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genecopoeia reverse transcription kit  (Genecopoeia)


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    Structured Review

    Genecopoeia genecopoeia reverse transcription kit
    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.
    Genecopoeia Reverse Transcription Kit, supplied by Genecopoeia, used in various techniques. Bioz Stars score: 97/100, based on 259 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/genecopoeia reverse transcription kit/product/Genecopoeia
    Average 97 stars, based on 259 article reviews
    genecopoeia reverse transcription kit - by Bioz Stars, 2026-03
    97/100 stars

    Images

    1) Product Images from "Estrogen upregulates NR4A1 to counter TGF beta induced pulmonary fibrosis therapeutic insights for IPF"

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

    Journal: iScience

    doi: 10.1016/j.isci.2026.114756

    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.
    Figure Legend 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.

    Techniques Used: Phospho-proteomics



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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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    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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    Image Search Results


    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