Review

tgf β2 neutralizing antibody (R&D Systems)

R&D Systems is a verified supplier

R&D Systems manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

R&D Systems tgf β2 neutralizing antibody
Tgf β2 Neutralizing Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 24 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tgf+%CE%B22/TGF-beta+2+Antibody/pmc12859453-497-243-246
Average 93 stars, based on 24 article reviews

tgf β2 neutralizing antibody - by Bioz Stars, 2026-09

93/100 stars

Images

Expressing:

Article Title: Physiological activation of liver X receptor provides protection against ocular inflammation in uveitic glaucoma
Article Snippet: .. To identify external inputs affecting the expression of LXRα, LXRβ, and ABCA1 in human TM cells, we evaluated the effects of physiologic agents previously implicated in the pathobiology of glaucoma, namely: LXR agonist, T091317 (10 μM, 48 hours; cat no. 71810–10, Cayman Chemical, Ann Arbor, Michigan, USA), TGF-β1 (10 ng/ml, 24 hours; cat no. 240-B, R&D Systems, Minneapolis MN), TGF-β2 (10 ng/ml, 24 hours; cat no. 302-B2, R&D Systems), lipopolysaccharide (LPS; 100 ng/ml, 48 hours; cat no. L5293, Sigma-Aldrich, Gillingham, UK). .. To assess the anti-inflammatory effects of LXRs, cells were additionally co-treated with T091317 (10 μM, 48 hours) or dexamethasone (100 nM, 48 hours; cat no. D4902, Sigma-Aldrich) in the presence of LPS stimulation (100 ng/ml, 48 hours) ( Supplementary Figure 6 ).

Article Title: Physiological activation of liver X receptor provides protection against ocular inflammation in uveitic glaucoma.
Article Snippet: Virus-induced trabeculitis is considered a significant cause of uveitic glaucoma, being marked by a sudden increase in intraocular pressure and relatively mild inflammation in the anterior chamber of the eye.. In previous proteome analyses of aqueous humor (AH) derived from Cytomegalovirus (CMV) uveitic glaucoma patients, we observed the liver X receptor (LXR) pathway to be among the most prominently activated canonical pathways.. In the present study, we explored the role of the LXR pathway in the etiology of glaucoma in association with ocular inflammation.

Control:

Article Title: TGFβ signaling regulates the response of the skeleton to phosphate
Article Snippet: Small molecule inhibitors (FGFR1 inhibitor, PD173074, 100nM, Cayman; TGFβRI inhibitor, SB525334, 80nM, Selleck Chemicals; MEK inhibitor, U0126, 10μM, Cell Signaling Technologies) or vehicle controls were added 30 minutes prior to addition of added NaPi. .. For treatment with TGF-β ligands, cells underwent a 30 minute or 1 hour pre-treatment in duplicate or triplicate with either a vehicle control (4mM HCl + 0.1% BSA) or 0.4 ng/ml recombinant mouse TGF-β1, TGF-β2, or TGF-β3 protein (TGF-β1, R&D Systems; TGF-β2, R&D Systems; TGF-β3, Sigma-Aldrich). ..

Recombinant:

Article Title: EPHB2 promotes diet-induced MASH liver fibrosis
Article Snippet: .. Subsequently, HSCs were serum-starved overnight in Dulbecco’s Modified Eagle Medium/F12 (DMEM/F12) containing 0.5% Bovine Serum Albumin (BSA) and exposed to recombinant human TGF-β1, TGF-β2, and TGF-β3 all at 10 ng/ml (R&D Systems) for 3h, 6h, 12h, 24h, and 48h. ..

Article Title: Transforming growth factor-β isoforms drive common and distinct signaling pathways in dermal fibroblasts: insights into the signaling diversity in keloid pathogenesis
Article Snippet: .. The medium was then replaced with serum- and antibiotic-free DMEM, and cells were stimulated with 5 ng/mL of recombinant human TGF-β1, TGF-β2, or TGFβ3 (R&D Systems, USA) in separate wells, with three biological replicates per condition. .. After 24 hours of stimulation, the total RNA was extracted from the cells using RNAiso Plus reagent (Takara, Japan) according to manufacturer’s instructions.

