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R&D Systems rabbit antip p53

FIGURE 5 PAI-1 induced <t>p53</t> upregulation is critical for the subsequent maladaptive response. A, Western blot assessments for total and p-p53 protein levels between CMV-Con and CMV-PAI-1 populations. B-C, Histograms depicting the relative expression of p53 levels (mean ± SD) for three independent studies, n = 3. D-G, Lysates of CMV-PAI-1+Con-shRNA and CMV-PAI-1+p53-shRNA double transductants are immunoblotted for p53 (D, E; P < .001), p21 (D, F; P < .01), p-H3 (D, G; P < .01), fibronectin (H, I; P < .01), collagen-1 (H, J; P < .01). Histograms in (E-G) and (I-J) depict the relative expression (mean ± SD) for indicated proteins from the immunoblots in (D) and (H), shown as biological triplicates for three independent studies (n = 3). K, Confluent monolayers of CMV-PAI-1+Con-shRNA and CMV-PAI-1+p53- shRNA HK2 cultures are serum-starved for 6 days. Phase contrast and crystal violet images are taken on day 0 and day 6 to assess cell monolayer detachment. Scale bar = 400 µm. L, Western blot analysis for FAK and p-ERK1/2 protein levels between CMV-Con and CMV-PAI-1 cultures, with ERK2 serving as a loading control, (n = 3). *P < .05, **P < .01, ***P < .001

Rabbit Antip P53, 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
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rabbit antip p53 - by Bioz Stars, 2026-06

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1) Product Images from "PAI‐1 induction during kidney injury promotes fibrotic epithelial dysfunction via deregulation of klotho, p53, and TGF‐β1‐receptor signaling"

Article Title: PAI‐1 induction during kidney injury promotes fibrotic epithelial dysfunction via deregulation of klotho, p53, and TGF‐β1‐receptor signaling

Journal: The FASEB Journal

doi: 10.1096/fj.202002652rr

FIGURE 5 PAI-1 induced p53 upregulation is critical for the subsequent maladaptive response. A, Western blot assessments for total and p-p53 protein levels between CMV-Con and CMV-PAI-1 populations. B-C, Histograms depicting the relative expression of p53 levels (mean ± SD) for three independent studies, n = 3. D-G, Lysates of CMV-PAI-1+Con-shRNA and CMV-PAI-1+p53-shRNA double transductants are immunoblotted for p53 (D, E; P < .001), p21 (D, F; P < .01), p-H3 (D, G; P < .01), fibronectin (H, I; P < .01), collagen-1 (H, J; P < .01). Histograms in (E-G) and (I-J) depict the relative expression (mean ± SD) for indicated proteins from the immunoblots in (D) and (H), shown as biological triplicates for three independent studies (n = 3). K, Confluent monolayers of CMV-PAI-1+Con-shRNA and CMV-PAI-1+p53- shRNA HK2 cultures are serum-starved for 6 days. Phase contrast and crystal violet images are taken on day 0 and day 6 to assess cell monolayer detachment. Scale bar = 400 µm. L, Western blot analysis for FAK and p-ERK1/2 protein levels between CMV-Con and CMV-PAI-1 cultures, with ERK2 serving as a loading control, (n = 3). *P < .05, **P < .01, ***P < .001

Figure Legend Snippet: FIGURE 5 PAI-1 induced p53 upregulation is critical for the subsequent maladaptive response. A, Western blot assessments for total and p-p53 protein levels between CMV-Con and CMV-PAI-1 populations. B-C, Histograms depicting the relative expression of p53 levels (mean ± SD) for three independent studies, n = 3. D-G, Lysates of CMV-PAI-1+Con-shRNA and CMV-PAI-1+p53-shRNA double transductants are immunoblotted for p53 (D, E; P < .001), p21 (D, F; P < .01), p-H3 (D, G; P < .01), fibronectin (H, I; P < .01), collagen-1 (H, J; P < .01). Histograms in (E-G) and (I-J) depict the relative expression (mean ± SD) for indicated proteins from the immunoblots in (D) and (H), shown as biological triplicates for three independent studies (n = 3). K, Confluent monolayers of CMV-PAI-1+Con-shRNA and CMV-PAI-1+p53- shRNA HK2 cultures are serum-starved for 6 days. Phase contrast and crystal violet images are taken on day 0 and day 6 to assess cell monolayer detachment. Scale bar = 400 µm. L, Western blot analysis for FAK and p-ERK1/2 protein levels between CMV-Con and CMV-PAI-1 cultures, with ERK2 serving as a loading control, (n = 3). *P < .05, **P < .01, ***P < .001

