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mouse kidney epithelial cell line  (ATCC)


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    ATCC mouse kidney epithelial cell line
    The mechanism diagram of the study. Upregulated ATF3 in damaged tubular <t>epithelial</t> cells (TECs) promotes the progression of kidney fibrosis. In TECs, under homeostatic conditions, SMAD7 transcripts with histone 3 lysine 14 acetylation and histone opening. Under fibrotic conditions, upregulated ATF3 recruits HDAC6 to the SMAD7 promoter, eradicating histone 3 lysine 14 acetylation (H3K14ac) and diminishing SMAD7 transcription, thus activates TGF-β1/Smad3 signaling and aggravates kidney fibrosis.
    Mouse Kidney Epithelial Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 206 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+kidney+epithelial+tcmk+1+cell+line/pmc12781174-59-0-20?v=ATCC
    Average 96 stars, based on 206 article reviews
    mouse kidney epithelial cell line - by Bioz Stars, 2026-07
    96/100 stars

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    1) Product Images from "ATF3 aggravates kidney fibrosis via HDAC6-dependent epigenetic reprogramming"

    Article Title: ATF3 aggravates kidney fibrosis via HDAC6-dependent epigenetic reprogramming

    Journal: International Journal of Biological Sciences

    doi: 10.7150/ijbs.125062

    The mechanism diagram of the study. Upregulated ATF3 in damaged tubular epithelial cells (TECs) promotes the progression of kidney fibrosis. In TECs, under homeostatic conditions, SMAD7 transcripts with histone 3 lysine 14 acetylation and histone opening. Under fibrotic conditions, upregulated ATF3 recruits HDAC6 to the SMAD7 promoter, eradicating histone 3 lysine 14 acetylation (H3K14ac) and diminishing SMAD7 transcription, thus activates TGF-β1/Smad3 signaling and aggravates kidney fibrosis.
    Figure Legend Snippet: The mechanism diagram of the study. Upregulated ATF3 in damaged tubular epithelial cells (TECs) promotes the progression of kidney fibrosis. In TECs, under homeostatic conditions, SMAD7 transcripts with histone 3 lysine 14 acetylation and histone opening. Under fibrotic conditions, upregulated ATF3 recruits HDAC6 to the SMAD7 promoter, eradicating histone 3 lysine 14 acetylation (H3K14ac) and diminishing SMAD7 transcription, thus activates TGF-β1/Smad3 signaling and aggravates kidney fibrosis.

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    The mechanism diagram of the study. Upregulated ATF3 in damaged tubular epithelial cells (TECs) promotes the progression of kidney fibrosis. In TECs, under homeostatic conditions, SMAD7 transcripts with histone 3 lysine 14 acetylation and histone opening. Under fibrotic conditions, upregulated ATF3 recruits HDAC6 to the SMAD7 promoter, eradicating histone 3 lysine 14 acetylation (H3K14ac) and diminishing SMAD7 transcription, thus activates TGF-β1/Smad3 signaling and aggravates kidney fibrosis.

    Journal: International Journal of Biological Sciences

    Article Title: ATF3 aggravates kidney fibrosis via HDAC6-dependent epigenetic reprogramming

    doi: 10.7150/ijbs.125062

    Figure Lengend Snippet: The mechanism diagram of the study. Upregulated ATF3 in damaged tubular epithelial cells (TECs) promotes the progression of kidney fibrosis. In TECs, under homeostatic conditions, SMAD7 transcripts with histone 3 lysine 14 acetylation and histone opening. Under fibrotic conditions, upregulated ATF3 recruits HDAC6 to the SMAD7 promoter, eradicating histone 3 lysine 14 acetylation (H3K14ac) and diminishing SMAD7 transcription, thus activates TGF-β1/Smad3 signaling and aggravates kidney fibrosis.

    Article Snippet: Mouse kidney epithelial cell line (TCMK-1), HEK 293T cells and rat renal interstitial fibroblasts (NRK-49F) cells were purchased from the American Type Culture Collection (Manassas, VA) and were cultured in DMEM (Sigma-Aldrich) containing 10% fetal bovine serum (FBS), at 37°C, 5% CO2, 95% air.

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