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rabbit polyclonal stat5 antibody  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology rabbit polyclonal stat5 antibody
    (A) Western blot analyses of JAK1, JAK2, as well as tyrosine phosphorylated STAT proteins in human pancreatic cancer cell lines ( n = 9) and untransformed pancreatic cells (HPNE). Beta-actin (ACTB) and GAPDH served as loading controls; mouse pancreatic tumor cells treated with human growth hormone (hGH) and IL-4 served as controls for the activation of <t>STAT5</t> and STAT6, respectively (b and c). Western blots are representative of three experimental replicates used for quantitative analysis in . (B) Quantitative analysis of nuclear STAT3 expression in primary human pancreatic cancers ( n = 28) and normal tissues ( n = 17). The right panel shows representative immunofluorescent (IF) images of normal and tumor tissues co-stained for tyrosine phosphorylated STAT3 (pSTAT3) and pan-cytokeratin (panCK). Slides were counterstained with DAPI; bars, 40 μm.
    Rabbit Polyclonal Stat5 Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+polyclonal+stat5+antibody/pmc11194014-10-2-4?v=Santa+Cruz+Biotechnology
    Average 90 stars, based on 1 article reviews
    rabbit polyclonal stat5 antibody - by Bioz Stars, 2026-08
    90/100 stars

    Images

    1) Product Images from "The Janus kinase 1 is critical for pancreatic cancer initiation and progression"

    Article Title: The Janus kinase 1 is critical for pancreatic cancer initiation and progression

    Journal: Cell reports

    doi: 10.1016/j.celrep.2024.114202

    (A) Western blot analyses of JAK1, JAK2, as well as tyrosine phosphorylated STAT proteins in human pancreatic cancer cell lines ( n = 9) and untransformed pancreatic cells (HPNE). Beta-actin (ACTB) and GAPDH served as loading controls; mouse pancreatic tumor cells treated with human growth hormone (hGH) and IL-4 served as controls for the activation of STAT5 and STAT6, respectively (b and c). Western blots are representative of three experimental replicates used for quantitative analysis in . (B) Quantitative analysis of nuclear STAT3 expression in primary human pancreatic cancers ( n = 28) and normal tissues ( n = 17). The right panel shows representative immunofluorescent (IF) images of normal and tumor tissues co-stained for tyrosine phosphorylated STAT3 (pSTAT3) and pan-cytokeratin (panCK). Slides were counterstained with DAPI; bars, 40 μm.
    Figure Legend Snippet: (A) Western blot analyses of JAK1, JAK2, as well as tyrosine phosphorylated STAT proteins in human pancreatic cancer cell lines ( n = 9) and untransformed pancreatic cells (HPNE). Beta-actin (ACTB) and GAPDH served as loading controls; mouse pancreatic tumor cells treated with human growth hormone (hGH) and IL-4 served as controls for the activation of STAT5 and STAT6, respectively (b and c). Western blots are representative of three experimental replicates used for quantitative analysis in . (B) Quantitative analysis of nuclear STAT3 expression in primary human pancreatic cancers ( n = 28) and normal tissues ( n = 17). The right panel shows representative immunofluorescent (IF) images of normal and tumor tissues co-stained for tyrosine phosphorylated STAT3 (pSTAT3) and pan-cytokeratin (panCK). Slides were counterstained with DAPI; bars, 40 μm.

    Techniques Used: Western Blot, Activation Assay, Expressing, Staining

    KEY RESOURCES TABLE
    Figure Legend Snippet: KEY RESOURCES TABLE

    Techniques Used: Recombinant, Transduction, Polymer, Virus, Western Blot, Software



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    Silencing of MRCKα inhibits the stimulatory effects of Met and Leu on mRNA abundance of genes related to milk protein synthesis in bovine mammary epithelial cells. Cells were transfected with scrambled siRNA (control, SC) or MRCKα siRNA (SI) and stimulated simultaneously with control (B, basal medium), additional Met (M, Met = 0.6 mM) or Leu (L, Leu = 0.6 mM). After 24 h, cells were collected and isolated for RT-qPCR analysis. Values are presented as mean ± SEM for three independent experiments. P AA , P -value of amino acid addition (AA); P SI , P -value of silencing of MRCKα (SI); P AA×SI , P -value of AA × SI interaction. CSN2 = β-casein; CSN1S1 = αS1-casein; CSN3 = κ-casein; LALBA = lactalbumin α; MRCKα = myotonic dystrophy-related CDC42-binding kinase alpha; mTOR = mechanistic target of rapamycin; JAK2 = Janus kinase 2; <t>STAT5</t> = signal transducers and activators of transcription 5.
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    (A) Western blot analyses of JAK1, JAK2, as well as tyrosine phosphorylated STAT proteins in human pancreatic cancer cell lines ( n = 9) and untransformed pancreatic cells (HPNE). Beta-actin (ACTB) and GAPDH served as loading controls; mouse pancreatic tumor cells treated with human growth hormone (hGH) and IL-4 served as controls for the activation of <t>STAT5</t> and STAT6, respectively (b and c). Western blots are representative of three experimental replicates used for quantitative analysis in . (B) Quantitative analysis of nuclear STAT3 expression in primary human pancreatic cancers ( n = 28) and normal tissues ( n = 17). The right panel shows representative immunofluorescent (IF) images of normal and tumor tissues co-stained for tyrosine phosphorylated STAT3 (pSTAT3) and pan-cytokeratin (panCK). Slides were counterstained with DAPI; bars, 40 μm.
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    (A) Western blot analyses of JAK1, JAK2, as well as tyrosine phosphorylated STAT proteins in human pancreatic cancer cell lines ( n = 9) and untransformed pancreatic cells (HPNE). Beta-actin (ACTB) and GAPDH served as loading controls; mouse pancreatic tumor cells treated with human growth hormone (hGH) and IL-4 served as controls for the activation of <t>STAT5</t> and STAT6, respectively (b and c). Western blots are representative of three experimental replicates used for quantitative analysis in . (B) Quantitative analysis of nuclear STAT3 expression in primary human pancreatic cancers ( n = 28) and normal tissues ( n = 17). The right panel shows representative immunofluorescent (IF) images of normal and tumor tissues co-stained for tyrosine phosphorylated STAT3 (pSTAT3) and pan-cytokeratin (panCK). Slides were counterstained with DAPI; bars, 40 μm.
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    Image Search Results