Modification:

Image Search Results

KGN@PB@CM modulates macrophage polarization and restores immune homeostasis in vitro. (A) Representative immunofluorescence images showing iNOS (M1 marker, red) expression in RAW 264.7 macrophages under different treatment conditions. DAPI (blue) was used for nuclear staining. (B) Quantitative analysis of iNOS fluorescence intensity. (C) Representative dual-staining images for CD206 (M2 marker, green) and F4/80 (pan-macrophage marker, red). (D) Quantification of CD86 (M1 marker) fluorescence intensity. (E) Representative immunofluorescence images showing CD206 + F4/80 + macrophages in different groups. (F) Quantitative analysis of CD206 fluorescence intensity. (G to L) RT-qPCR analysis of M1-related genes ( iNOS , CD86 , TNF-α , and IL-6 ) and M2-related genes ( Arg-1 , CD206 , and IL-10 ) in different treatment groups. (M to Q) ELISA results showing the concentrations of inflammatory cytokines IL-1β, IL-6, TNF-α and anti-inflammatory cytokines IL-10 and TGF-β1 in macrophage supernatants. Data are presented as means ± SD, n = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Journal: Cyborg and Bionic Systems

Article Title: Bioinspired Nanocomposite for Targeted Immunoengineering and Improved Tendon Regeneration

doi: 10.34133/cbsystems.0503

Figure Lengend Snippet: KGN@PB@CM modulates macrophage polarization and restores immune homeostasis in vitro. (A) Representative immunofluorescence images showing iNOS (M1 marker, red) expression in RAW 264.7 macrophages under different treatment conditions. DAPI (blue) was used for nuclear staining. (B) Quantitative analysis of iNOS fluorescence intensity. (C) Representative dual-staining images for CD206 (M2 marker, green) and F4/80 (pan-macrophage marker, red). (D) Quantification of CD86 (M1 marker) fluorescence intensity. (E) Representative immunofluorescence images showing CD206 + F4/80 + macrophages in different groups. (F) Quantitative analysis of CD206 fluorescence intensity. (G to L) RT-qPCR analysis of M1-related genes ( iNOS , CD86 , TNF-α , and IL-6 ) and M2-related genes ( Arg-1 , CD206 , and IL-10 ) in different treatment groups. (M to Q) ELISA results showing the concentrations of inflammatory cytokines IL-1β, IL-6, TNF-α and anti-inflammatory cytokines IL-10 and TGF-β1 in macrophage supernatants. Data are presented as means ± SD, n = 5; * P < 0.05, ** P < 0.01, *** P < 0.001, and **** P < 0.0001.

Article Snippet: IL-1β, IL-6, TNF-α, IL-10, and TGF-β1 levels were assessed by ELISA kits (MULTI SCIENCES, China) following the manufacturer’s instructions.

Techniques: In Vitro, Immunofluorescence, Marker, Expressing, Staining, Fluorescence, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

Wild-type C57BL/6 mice (n=12/group) were injected intravitreally with either LV-TGF-β2 or LV-null vectors. ( A ) Weekly IOP measurements demonstrate significant and sustained IOP elevation in LV-TGF-β2-injected mice compared with LV-null controls. ( B ) Immunofluorescence staining of anterior segment cross-sections for α-SMA and MIF shows co-localization of MIF with the TM marker α-SMA, indicating increased MIF expression in the TM of LV-TGF-β2 injected mice. ( C-E ) qPCR ( C ) and western blot ( D, E ) analyses of anterior segment tissues show upregulation of MIF and CD74 accompanied by suppression of Blimp-1 in LV-TGF-β2-injected mice. Increased expression of profibrotic markers, including α-SMA, Fn-1, and MYOC, was also evident in LV-TGF-β2-injected mice. Western blot bands were quantified by densitometric analysis using ImageJ and normalized to the housekeeping control β-actin, and protein levels are presented as relative expression (AU) ( E ). Data represent mean ± SD. **p<0.005, ***p<0.0005, and ****p<0.0001. Two-way ANOVA with Tukey’s multiple-comparison test (A), unpaired t-test (C, E).

