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anti stat1 rabbit polyclonal antibody  (Proteintech)


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    Structured Review

    Proteintech anti stat1 rabbit polyclonal antibody
    CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and <t>STAT1</t> . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).
    Anti Stat1 Rabbit Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 382 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+polyclonal+anti+stat1/pmc12754513-77-74-79?v=Proteintech
    Average 96 stars, based on 382 article reviews
    anti stat1 rabbit polyclonal antibody - by Bioz Stars, 2026-07
    96/100 stars

    Images

    1) Product Images from "Transcriptomic analysis identifies CXCL12 as a novel candidate gene for litter size in rabbits"

    Article Title: Transcriptomic analysis identifies CXCL12 as a novel candidate gene for litter size in rabbits

    Journal: Animal Bioscience

    doi: 10.5713/ab.24.0640

    CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and STAT1 . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).
    Figure Legend Snippet: CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and STAT1 . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).

    Techniques Used: Binding Assay, Immunofluorescence, Staining, Over Expression, Expressing, Phospho-proteomics



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    (A) Immunoblot analysis of the expression and activation of selected STAT proteins in mammary epithelial cells from STAT3 and STAT5a/b conditional triple-knockout mice (MMTV-Cre Stat3/5 fl/fl ; N = 4) and age-matched Stat3/5 fl/wt controls ( N = 2 and 4, respectively). E-cadherin (CDH1) and beta-actin (ACTB) were used as loading controls. PC, wild-type control epithelial cells treated with IL-4 served as a positive control for tyrosine-phosphorylated STAT6 (pY-STAT6). (B) Immunohistochemistry of tyrosine-phosphorylated <t>STAT1</t> (pY-STAT1) on histologic sections of mammary glands from postpartum STAT3/5 triple-knockout and control females; bars, 20 μm. (C and D) Immunoblot analysis of active and total levels of STAT1 before and after the retroviralbased expression of Cre recombinase in three immortalized mammary epithelial cell lines (C) and three mouse embryonic fibroblast lines (D). Wild-type mammary epithelial cells and interferon gamma-treated wild-type mouse fibroblasts served as positive controls (C) for STAT5a and active STAT1, respectively. The densitometry results of the STAT proteins in (C) from 3 technical repeats of the 3 biological repeats are shown in . (E) Immunohistochemistry of active STAT1 (pY-STAT1) in alveolar cells of mammary glands of a postpartum WAP-Cre Stat3/5 fl/fl female and an age-matched control; bars, 20 μm.
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    CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and <t>STAT1</t> . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).
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    The antiviral activity of EHMT2 inhibitors is independent of the interferon pathway. (A) The effects of EHMT2 inhibitors, BIX01294 (left), UNC0638 (middle), and UNC0642 (right), on the interferon responses induced by high-molecular weight poly(I:C) were investigated. A549-ACE2 cells were transfected with poly(I:C) for 6 h after treating with varying concentrations of the inhibitors. The change of IFN-β was detected with RT-qPCR using GAPDH as an internal control. (B and C) <t>A549-ACE2-STAT1</t> −/− cells were treated with EHMT2 inhibitors at indicated doses and then were infected with SARS-CoV-2 at an MOI of 0.1 for 24 h. Intracellular SARS-CoV-2 RNA levels were quantified with RT-qPCR, using GAPDH as the internal control ( B ). Intracellular SARS-CoV-2 protein levels were quantified with western blotting ( C ). Data are means ± SD. These experiments were repeated at least twice.
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    Image Search Results