Techniques Used: Western Blot, Expressing, shRNA, Control

FIGURE 6 Klotho downregulation consequent to PAI-1 induction contributes to epithelial dysfunction. A-C, Immunoblot analysis of CMV- Con and CMV-PAI-1 cell lysates for PAI-1 (A, B; P < .001) and klotho (A, C; P < .01) expression. Histograms in (B-C) represent the relative expression of the indicated proteins as (mean ± SD) for three independent studies (n = 3). D-I, Protein extracts of CMV-PAI-1+CMV-Con and CMV-PAI-1+CMV-Klotho double transgenic cultures are immunoblotted for klotho (D, E; P < .001), CCN2 (D, F; P < .001), p21 (D, G; P < .01), p53 (D, H; P < .001), p-SMAD3 (D, I; P < .01). GAPDH serves as loading control. Histograms in (E-I) depict the relative levels (mean ± SD) of the indicated proteins for three separate experiments (n = 3). **P < .01, ***P < .001

Figure Legend Snippet: FIGURE 6 Klotho downregulation consequent to PAI-1 induction contributes to epithelial dysfunction. A-C, Immunoblot analysis of CMV- Con and CMV-PAI-1 cell lysates for PAI-1 (A, B; P < .001) and klotho (A, C; P < .01) expression. Histograms in (B-C) represent the relative expression of the indicated proteins as (mean ± SD) for three independent studies (n = 3). D-I, Protein extracts of CMV-PAI-1+CMV-Con and CMV-PAI-1+CMV-Klotho double transgenic cultures are immunoblotted for klotho (D, E; P < .001), CCN2 (D, F; P < .001), p21 (D, G; P < .01), p53 (D, H; P < .001), p-SMAD3 (D, I; P < .01). GAPDH serves as loading control. Histograms in (E-I) depict the relative levels (mean ± SD) of the indicated proteins for three separate experiments (n = 3). **P < .01, ***P < .001

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

FIGURE 8 Dysfunction driven by PAI-1 overexpression is independent of TGF-β1 ligand synthesis or release. A, ELISA analysis for active TGF-β1 ligand concentrations in the conditioned media isolated from serum-starved CMV-Con and CMV-PAI-1 cultures. n = 3. B-D, Cytokine protein array analysis of CMV-Con and CMV-PAI-1 conditioned media for active TGF-β1 (B), TGF-β2 (C), and TGF-β3 (D). Graphs depict the relative levels of secreted ligands (mean ± SD), n = 3. E, Immunoblot comparison of fibrotic responses in the cellular lysates of TGF-β1 stimulated or unstimulated CMV-Con and untreated CMV-PAI-1 culture extracted in parallel. F, CMV-Con HK2 cells pretreated with 20 μg/mL of TGF-β1 neutralizing antibody or 20 μg/mL IgY control antisera are stimulated with 2 ng/mL TGF-β1. Cells are harvested after 24 hours and expression of p-SMAD3, fibronectin and E-cadherin are analyzed by western blot. n = 3. G, Equally seeded CMV-PAI-1 HK2s are treated with various concentrations of TGF-β1 neutralizing antibody (0, 20, 40, 60 μg/mL) or 60 μg/mL IgY control antisera for 24 hours prior to western blot analysis of extracts for p-SMAD3, fibronectin, collagen-1, vimentin, p53 and p21, with GAPDH is serving as a loading marker. n = 3, *P < .05, **P < .01, ***P < .001, n.s., not significant. H, Western blot analysis of cell lysate extracts from CMV-PAI-1+Con shRNA and CMV-PAI-1+TGF-β1 shRNA HK2 cells for the indicated fibrotic markers. Cytokine protein array analysis of whole cell lysates (I) and conditioned media (J) used to validate TGF-β1 knockdown