Journal: bioRxiv

Article Title: Macrophage Migration Inhibitory Factor (MIF)-CD74 Signaling Pathway Mediates Trabecular Meshwork Dysfunction in Glaucoma

doi: 10.64898/2026.03.18.712673

Figure Lengend Snippet: Wild-type C57BL/6 mice (n=12/group) were injected intravitreally with either LV-TGF-β2 or LV-null vectors. ( A ) Weekly IOP measurements demonstrate significant and sustained IOP elevation in LV-TGF-β2-injected mice compared with LV-null controls. ( B ) Immunofluorescence staining of anterior segment cross-sections for α-SMA and MIF shows co-localization of MIF with the TM marker α-SMA, indicating increased MIF expression in the TM of LV-TGF-β2 injected mice. ( C-E ) qPCR ( C ) and western blot ( D, E ) analyses of anterior segment tissues show upregulation of MIF and CD74 accompanied by suppression of Blimp-1 in LV-TGF-β2-injected mice. Increased expression of profibrotic markers, including α-SMA, Fn-1, and MYOC, was also evident in LV-TGF-β2-injected mice. Western blot bands were quantified by densitometric analysis using ImageJ and normalized to the housekeeping control β-actin, and protein levels are presented as relative expression (AU) ( E ). Data represent mean ± SD. **p<0.005, ***p<0.0005, and ****p<0.0001. Two-way ANOVA with Tukey’s multiple-comparison test (A), unpaired t-test (C, E).

Article Snippet: Recombinant human TGF-β2 (302-B2-010/CF) protein was purchased from R&D Systems (Minneapolis, MN).

Techniques: Injection, Immunofluorescence, Staining, Marker, Expressing, Western Blot, Control, Comparison

Primary HTMCs (n=3) were challenged with TGF-β2 (10ng/mL), rMIF (100ng/mL), or pro-inflammatory cytokine pool (CP; TNF-α, IL-1β, IL-6, and IL-17 100ng/mL) for 24h. (A) qPCR analysis shows significant upregulation of MIF and CD74 transcripts accompanied by reduced Blimp-1 expression in response to glaucomatous stressors. ( B ) Immunofluorescence staining demonstrates increased MIF expression following TGF-β2 or CP treatment. (C) Western blot analysis confirms induction of MIF and CD74 with concurrent suppression of Blimp-1 at the protein level. Data represent mean ± SD. **p<0.005, ***p<0.0005, and ***p<0.0001, One-way ANOVA with Dunnett’s multiple-comparison test.

Journal: bioRxiv

Article Title: Macrophage Migration Inhibitory Factor (MIF)-CD74 Signaling Pathway Mediates Trabecular Meshwork Dysfunction in Glaucoma

doi: 10.64898/2026.03.18.712673

Figure Lengend Snippet: Primary HTMCs (n=3) were challenged with TGF-β2 (10ng/mL), rMIF (100ng/mL), or pro-inflammatory cytokine pool (CP; TNF-α, IL-1β, IL-6, and IL-17 100ng/mL) for 24h. (A) qPCR analysis shows significant upregulation of MIF and CD74 transcripts accompanied by reduced Blimp-1 expression in response to glaucomatous stressors. ( B ) Immunofluorescence staining demonstrates increased MIF expression following TGF-β2 or CP treatment. (C) Western blot analysis confirms induction of MIF and CD74 with concurrent suppression of Blimp-1 at the protein level. Data represent mean ± SD. **p<0.005, ***p<0.0005, and ***p<0.0001, One-way ANOVA with Dunnett’s multiple-comparison test.

Article Snippet: Recombinant human TGF-β2 (302-B2-010/CF) protein was purchased from R&D Systems (Minneapolis, MN).