    (A) Immunoblot analysis of the expression and activation of selected STAT proteins in mammary epithelial cells from STAT3 and STAT5a/b conditional triple-knockout mice (MMTV-Cre Stat3/5 fl/fl ; N = 4) and age-matched Stat3/5 fl/wt controls ( N = 2 and 4, respectively). E-cadherin (CDH1) and beta-actin (ACTB) were used as loading controls. PC, wild-type control epithelial cells treated with IL-4 served as a positive control for tyrosine-phosphorylated STAT6 (pY-STAT6). (B) Immunohistochemistry of tyrosine-phosphorylated STAT1 (pY-STAT1) on histologic sections of mammary glands from postpartum STAT3/5 triple-knockout and control females; bars, 20 μm. (C and D) Immunoblot analysis of active and total levels of STAT1 before and after the retroviralbased expression of Cre recombinase in three immortalized mammary epithelial cell lines (C) and three mouse embryonic fibroblast lines (D). Wild-type mammary epithelial cells and interferon gamma-treated wild-type mouse fibroblasts served as positive controls (C) for STAT5a and active STAT1, respectively. The densitometry results of the STAT proteins in (C) from 3 technical repeats of the 3 biological repeats are shown in . (E) Immunohistochemistry of active STAT1 (pY-STAT1) in alveolar cells of mammary glands of a postpartum WAP-Cre Stat3/5 fl/fl female and an age-matched control; bars, 20 μm.

    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) Immunoblot analysis of the expression and activation of selected STAT proteins in mammary epithelial cells from STAT3 and STAT5a/b conditional triple-knockout mice (MMTV-Cre Stat3/5 fl/fl ; N = 4) and age-matched Stat3/5 fl/wt controls ( N = 2 and 4, respectively). E-cadherin (CDH1) and beta-actin (ACTB) were used as loading controls. PC, wild-type control epithelial cells treated with IL-4 served as a positive control for tyrosine-phosphorylated STAT6 (pY-STAT6). (B) Immunohistochemistry of tyrosine-phosphorylated STAT1 (pY-STAT1) on histologic sections of mammary glands from postpartum STAT3/5 triple-knockout and control females; bars, 20 μm. (C and D) Immunoblot analysis of active and total levels of STAT1 before and after the retroviralbased expression of Cre recombinase in three immortalized mammary epithelial cell lines (C) and three mouse embryonic fibroblast lines (D). Wild-type mammary epithelial cells and interferon gamma-treated wild-type mouse fibroblasts served as positive controls (C) for STAT5a and active STAT1, respectively. The densitometry results of the STAT proteins in (C) from 3 technical repeats of the 3 biological repeats are shown in . (E) Immunohistochemistry of active STAT1 (pY-STAT1) in alveolar cells of mammary glands of a postpartum WAP-Cre Stat3/5 fl/fl female and an age-matched control; bars, 20 μm.

    Article Snippet: Rabbit polyclonal, pY-STAT1 (Y701) , Origene , Cat#TA309955.

    Techniques: Western Blot, Expressing, Activation Assay, Triple Knockout, Control, Positive Control, Immunohistochemistry

    (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 polyclonal, pY-STAT1 (Y701) , Origene , Cat#TA309955.

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

    (A) Immunoblot analysis of STAT1 and JAK1 expression and activation in response to the pharmacological inhibition of JAK1 using 1 μM itacitinib in three mammary epithelial cell lines co-deficient in STAT3, STAT5a, and STAT5b. Beta-actin (ACTB) was used as a loading control. The densitometry results of immunoblots from 2 technical repeats of the 3 biological repeats are shown in . (B) Schematic of a quadruple knockout of STAT3, STAT5a, and STAT5b along with JAK1 to genetically ablate the compensatory activation of STAT1 in the STAT3/5a/5b triple-knockout mammary epithelium and to determine the STAT-independent contribution of JAK2 to mammary gland development. (C) Carmine alum-stained mammary gland whole-mounts of 4- and 6-week-old nulliparous females that are conditionally deficient inSTAT3, STAT5a/b, and JAK1 (MMTV-Cre Stat3/5 fl/fl Jak1 fl/fl ) and littermate controls without the MMTV-Cre transgene; bars, 1 mm. Dotted lines mark the invasive fronts of the terminal ends of ducts. (D) Immunoblot analysis of STAT1 expression and activation in response to the knockout of JAK1 in the mammary epithelium of STAT3/5a/5b triple-knockout females; 4 biological repeats of quadruple-knockout females compared to 2 wild-type controls and 2 STAT3/5a/5b triple-knockout mice. Beta-actin (ACTB) served as a loading control. The densitometry results of immunoblots from the 4 biological and 2 technical repeats are shown in .

