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iscript cdna synthesis kit  (Bio-Rad)


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    Structured Review

    Bio-Rad iscript cdna synthesis kit
    Iscript Cdna Synthesis Kit, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 99/100, based on 47380 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/iscript cdna synthesis kit/product/Bio-Rad
    Average 99 stars, based on 47380 article reviews
    iscript cdna synthesis kit - by Bioz Stars, 2026-03
    99/100 stars

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    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.
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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 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