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

Primary HTMCs (n=3) were challenged with rMIF (100 ng/mL) in the presence or absence of MIF inhibitor 4-IPP (100µM) or the metabolites Agm or Thia (100 ng/mL) for 24h. Cells treated with TGF-β2 (10ng/mL) served as a positive control. (A-B) Western blot analysis confirms activation of the RhoA/ROCK/pMLC signaling pathway in response to MIF treatment, which is significantly attenuated by MIF inhibition with 4-IPP, Agm, or Thia ( A ). Western blot bands were quantified by densitometric analysis using ImageJ and normalized to the housekeeping control β-actin, and protein levels are presented as relative expression (AU) ( B ). (C) Immunofluorescence analysis shows that MIF induces pMLC staining, comparable to that observed with TGF-β2 stimulation, which is significantly attenuated by MIF inhibition with 4-IPP, Agm, or Thia. Data represent mean ± SD. *p<0.05, **p<0.005, ***p<0.0005, and ****p<0.0001, One-way ANOVA with Dunnett’s multiple-comparison test.

Journal: bioRxiv

Article Title: Macrophage Migration Inhibitory Factor (MIF)-CD74 Signaling Pathway Mediates Trabecular Meshwork Dysfunction in Glaucoma

doi: 10.64898/2026.03.18.712673

Figure Lengend Snippet: Primary HTMCs (n=3) were challenged with rMIF (100 ng/mL) in the presence or absence of MIF inhibitor 4-IPP (100µM) or the metabolites Agm or Thia (100 ng/mL) for 24h. Cells treated with TGF-β2 (10ng/mL) served as a positive control. (A-B) Western blot analysis confirms activation of the RhoA/ROCK/pMLC signaling pathway in response to MIF treatment, which is significantly attenuated by MIF inhibition with 4-IPP, Agm, or Thia ( A ). Western blot bands were quantified by densitometric analysis using ImageJ and normalized to the housekeeping control β-actin, and protein levels are presented as relative expression (AU) ( B ). (C) Immunofluorescence analysis shows that MIF induces pMLC staining, comparable to that observed with TGF-β2 stimulation, which is significantly attenuated by MIF inhibition with 4-IPP, Agm, or Thia. Data represent mean ± SD. *p<0.05, **p<0.005, ***p<0.0005, and ****p<0.0001, One-way ANOVA with Dunnett’s multiple-comparison test.

Article Snippet: Recombinant human TGF-β2 (302-B2-010/CF) protein was purchased from R&D Systems (Minneapolis, MN).

Techniques: Positive Control, Western Blot, Activation Assay, Inhibition, Control, Expressing, Immunofluorescence, Staining, Comparison

OHT was induced in WT C57BL/6 mice (n=12) by intravitreal injection of LV-TGF-β2. LV-null-injected mcie served as controls. Following OHT induction, extracellular vesicle-loaded agmatine (EV-Agm; 0.1 µg/eye) was applied topically once daily. (A) Weekly IOP measurements over 9 weeks show that EV-Agm treatment significantly reduces IOP compared with untreated LV-TGF-β2-injected mice. (B) qPCR analysis of anterior segment tissue demonstrates that EV-Agm significantly reduces expression of Mif, Cd74, pro-inflammatory cytokines ( Il-1 β , Il-6 ), and cytoskeletal/ECM markers (α -Sma, Myoc, Fn-1 ), while restoring Blimp-1 expression compared with untreated LV-TGF-β2-injected mice. *p<0.05, **p<0.005, ###,***p<0.0005, and ####,****p<0.0001. Two-way ANOVA with Tukey’s multiple comparison (A), one-way ANOVA with Tukey’s multiple comparison (B). In panel A, * denotes LV-null vs. LV-TGF-β2, and # denotes LV-TGF-β2 vs. LV-TGF-β2+EV-Agm comparisons.

