGF-β1 group; ##p < 0.01 vs. TGF-β1+in-miR group; &&p < 0.01 vs. TGF-β1+si-SPRY1 group.

Article Snippet: Solid recombinant human TGF-β1 protein was purchased from MedChemExpress (United States).

Techniques: Transformation Assay, Western Blot, Expressing, CCK-8 Assay, Transwell Assay, Migration

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