Figure Legend Snippet: FIGURE 8 Dysfunction driven by PAI-1 overexpression is independent of TGF-β1 ligand synthesis or release. A, ELISA analysis for active TGF-β1 ligand concentrations in the conditioned media isolated from serum-starved CMV-Con and CMV-PAI-1 cultures. n = 3. B-D, Cytokine protein array analysis of CMV-Con and CMV-PAI-1 conditioned media for active TGF-β1 (B), TGF-β2 (C), and TGF-β3 (D). Graphs depict the relative levels of secreted ligands (mean ± SD), n = 3. E, Immunoblot comparison of fibrotic responses in the cellular lysates of TGF-β1 stimulated or unstimulated CMV-Con and untreated CMV-PAI-1 culture extracted in parallel. F, CMV-Con HK2 cells pretreated with 20 μg/mL of TGF-β1 neutralizing antibody or 20 μg/mL IgY control antisera are stimulated with 2 ng/mL TGF-β1. Cells are harvested after 24 hours and expression of p-SMAD3, fibronectin and E-cadherin are analyzed by western blot. n = 3. G, Equally seeded CMV-PAI-1 HK2s are treated with various concentrations of TGF-β1 neutralizing antibody (0, 20, 40, 60 μg/mL) or 60 μg/mL IgY control antisera for 24 hours prior to western blot analysis of extracts for p-SMAD3, fibronectin, collagen-1, vimentin, p53 and p21, with GAPDH is serving as a loading marker. n = 3, *P < .05, **P < .01, ***P < .001, n.s., not significant. H, Western blot analysis of cell lysate extracts from CMV-PAI-1+Con shRNA and CMV-PAI-1+TGF-β1 shRNA HK2 cells for the indicated fibrotic markers. Cytokine protein array analysis of whole cell lysates (I) and conditioned media (J) used to validate TGF-β1 knockdown

Techniques Used: Over Expression, Enzyme-linked Immunosorbent Assay, Isolation, Protein Array, Western Blot, Comparison, Control, Expressing, Marker, shRNA, Knockdown

FIGURE 9 Model. PAI-1 upregulation leads to downregulation of klotho, upregulation of p53, and induction of TGF-β1 receptor signaling independent of the TGF-β1 ligand, resulting in expression and secretion of fibrotic markers, downregulation of E-cadherin and upregulation of vimentin, leading to dedifferentiation, and upregulation of p21, p-H3, causing G2/M cell cycle arrest and a propensity to cell death, collectively establishing a role for PAI-1 in tubular epithelial dysfunction. Klotho regulates both p53 and SMAD3 signaling, promoting PAI-1-mediated tubular maladaptive responses

Figure Legend Snippet: FIGURE 9 Model. PAI-1 upregulation leads to downregulation of klotho, upregulation of p53, and induction of TGF-β1 receptor signaling independent of the TGF-β1 ligand, resulting in expression and secretion of fibrotic markers, downregulation of E-cadherin and upregulation of vimentin, leading to dedifferentiation, and upregulation of p21, p-H3, causing G2/M cell cycle arrest and a propensity to cell death, collectively establishing a role for PAI-1 in tubular epithelial dysfunction. Klotho regulates both p53 and SMAD3 signaling, promoting PAI-1-mediated tubular maladaptive responses

Techniques Used: Expressing

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Fig. 1. Impact of Acute NO exposure on RWPE-1 activation of p53 signalling and the DNA damage repair response: (a) Western blot analysis of p53, p21, p16, γH2AX and PARP cleavage 1–48 h post 500 μM DETA/NO treatment; (b) Accumulation of γH2AX foci post 500 μM DETA/NO treatment; (c) Accumulation of 53BP1 foci post 500 μM DETA/NO treatment.

Journal: Nitric oxide : biology and chemistry

Article Title: Chronic nitric oxide exposure induces prostate cell carcinogenesis, involving genetic instability and a pro-tumorigenic secretory phenotype.

doi: 10.1016/j.niox.2022.07.005

Figure Lengend Snippet: Fig. 1. Impact of Acute NO exposure on RWPE-1 activation of p53 signalling and the DNA damage repair response: (a) Western blot analysis of p53, p21, p16, γH2AX and PARP cleavage 1–48 h post 500 μM DETA/NO treatment; (b) Accumulation of γH2AX foci post 500 μM DETA/NO treatment; (c) Accumulation of 53BP1 foci post 500 μM DETA/NO treatment.