Journal: bioRxiv

Article Title: Macrophage Migration Inhibitory Factor (MIF)-CD74 Signaling Pathway Mediates Trabecular Meshwork Dysfunction in Glaucoma

doi: 10.64898/2026.03.18.712673

Figure Lengend Snippet: OHT was induced in WT C57BL/6 mice (n=12) by intravitreal injection of LV-TGF-β2. LV-null-injected mcie served as controls. Following OHT induction, extracellular vesicle-loaded agmatine (EV-Agm; 0.1 µg/eye) was applied topically once daily. (A) Weekly IOP measurements over 9 weeks show that EV-Agm treatment significantly reduces IOP compared with untreated LV-TGF-β2-injected mice. (B) qPCR analysis of anterior segment tissue demonstrates that EV-Agm significantly reduces expression of Mif, Cd74, pro-inflammatory cytokines ( Il-1 β , Il-6 ), and cytoskeletal/ECM markers (α -Sma, Myoc, Fn-1 ), while restoring Blimp-1 expression compared with untreated LV-TGF-β2-injected mice. *p<0.05, **p<0.005, ###,***p<0.0005, and ####,****p<0.0001. Two-way ANOVA with Tukey’s multiple comparison (A), one-way ANOVA with Tukey’s multiple comparison (B). In panel A, * denotes LV-null vs. LV-TGF-β2, and # denotes LV-TGF-β2 vs. LV-TGF-β2+EV-Agm comparisons.

Article Snippet: Recombinant human TGF-β2 (302-B2-010/CF) protein was purchased from R&D Systems (Minneapolis, MN).

Techniques: Injection, Expressing, Comparison

GO and KEGG pathway enrichment analyses of DEGs in MCF-7 cells after GGCT knockdown. (A) GO enrichment analysis for biological processes (up-regulated and down-regulated genes), and KEGG pathway analysis of DEGs, using samples collected 3 days after knockdown. The top 10 biological process terms ranked according to p-Values are shown. (B) Hypothetical schema of cell cycle regulation following GGCT knockdown in MCF-7 cells, constructed based on DEGs enriched in the KEGG pathway ‘hsa04110: Cell cycle’ (http://www.kegg.jp). (C) Relative mRNA expression patterns of GGCT, TGF-β2, CDKN1A (p21 Cip1 ), and CDKN2B (p15 INK4b ) were measured with qRT-PCR. n=3 per group; *p<0.05, **p<0.01, and ***p<0.001 using two-tailed Student’s t-test for pairwise comparisons. CDKN1A, Cyclin dependent kinase inhibitor 1A; CDKN2B, cyclin dependent kinase inhibitor 2B; DEGs, differentially expressed genes; GGCT, γ-glutamylcyclotransferase; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; qRT-PCR, quantitative reverse-transcription-polymerase chain reaction; TGF-β2, transforming growth factor-β2.

Journal: Cancer Genomics & Proteomics

Article Title: γ-Glutamylcyclotransferase Depletion Induces p15INK4b and p21Cip1-mediated Senescence via TGF-β2/SMAD3 Pathway Activation in Breast Cancer Cells

doi: 10.21873/cgp.20571

Figure Lengend Snippet: GO and KEGG pathway enrichment analyses of DEGs in MCF-7 cells after GGCT knockdown. (A) GO enrichment analysis for biological processes (up-regulated and down-regulated genes), and KEGG pathway analysis of DEGs, using samples collected 3 days after knockdown. The top 10 biological process terms ranked according to p-Values are shown. (B) Hypothetical schema of cell cycle regulation following GGCT knockdown in MCF-7 cells, constructed based on DEGs enriched in the KEGG pathway ‘hsa04110: Cell cycle’ (http://www.kegg.jp). (C) Relative mRNA expression patterns of GGCT, TGF-β2, CDKN1A (p21 Cip1 ), and CDKN2B (p15 INK4b ) were measured with qRT-PCR. n=3 per group; *p<0.05, **p<0.01, and ***p<0.001 using two-tailed Student’s t-test for pairwise comparisons. CDKN1A, Cyclin dependent kinase inhibitor 1A; CDKN2B, cyclin dependent kinase inhibitor 2B; DEGs, differentially expressed genes; GGCT, γ-glutamylcyclotransferase; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; qRT-PCR, quantitative reverse-transcription-polymerase chain reaction; TGF-β2, transforming growth factor-β2.

