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anti stat4  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti stat4
    Anti Stat4, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 119 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+stat4/pm41826817-101-59-63?v=Cell+Signaling+Technology+Inc
    Average 95 stars, based on 119 article reviews
    anti stat4 - by Bioz Stars, 2026-07
    95/100 stars

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    Image Search Results


    (A) Schematic of the knockout of STAT1, STAT3, STAT5a, and STAT5b in canonical JAK/STAT signaling cascades of the mammary gland. (B) Carmine alum-stained mammary gland wholemounts of nulliparous female mice with a targeted deletion of four Stat genes in the mammary epithelium MMTV-Cre Stat3/5 fl/fl Stat1 −/− ) and a STAT1 single-knockout littermate control; bars, 1 mm. (C) Immunoblot analysis of the seven known mammalian STAT proteins in mammary epithelial cells (MECs) from STAT1/3/5a/5b quadruple-knockout females ( N = 4) in comparison to age-matched STAT3/5a/5b triple-knockout mice ( N = 2). Other controls: C1 and C2, positive controls for active STAT3 and STAT5, mammary gland tissues from wild-type mice on day 1 of involution and lactation, respectively; C3, spleen as a positive control for STAT4; C4, wild-type MECs as a negative control for STAT4; C5 and C6 interferon-treated and untreated MECs as positive and negative controls for STAT2; C7 and C8, IL-4-treated and untreated wild-type MECs as positive and negative controls for active STAT6. GAPDH and ACTB served as loading controls.

    Journal: Cell reports

    Article Title: STAT-independent functions of Janus kinases 1 and 2 are obligatory for the postnatal development of mammary epithelial ducts

    doi: 10.1016/j.celrep.2025.116703

    Figure Lengend Snippet: (A) Schematic of the knockout of STAT1, STAT3, STAT5a, and STAT5b in canonical JAK/STAT signaling cascades of the mammary gland. (B) Carmine alum-stained mammary gland wholemounts of nulliparous female mice with a targeted deletion of four Stat genes in the mammary epithelium MMTV-Cre Stat3/5 fl/fl Stat1 −/− ) and a STAT1 single-knockout littermate control; bars, 1 mm. (C) Immunoblot analysis of the seven known mammalian STAT proteins in mammary epithelial cells (MECs) from STAT1/3/5a/5b quadruple-knockout females ( N = 4) in comparison to age-matched STAT3/5a/5b triple-knockout mice ( N = 2). Other controls: C1 and C2, positive controls for active STAT3 and STAT5, mammary gland tissues from wild-type mice on day 1 of involution and lactation, respectively; C3, spleen as a positive control for STAT4; C4, wild-type MECs as a negative control for STAT4; C5 and C6 interferon-treated and untreated MECs as positive and negative controls for STAT2; C7 and C8, IL-4-treated and untreated wild-type MECs as positive and negative controls for active STAT6. GAPDH and ACTB served as loading controls.

    Article Snippet: Rabbit monoclonal, STAT4 , Cell Signaling , Cat#2653; RRID:AB_ 2255156.

    Techniques: Knock-Out, Staining, Control, Western Blot, Quadruple Knockout, Comparison, Triple Knockout, Positive Control, Negative Control

    (A and B) Immunoblot analysis of tyrosine-phosphorylated JAK1 and JAK2 and expression of selected STAT proteins in mammary epithelial cells from quadruple STAT1/3/5a/5b conditional knockout mice and wild-type controls that were treated with either oncostatin M (OSM) alone and human growth hormone (hGH) alone (A) or a combination of both (B); 2 biological repeats of experimental and control animals. GAPDH served as a loading control. (C) Immunoblot analysis to assess the activation of STAT6 and tyrosine phosphorylation of JAK1 in STAT1/3/5a/5b-deficient quadruple-knockout cells and controls following stimulation with IL-4. GAPDH was used as a loading control. PC, splenocytes as positive controls for the validated absence of STAT2 and STAT4 in the quadruple-knockout epithelial cells. (D) Summary of canonical and noncanonical signaling mechanisms by which JAK2, in cooperation with JAK1, drives the postnatal development of the mammary gland.

    Journal: Cell reports

    Article Title: STAT-independent functions of Janus kinases 1 and 2 are obligatory for the postnatal development of mammary epithelial ducts

    doi: 10.1016/j.celrep.2025.116703

    Figure Lengend Snippet: (A and B) Immunoblot analysis of tyrosine-phosphorylated JAK1 and JAK2 and expression of selected STAT proteins in mammary epithelial cells from quadruple STAT1/3/5a/5b conditional knockout mice and wild-type controls that were treated with either oncostatin M (OSM) alone and human growth hormone (hGH) alone (A) or a combination of both (B); 2 biological repeats of experimental and control animals. GAPDH served as a loading control. (C) Immunoblot analysis to assess the activation of STAT6 and tyrosine phosphorylation of JAK1 in STAT1/3/5a/5b-deficient quadruple-knockout cells and controls following stimulation with IL-4. GAPDH was used as a loading control. PC, splenocytes as positive controls for the validated absence of STAT2 and STAT4 in the quadruple-knockout epithelial cells. (D) Summary of canonical and noncanonical signaling mechanisms by which JAK2, in cooperation with JAK1, drives the postnatal development of the mammary gland.

    Article Snippet: Rabbit monoclonal, STAT4 , Cell Signaling , Cat#2653; RRID:AB_ 2255156.

    Techniques: Western Blot, Expressing, Knock-Out, Control, Activation Assay, Phospho-proteomics, Quadruple Knockout