Article Snippet: Membranes were blocked in 5% milk (Sigma) or BSA (Sigma in 0.01% TBS-tween) and incubated with primary antibody (1:20000 Anti-β-actin (A5441; Sigma), 1:1000 Anti-Caspase-3 (cleaved) (9665; Cell Signaling Technology), 1:1000 anti-E-cadherin (3195; Cell Signaling Technology), 1:1000 anti-PARP (9542; Cell Signaling Technology), 1:1000 Anti-p16 (550834; BD Pharmingen), 1:1000 Anti-p21Waf1/Cip1 (2947; Cell Signaling Technology), 1:1000 Anti-p27 Kip1 (3688; Cell Signaling Technology), 1:1000 Anti-p53 (DO-1) (F1113; Santa Cruz), 1:1000 Antip-p53 (ser 15) (9284; Cell Signaling Technology), 1:1000 anti-vimentin (5741; Cell Signaling Technology), 1:1000 Anti-γH2AX (07164; Upstate), 1:1000 Anti-Total H2AX (07476; Upstate), 1:1000 anti-vimentin rabbit monoclonal antibody (#5741; Cell Signaling Technology, UK).

Techniques: Activation Assay, Western Blot

Fig. 6. Impact of Chronic NO on resistance to chemotherapeutic agents: RW/NOw cells display reduced cell death compared to control when treated with etoposide (a) or doxorubicin (b) for 72 h (2-way ANOVA with Bonferroni correction; *p < 0.05, **p < 0.01) (c) Phospho-p53, p53 and p21 protein induction was reduced in etoposide treated (50 μM) RW/NO_LT cells compared to control or RW/NOw cells treated with etoposide (24 h). (d) RW/NO_LT maintained similar γH2AX induction in upon etoposide treatment as compared to control cells, indicating DNA damage still occurs; (e) RW/NO_LT and RW/NOw cells treated with etoposide had decreased levels of both cleaved caspase-3 and cleaved PARP as compared to etoposide treated vehicle control cells.

Journal: Nitric oxide : biology and chemistry

Article Title: Chronic nitric oxide exposure induces prostate cell carcinogenesis, involving genetic instability and a pro-tumorigenic secretory phenotype.

doi: 10.1016/j.niox.2022.07.005

Figure Lengend Snippet: Fig. 6. Impact of Chronic NO on resistance to chemotherapeutic agents: RW/NOw cells display reduced cell death compared to control when treated with etoposide (a) or doxorubicin (b) for 72 h (2-way ANOVA with Bonferroni correction; *p < 0.05, **p < 0.01) (c) Phospho-p53, p53 and p21 protein induction was reduced in etoposide treated (50 μM) RW/NO_LT cells compared to control or RW/NOw cells treated with etoposide (24 h). (d) RW/NO_LT maintained similar γH2AX induction in upon etoposide treatment as compared to control cells, indicating DNA damage still occurs; (e) RW/NO_LT and RW/NOw cells treated with etoposide had decreased levels of both cleaved caspase-3 and cleaved PARP as compared to etoposide treated vehicle control cells.

Techniques: Control

Fig. 5. Impact of chronic NO exposure on prolifera tion in serum containing and serum free media: (a) RW/NO_LT and RW/NOw cells have a slightly decreased growth rate as compared to control cells in complete media; (b) Under serum/supplement free conditions, both the RW/NO_LT and RW/NOw cells had the ability to proliferate, whereas the control cells did not. RW/NO_LT and RW/NOw cells had a statistically significant increased proliferation at 8 and 10 days (2 way ANOVA with Bonferroni correc tion p < 0.05); (c) Western blots of phospho-p53, p- 53, p21, p27 and PARP cleavage showed levels were all reduced if not completely abolished in serum free RW/NOw cells as compared to serum free vehicle control cells. p16 levels remain unchanged.

Journal: Nitric oxide : biology and chemistry

Article Title: Chronic nitric oxide exposure induces prostate cell carcinogenesis, involving genetic instability and a pro-tumorigenic secretory phenotype.

doi: 10.1016/j.niox.2022.07.005

Figure Lengend Snippet: Fig. 5. Impact of chronic NO exposure on prolifera tion in serum containing and serum free media: (a) RW/NO_LT and RW/NOw cells have a slightly decreased growth rate as compared to control cells in complete media; (b) Under serum/supplement free conditions, both the RW/NO_LT and RW/NOw cells had the ability to proliferate, whereas the control cells did not. RW/NO_LT and RW/NOw cells had a statistically significant increased proliferation at 8 and 10 days (2 way ANOVA with Bonferroni correc tion p < 0.05); (c) Western blots of phospho-p53, p- 53, p21, p27 and PARP cleavage showed levels were all reduced if not completely abolished in serum free RW/NOw cells as compared to serum free vehicle control cells. p16 levels remain unchanged.