Article Snippet: Antibodies against various proteins were obtained from the following sources: mouse monoclonal antibodies; p15 INK4b (1:500; cat. no. sc-271791; Santa Cruz Biotechnology, Dallas, TX, USA); p21 WAF1/CIP1 (1:500; cat. no. 556430; BD Biosciences, San Jose, CA, USA); α-tubulin (1:1,000; cat. no. T9026; Sigma–Aldrich Co. LCC, Tokyo, Japan); GGCT (1:500; cat. no. HPA020735; Sigma–Aldrich Co. LCC); TGF-β2 (1:1,000; cat no. 19999-1-AP; Proteintech, Rosemont, IL, USA), phospho-SMAD2 (1:500; cat. no. 3108; Cell Signaling Technology, Danvers, MA, USA); phospho-SMAD3 (1:500; cat. no. 9520; Cell Signaling Technology); SMAD2/3 (1:500; cat. no. 3102; Cell Signaling Technology).

Techniques: Knockdown, Construct, Expressing, Quantitative RT-PCR, Two Tailed Test, Reverse Transcription, Polymerase Chain Reaction

TGF-β2/SMAD signaling axis regulates p15 INK4b and p21 Cip1 expression in GGCT-depleted MCF-7 cells. (A) mRNA expression levels of GGCT and TGF-β2 were analyzed by qRT-PCR 3 days after transfection with GGCT- and/or TGF-β2-siRNA. (B) Western blot analysis of GGCT and TGF-β2 expression 4 days after transfection with GGCT- and/or TGF-β2-siRNA. (C) Western blotting analysis of p15 INK4b , p21 Cip1 , phospho-SMAD2 (pSMAD2), SMAD2, phospho-SMAD3 (pSMAD3), SMAD3, GGCT, and α-tubulin in MCF-7 at 4 days after transfection with GGCT-siRNA and/or TGF-β2-siRNA, or non-target control siRNA. (D) Western blotting analysis of p15 INK4b , p21 Cip1 , pSMAD3, SMAD3, GGCT, and α-tubulin in MCF-7 cells at 4 days after transfection with GGCT-siRNA and/ or SMAD3-siRNA, or non-target control siRNA. (E) The number of viable cells in the trypan blue dye exclusion test and (F) representative images of MCF- 7 cells at 4 days after transfection with the indicated siRNAs. Scale bar: 200 μm; n=3 per group; *p<0.05, **p<0.01, and ***p<0.001 vs. control, †p<0.05; ††p<0.01, and †††p<0.001 vs. GGCT, one-way ANOVA followed by Tukey’s post hoc test. ANOVA, Analysis of variance; GGCT, γ-glutamylcyclotransferase; pSMAD, phosphorylated SMAD; qRT-PCR, quantitative reverse-transcription-polymerase chain reaction; siRNA, small-interfering RNA.

Journal: Cancer Genomics & Proteomics

Article Title: γ-Glutamylcyclotransferase Depletion Induces p15INK4b and p21Cip1-mediated Senescence via TGF-β2/SMAD3 Pathway Activation in Breast Cancer Cells