    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) Immunoblot analysis of STAT1 and JAK1 expression and activation in response to the pharmacological inhibition of JAK1 using 1 μM itacitinib in three mammary epithelial cell lines co-deficient in STAT3, STAT5a, and STAT5b. Beta-actin (ACTB) was used as a loading control. The densitometry results of immunoblots from 2 technical repeats of the 3 biological repeats are shown in . (B) Schematic of a quadruple knockout of STAT3, STAT5a, and STAT5b along with JAK1 to genetically ablate the compensatory activation of STAT1 in the STAT3/5a/5b triple-knockout mammary epithelium and to determine the STAT-independent contribution of JAK2 to mammary gland development. (C) Carmine alum-stained mammary gland whole-mounts of 4- and 6-week-old nulliparous females that are conditionally deficient inSTAT3, STAT5a/b, and JAK1 (MMTV-Cre Stat3/5 fl/fl Jak1 fl/fl ) and littermate controls without the MMTV-Cre transgene; bars, 1 mm. Dotted lines mark the invasive fronts of the terminal ends of ducts. (D) Immunoblot analysis of STAT1 expression and activation in response to the knockout of JAK1 in the mammary epithelium of STAT3/5a/5b triple-knockout females; 4 biological repeats of quadruple-knockout females compared to 2 wild-type controls and 2 STAT3/5a/5b triple-knockout mice. Beta-actin (ACTB) served as a loading control. The densitometry results of immunoblots from the 4 biological and 2 technical repeats are shown in .

    Article Snippet: Rabbit polyclonal, pY-STAT1 (Y701) , Origene , Cat#TA309955.

    Techniques: Western Blot, Expressing, Activation Assay, Inhibition, Control, Quadruple Knockout, Triple Knockout, Staining, Knock-Out

    (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 polyclonal, pY-STAT1 (Y701) , Origene , Cat#TA309955.

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

    CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and STAT1 . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).

    Journal: Animal Bioscience

    Article Title: Transcriptomic analysis identifies CXCL12 as a novel candidate gene for litter size in rabbits

    doi: 10.5713/ab.24.0640

    Figure Lengend Snippet: CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and STAT1 . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).

    Article Snippet: Protein detection was achieved using the following antibodies: anti-CCND1 mouse monoclonal antibody (1:250, Proteintech), anti-PCNA rabbit polyclonal antibody (1:250, Proteintech), anti-Bcl2 rabbit polyclonal antibody (1:250, Proteintech), anti-Bax rabbit polyclonal antibody (1:250, Proteintech), anti-CITED1 rabbit polyclonal antibody (1:50, Proteintech), anti-WNT10B mouse monoclonal polyclonal antibody (1:250, Proteintech), anti-CXCR4 mouse monoclonal polyclonal antibody (1:250, Proteintech), anti-phospho-JAK2 rabbit monoclonal polyclonal antibody (1:250, Abcam, Cambridge, UK), anti-JAK2 rabbit monoclonal polyclonal antibody (1:250, Abcam), anti-phospho-STAT1 rabbit polyclonal antibody (1:250, Proteintech), anti-STAT1 rabbit polyclonal antibody (1:250, Proteintech), anti-GAPDH mouse monoclonal antibody (1:2,500, Proteintech), 1:1,000 goat anti-rabbit secondary antibody IgG (Proteintech) and 1:1,000 goat anti-mouse secondary antibody IgG (Proteintech).

    Techniques: Binding Assay, Immunofluorescence, Staining, Over Expression, Expressing, Phospho-proteomics

    CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and STAT1 . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).