Techniques: Control, Western Blot

Journal: The FASEB Journal

Article Title: PAI‐1 induction during kidney injury promotes fibrotic epithelial dysfunction via deregulation of klotho, p53, and TGF‐β1‐receptor signaling

doi: 10.1096/fj.202002652rr

Figure Lengend Snippet: FIGURE 5 PAI-1 induced p53 upregulation is critical for the subsequent maladaptive response. A, Western blot assessments for total and p-p53 protein levels between CMV-Con and CMV-PAI-1 populations. B-C, Histograms depicting the relative expression of p53 levels (mean ± SD) for three independent studies, n = 3. D-G, Lysates of CMV-PAI-1+Con-shRNA and CMV-PAI-1+p53-shRNA double transductants are immunoblotted for p53 (D, E; P < .001), p21 (D, F; P < .01), p-H3 (D, G; P < .01), fibronectin (H, I; P < .01), collagen-1 (H, J; P < .01). Histograms in (E-G) and (I-J) depict the relative expression (mean ± SD) for indicated proteins from the immunoblots in (D) and (H), shown as biological triplicates for three independent studies (n = 3). K, Confluent monolayers of CMV-PAI-1+Con-shRNA and CMV-PAI-1+p53- shRNA HK2 cultures are serum-starved for 6 days. Phase contrast and crystal violet images are taken on day 0 and day 6 to assess cell monolayer detachment. Scale bar = 400 µm. L, Western blot analysis for FAK and p-ERK1/2 protein levels between CMV-Con and CMV-PAI-1 cultures, with ERK2 serving as a loading control, (n = 3). *P < .05, **P < .01, ***P < .001

Article Snippet: Overnight incubation at 4°C utilized the following primary antibodies; rabbit anti- PAI- 1 (1:3000) and rabbit anti- collagen- 1 (1:5000) as previously described,15 rat anti- klotho (1:5000; Transgenic Inc.- KM2119), rabbit anti- SMAD3 (1:1000; Cell Signaling- 9523), rabbit anti- p- Histone3 (1:1000; Cell Signaling- 9701), rabbit anti- p21 (1:1000; Cell Signaling- 2947), rabbit anti- caspase- 9 (1:1000; Cell Signaling- 9502), rabbit anti- c- caspase- 3 (1:1000; Cell Signaling- 9661), rabbit antiSnail1 (1:1000; Cell Signaling- 38798s), rabbit anti- α- SMA (1:1000; Abcam- ab32575), rabbit anti- phospho- SMAD3 (1:1000; Abcam- ab52903), rabbit anti- fibronectin (1:100,000; Abcam- ab2413), rabbit anti- LOXL2 (1:1000; Abcam- ab96233), rabbit anti- MMP- 9 (1:1000; Abcam- ab38898), rabbit antiMMP- 2 (1:1000; Abcam- ab97779), rabbit anti- VEGF- C (1:1000; Abcam- ab9546), rabbit anti- endothelin- 1 (1:1000; 18201- IBL America, Minneapolis, MN, USA), rabbit antivimentin (1:10,000; Santa Cruz- sc5565), rabbit anti- GAPDH (1:5000; Santa Cruz- sc25778), goat anti- CCN2 (1:500; Santa Cruz- sc14939), rabbit anti- TGF- βRI (1:1000; Santa Cruz- sc9048), rabbit anti- TGF- βRII (1:1000; Santa Cruz- sc220), mouse anti- p53 (1:1000; Santa Cruz- sc126), mouse anti- Ecadherin (1:1000; BD Biosciences- 610181), and rabbit antip- p53 (1:1000; AF1043- R&D systems, Minneapolis, MN, USA).

