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PUM2 knockdown inhibits viability in H9C2 cells. (A) Reverse <t>transcription-quantitative</t> PCR results after PUM2 knockdown. (B) Representative western blot bands after PUM2 knockdown. (C) PUM2 inhibited viability at 48 and 72 h after transfection. ** P≤0.01 and **** P<0.0001. PUM2, pumilio RNA-binding family member 2; NC, negative control; DSI, dicer-substrate small interfering RNA.
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PUM2 knockdown inhibits viability in H9C2 cells. (A) Reverse <t>transcription-quantitative</t> PCR results after PUM2 knockdown. (B) Representative western blot bands after PUM2 knockdown. (C) PUM2 inhibited viability at 48 and 72 h after transfection. ** P≤0.01 and **** P<0.0001. PUM2, pumilio RNA-binding family member 2; NC, negative control; DSI, dicer-substrate small interfering RNA.
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PUM2 knockdown inhibits viability in H9C2 cells. (A) Reverse <t>transcription-quantitative</t> PCR results after PUM2 knockdown. (B) Representative western blot bands after PUM2 knockdown. (C) PUM2 inhibited viability at 48 and 72 h after transfection. ** P≤0.01 and **** P<0.0001. PUM2, pumilio RNA-binding family member 2; NC, negative control; DSI, dicer-substrate small interfering RNA.
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PUM2 knockdown inhibits viability in H9C2 cells. (A) Reverse <t>transcription-quantitative</t> PCR results after PUM2 knockdown. (B) Representative western blot bands after PUM2 knockdown. (C) PUM2 inhibited viability at 48 and 72 h after transfection. ** P≤0.01 and **** P<0.0001. PUM2, pumilio RNA-binding family member 2; NC, negative control; DSI, dicer-substrate small interfering RNA.
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Regulatory role of NR4A1 in TGF-β signaling in normal, IPF, and estrogen treatment conditions (A) Under normal physiological conditions, brief TGF-β stimulation induces the upregulation of NR4A1. NR4A1 then suppresses epithelial-mesenchymal transition (EMT) and collagen deposition via a negative feedback mechanism. (B) In the IPF state, sustained TGF-β signaling leads to prolonged EMT and collagen deposition, while promoting NR4A1 phosphorylation, which disables its negative feedback regulation of TGF-β signaling. (C) Estrogen treatment enhances NR4A1 <t>transcription</t> and inhibits NR4A1 phosphorylation, thereby restoring its negative feedback regulation on TGF-β signaling.
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PUM2 knockdown inhibits viability in H9C2 cells. (A) Reverse transcription-quantitative PCR results after PUM2 knockdown. (B) Representative western blot bands after PUM2 knockdown. (C) PUM2 inhibited viability at 48 and 72 h after transfection. ** P≤0.01 and **** P<0.0001. PUM2, pumilio RNA-binding family member 2; NC, negative control; DSI, dicer-substrate small interfering RNA.

Journal: Experimental and Therapeutic Medicine

Article Title: PUM2 knockdown regulates the expression and alternative splicing of genes associated with myocardial fibrosis in H9C2 cells

doi: 10.3892/etm.2026.13089

Figure Lengend Snippet: PUM2 knockdown inhibits viability in H9C2 cells. (A) Reverse transcription-quantitative PCR results after PUM2 knockdown. (B) Representative western blot bands after PUM2 knockdown. (C) PUM2 inhibited viability at 48 and 72 h after transfection. ** P≤0.01 and **** P<0.0001. PUM2, pumilio RNA-binding family member 2; NC, negative control; DSI, dicer-substrate small interfering RNA.

Article Snippet: The integrity of RNA was further verified by 1.0% agarose gel electrophoresis. cDNA was synthesized utilizing a reverse transcription kit (cat. no. R323-01; Vazyme Biotech Co., Ltd.).

Techniques: Knockdown, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Transfection, RNA Binding Assay, Negative Control, Small Interfering RNA

Regulatory role of NR4A1 in TGF-β signaling in normal, IPF, and estrogen treatment conditions (A) Under normal physiological conditions, brief TGF-β stimulation induces the upregulation of NR4A1. NR4A1 then suppresses epithelial-mesenchymal transition (EMT) and collagen deposition via a negative feedback mechanism. (B) In the IPF state, sustained TGF-β signaling leads to prolonged EMT and collagen deposition, while promoting NR4A1 phosphorylation, which disables its negative feedback regulation of TGF-β signaling. (C) Estrogen treatment enhances NR4A1 transcription and inhibits NR4A1 phosphorylation, thereby restoring its negative feedback regulation on TGF-β signaling.

Journal: iScience

Article Title: Estrogen upregulates NR4A1 to counter TGF beta induced pulmonary fibrosis therapeutic insights for IPF

doi: 10.1016/j.isci.2026.114756

Figure Lengend Snippet: Regulatory role of NR4A1 in TGF-β signaling in normal, IPF, and estrogen treatment conditions (A) Under normal physiological conditions, brief TGF-β stimulation induces the upregulation of NR4A1. NR4A1 then suppresses epithelial-mesenchymal transition (EMT) and collagen deposition via a negative feedback mechanism. (B) In the IPF state, sustained TGF-β signaling leads to prolonged EMT and collagen deposition, while promoting NR4A1 phosphorylation, which disables its negative feedback regulation of TGF-β signaling. (C) Estrogen treatment enhances NR4A1 transcription and inhibits NR4A1 phosphorylation, thereby restoring its negative feedback regulation on TGF-β signaling.

Article Snippet: RNA was then reverse transcribed into complementary DNA (cDNA) using the GeneCopoeia reverse transcription kit (QP056, USA).

Techniques: Phospho-proteomics