    Journal: Animal Bioscience

    Article Title: Transcriptomic analysis identifies CXCL12 as a novel candidate gene for litter size in rabbits

    doi: 10.5713/ab.24.0640

    Figure Lengend Snippet: CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and STAT1 . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).

    Article Snippet: Protein detection was achieved using the following antibodies: anti-CCND1 mouse monoclonal antibody (1:250, Proteintech), anti-PCNA rabbit polyclonal antibody (1:250, Proteintech), anti-Bcl2 rabbit polyclonal antibody (1:250, Proteintech), anti-Bax rabbit polyclonal antibody (1:250, Proteintech), anti-CITED1 rabbit polyclonal antibody (1:50, Proteintech), anti-WNT10B mouse monoclonal polyclonal antibody (1:250, Proteintech), anti-CXCR4 mouse monoclonal polyclonal antibody (1:250, Proteintech), anti-phospho-JAK2 rabbit monoclonal polyclonal antibody (1:250, Abcam, Cambridge, UK), anti-JAK2 rabbit monoclonal polyclonal antibody (1:250, Abcam), anti-phospho-STAT1 rabbit polyclonal antibody (1:250, Proteintech), anti-STAT1 rabbit polyclonal antibody (1:250, Proteintech), anti-GAPDH mouse monoclonal antibody (1:2,500, Proteintech), 1:1,000 goat anti-rabbit secondary antibody IgG (Proteintech) and 1:1,000 goat anti-mouse secondary antibody IgG (Proteintech).

    Techniques: Binding Assay, Immunofluorescence, Staining, Over Expression, Expressing, Phospho-proteomics

    The antiviral activity of EHMT2 inhibitors is independent of the interferon pathway. (A) The effects of EHMT2 inhibitors, BIX01294 (left), UNC0638 (middle), and UNC0642 (right), on the interferon responses induced by high-molecular weight poly(I:C) were investigated. A549-ACE2 cells were transfected with poly(I:C) for 6 h after treating with varying concentrations of the inhibitors. The change of IFN-β was detected with RT-qPCR using GAPDH as an internal control. (B and C) A549-ACE2-STAT1 −/− cells were treated with EHMT2 inhibitors at indicated doses and then were infected with SARS-CoV-2 at an MOI of 0.1 for 24 h. Intracellular SARS-CoV-2 RNA levels were quantified with RT-qPCR, using GAPDH as the internal control ( B ). Intracellular SARS-CoV-2 protein levels were quantified with western blotting ( C ). Data are means ± SD. These experiments were repeated at least twice.

    Journal: Journal of Virology

    Article Title: UNC0638 inhibits SARS-CoV-2 entry by blocking cathepsin L maturation

    doi: 10.1128/jvi.00741-25

    Figure Lengend Snippet: The antiviral activity of EHMT2 inhibitors is independent of the interferon pathway. (A) The effects of EHMT2 inhibitors, BIX01294 (left), UNC0638 (middle), and UNC0642 (right), on the interferon responses induced by high-molecular weight poly(I:C) were investigated. A549-ACE2 cells were transfected with poly(I:C) for 6 h after treating with varying concentrations of the inhibitors. The change of IFN-β was detected with RT-qPCR using GAPDH as an internal control. (B and C) A549-ACE2-STAT1 −/− cells were treated with EHMT2 inhibitors at indicated doses and then were infected with SARS-CoV-2 at an MOI of 0.1 for 24 h. Intracellular SARS-CoV-2 RNA levels were quantified with RT-qPCR, using GAPDH as the internal control ( B ). Intracellular SARS-CoV-2 protein levels were quantified with western blotting ( C ). Data are means ± SD. These experiments were repeated at least twice.

    Article Snippet: Rabbit monoclonal anti-EGFR antibody (4267), rabbit monoclonal anti-LAMP1 antibody (9090), and rabbit polyclonal anti-STAT1 antibody (9172) were from Cell Signaling Technology.

    Techniques: Activity Assay, High Molecular Weight, Transfection, Quantitative RT-PCR, Control, Infection, Western Blot