doi: 10.21873/cgp.20571

Figure Lengend Snippet: TGF-β2/SMAD signaling axis regulates p15 INK4b and p21 Cip1 expression in GGCT-depleted MCF-7 cells. (A) mRNA expression levels of GGCT and TGF-β2 were analyzed by qRT-PCR 3 days after transfection with GGCT- and/or TGF-β2-siRNA. (B) Western blot analysis of GGCT and TGF-β2 expression 4 days after transfection with GGCT- and/or TGF-β2-siRNA. (C) Western blotting analysis of p15 INK4b , p21 Cip1 , phospho-SMAD2 (pSMAD2), SMAD2, phospho-SMAD3 (pSMAD3), SMAD3, GGCT, and α-tubulin in MCF-7 at 4 days after transfection with GGCT-siRNA and/or TGF-β2-siRNA, or non-target control siRNA. (D) Western blotting analysis of p15 INK4b , p21 Cip1 , pSMAD3, SMAD3, GGCT, and α-tubulin in MCF-7 cells at 4 days after transfection with GGCT-siRNA and/ or SMAD3-siRNA, or non-target control siRNA. (E) The number of viable cells in the trypan blue dye exclusion test and (F) representative images of MCF- 7 cells at 4 days after transfection with the indicated siRNAs. Scale bar: 200 μm; n=3 per group; *p<0.05, **p<0.01, and ***p<0.001 vs. control, †p<0.05; ††p<0.01, and †††p<0.001 vs. GGCT, one-way ANOVA followed by Tukey’s post hoc test. ANOVA, Analysis of variance; GGCT, γ-glutamylcyclotransferase; pSMAD, phosphorylated SMAD; qRT-PCR, quantitative reverse-transcription-polymerase chain reaction; siRNA, small-interfering RNA.

Techniques: Expressing, Quantitative RT-PCR, Transfection, Western Blot, Control, Reverse Transcription, Polymerase Chain Reaction, Small Interfering RNA

p15 INK4b , p21 Cip1 , and their upstream regulator TGF-β2 are involved in the induction of cellular senescence following GGCT-KD in MCF-7 cells. (A) Representative images of SA-β-Gal staining 4 days after transfection with the indicated siRNAs, including simultaneous knockdown of GGCT, p15, and p21. Scale bar: 50 μm. (B) The proportion of SA-β-Gal-positive cells in MCF-7 cells are shown. (C) Representative images of SA-β-Gal staining at 4 days after transfection with the indicated siRNAs, including simultaneous knockdown of GGCT and TGF-β2. Scale bar: 50 μm. (D) The proportion of SA-β-Gal-positive cells in MCF-7 cells are shown. n=3 per group; *p<0.05, **p<0.01, ***p<0.001, using one-way ANOVA followed by Tukey’s post hoc test. ANOVA, Analysis of variance; GGCT, γ-glutamylcyclotransferase; KD, knockdown; SA-β-Gal, senescence-associated β-galactosidase; siRNA, smallinterfering RNA; TGF-β2, transforming growth factor-β2.

Journal: Cancer Genomics & Proteomics

Article Title: γ-Glutamylcyclotransferase Depletion Induces p15INK4b and p21Cip1-mediated Senescence via TGF-β2/SMAD3 Pathway Activation in Breast Cancer Cells

doi: 10.21873/cgp.20571

Figure Lengend Snippet: p15 INK4b , p21 Cip1 , and their upstream regulator TGF-β2 are involved in the induction of cellular senescence following GGCT-KD in MCF-7 cells. (A) Representative images of SA-β-Gal staining 4 days after transfection with the indicated siRNAs, including simultaneous knockdown of GGCT, p15, and p21. Scale bar: 50 μm. (B) The proportion of SA-β-Gal-positive cells in MCF-7 cells are shown. (C) Representative images of SA-β-Gal staining at 4 days after transfection with the indicated siRNAs, including simultaneous knockdown of GGCT and TGF-β2. Scale bar: 50 μm. (D) The proportion of SA-β-Gal-positive cells in MCF-7 cells are shown. n=3 per group; *p<0.05, **p<0.01, ***p<0.001, using one-way ANOVA followed by Tukey’s post hoc test. ANOVA, Analysis of variance; GGCT, γ-glutamylcyclotransferase; KD, knockdown; SA-β-Gal, senescence-associated β-galactosidase; siRNA, smallinterfering RNA; TGF-β2, transforming growth factor-β2.

Techniques: Staining, Transfection, Knockdown

Review

tgf β2 neutralizing antibody (R&D Systems)

Structured Review

Images

Related Articles

Expressing:

Control:

Recombinant:

Modification:

Similar Products

Image Search Results