Techniques: Western Blot, Expressing, shRNA, Control

Journal: The FASEB Journal

Article Title: PAI‐1 induction during kidney injury promotes fibrotic epithelial dysfunction via deregulation of klotho, p53, and TGF‐β1‐receptor signaling

doi: 10.1096/fj.202002652rr

Figure Lengend Snippet: FIGURE 6 Klotho downregulation consequent to PAI-1 induction contributes to epithelial dysfunction. A-C, Immunoblot analysis of CMV- Con and CMV-PAI-1 cell lysates for PAI-1 (A, B; P < .001) and klotho (A, C; P < .01) expression. Histograms in (B-C) represent the relative expression of the indicated proteins as (mean ± SD) for three independent studies (n = 3). D-I, Protein extracts of CMV-PAI-1+CMV-Con and CMV-PAI-1+CMV-Klotho double transgenic cultures are immunoblotted for klotho (D, E; P < .001), CCN2 (D, F; P < .001), p21 (D, G; P < .01), p53 (D, H; P < .001), p-SMAD3 (D, I; P < .01). GAPDH serves as loading control. Histograms in (E-I) depict the relative levels (mean ± SD) of the indicated proteins for three separate experiments (n = 3). **P < .01, ***P < .001

Techniques: Western Blot, Expressing, Transgenic Assay, Control

Journal: The FASEB Journal

Article Title: PAI‐1 induction during kidney injury promotes fibrotic epithelial dysfunction via deregulation of klotho, p53, and TGF‐β1‐receptor signaling

doi: 10.1096/fj.202002652rr

Figure Lengend Snippet: FIGURE 8 Dysfunction driven by PAI-1 overexpression is independent of TGF-β1 ligand synthesis or release. A, ELISA analysis for active TGF-β1 ligand concentrations in the conditioned media isolated from serum-starved CMV-Con and CMV-PAI-1 cultures. n = 3. B-D, Cytokine protein array analysis of CMV-Con and CMV-PAI-1 conditioned media for active TGF-β1 (B), TGF-β2 (C), and TGF-β3 (D). Graphs depict the relative levels of secreted ligands (mean ± SD), n = 3. E, Immunoblot comparison of fibrotic responses in the cellular lysates of TGF-β1 stimulated or unstimulated CMV-Con and untreated CMV-PAI-1 culture extracted in parallel. F, CMV-Con HK2 cells pretreated with 20 μg/mL of TGF-β1 neutralizing antibody or 20 μg/mL IgY control antisera are stimulated with 2 ng/mL TGF-β1. Cells are harvested after 24 hours and expression of p-SMAD3, fibronectin and E-cadherin are analyzed by western blot. n = 3. G, Equally seeded CMV-PAI-1 HK2s are treated with various concentrations of TGF-β1 neutralizing antibody (0, 20, 40, 60 μg/mL) or 60 μg/mL IgY control antisera for 24 hours prior to western blot analysis of extracts for p-SMAD3, fibronectin, collagen-1, vimentin, p53 and p21, with GAPDH is serving as a loading marker. n = 3, *P < .05, **P < .01, ***P < .001, n.s., not significant. H, Western blot analysis of cell lysate extracts from CMV-PAI-1+Con shRNA and CMV-PAI-1+TGF-β1 shRNA HK2 cells for the indicated fibrotic markers. Cytokine protein array analysis of whole cell lysates (I) and conditioned media (J) used to validate TGF-β1 knockdown

Techniques: Over Expression, Enzyme-linked Immunosorbent Assay, Isolation, Protein Array, Western Blot, Comparison, Control, Expressing, Marker, shRNA, Knockdown

Journal: The FASEB Journal

Article Title: PAI‐1 induction during kidney injury promotes fibrotic epithelial dysfunction via deregulation of klotho, p53, and TGF‐β1‐receptor signaling

doi: 10.1096/fj.202002652rr

Figure Lengend Snippet: FIGURE 9 Model. PAI-1 upregulation leads to downregulation of klotho, upregulation of p53, and induction of TGF-β1 receptor signaling independent of the TGF-β1 ligand, resulting in expression and secretion of fibrotic markers, downregulation of E-cadherin and upregulation of vimentin, leading to dedifferentiation, and upregulation of p21, p-H3, causing G2/M cell cycle arrest and a propensity to cell death, collectively establishing a role for PAI-1 in tubular epithelial dysfunction. Klotho regulates both p53 and SMAD3 signaling, promoting PAI-1-mediated tubular maladaptive responses

Techniques: Expressing

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1) Product Images from "PAI‐1 induction during kidney injury promotes fibrotic epithelial dysfunction via deregulation of klotho, p53, and TGF‐β1‐receptor signaling"

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