    Silencing of MRCKα inhibits the stimulatory effects of Met and Leu on mRNA abundance of genes related to milk protein synthesis in bovine mammary epithelial cells. Cells were transfected with scrambled siRNA (control, SC) or MRCKα siRNA (SI) and stimulated simultaneously with control (B, basal medium), additional Met (M, Met = 0.6 mM) or Leu (L, Leu = 0.6 mM). After 24 h, cells were collected and isolated for RT-qPCR analysis. Values are presented as mean ± SEM for three independent experiments. P AA , P -value of amino acid addition (AA); P SI , P -value of silencing of MRCKα (SI); P AA×SI , P -value of AA × SI interaction. CSN2 = β-casein; CSN1S1 = αS1-casein; CSN3 = κ-casein; LALBA = lactalbumin α; MRCKα = myotonic dystrophy-related CDC42-binding kinase alpha; mTOR = mechanistic target of rapamycin; JAK2 = Janus kinase 2; STAT5 = signal transducers and activators of transcription 5.

    Journal: Animal Nutrition

    Article Title: Myotonic dystrophy-related CDC42-binding kinase alpha (MRCKα) mediates methionine- and leucine-stimulated β-casein synthesis in bovine mammary epithelial cells via targeting mTOR

    doi: 10.1016/j.aninu.2025.01.003

    Figure Lengend Snippet: Silencing of MRCKα inhibits the stimulatory effects of Met and Leu on mRNA abundance of genes related to milk protein synthesis in bovine mammary epithelial cells. Cells were transfected with scrambled siRNA (control, SC) or MRCKα siRNA (SI) and stimulated simultaneously with control (B, basal medium), additional Met (M, Met = 0.6 mM) or Leu (L, Leu = 0.6 mM). After 24 h, cells were collected and isolated for RT-qPCR analysis. Values are presented as mean ± SEM for three independent experiments. P AA , P -value of amino acid addition (AA); P SI , P -value of silencing of MRCKα (SI); P AA×SI , P -value of AA × SI interaction. CSN2 = β-casein; CSN1S1 = αS1-casein; CSN3 = κ-casein; LALBA = lactalbumin α; MRCKα = myotonic dystrophy-related CDC42-binding kinase alpha; mTOR = mechanistic target of rapamycin; JAK2 = Janus kinase 2; STAT5 = signal transducers and activators of transcription 5.

    Article Snippet: Rabbit polyclonal anti-human signal transducer and activator of transcription 5 (STAT5) antibody, rabbit polyclonal anti-human phosphorylated STAT5 (Tyr 694 ) antibody, rabbit polyclonal anti-human PI3K antibody and rabbit polyclonal anti-human phosphorylated PI3K (Tyr 317 ) antibody were purchased from Bioss antibodies (Beijing, China).

    Techniques: Transfection, Control, Isolation, Quantitative RT-PCR, Binding Assay

    (A) Western blot analyses of JAK1, JAK2, as well as tyrosine phosphorylated STAT proteins in human pancreatic cancer cell lines ( n = 9) and untransformed pancreatic cells (HPNE). Beta-actin (ACTB) and GAPDH served as loading controls; mouse pancreatic tumor cells treated with human growth hormone (hGH) and IL-4 served as controls for the activation of STAT5 and STAT6, respectively (b and c). Western blots are representative of three experimental replicates used for quantitative analysis in . (B) Quantitative analysis of nuclear STAT3 expression in primary human pancreatic cancers ( n = 28) and normal tissues ( n = 17). The right panel shows representative immunofluorescent (IF) images of normal and tumor tissues co-stained for tyrosine phosphorylated STAT3 (pSTAT3) and pan-cytokeratin (panCK). Slides were counterstained with DAPI; bars, 40 μm.

    Journal: Cell reports

    Article Title: The Janus kinase 1 is critical for pancreatic cancer initiation and progression

    doi: 10.1016/j.celrep.2024.114202

    Figure Lengend Snippet: (A) Western blot analyses of JAK1, JAK2, as well as tyrosine phosphorylated STAT proteins in human pancreatic cancer cell lines ( n = 9) and untransformed pancreatic cells (HPNE). Beta-actin (ACTB) and GAPDH served as loading controls; mouse pancreatic tumor cells treated with human growth hormone (hGH) and IL-4 served as controls for the activation of STAT5 and STAT6, respectively (b and c). Western blots are representative of three experimental replicates used for quantitative analysis in . (B) Quantitative analysis of nuclear STAT3 expression in primary human pancreatic cancers ( n = 28) and normal tissues ( n = 17). The right panel shows representative immunofluorescent (IF) images of normal and tumor tissues co-stained for tyrosine phosphorylated STAT3 (pSTAT3) and pan-cytokeratin (panCK). Slides were counterstained with DAPI; bars, 40 μm.

    Article Snippet: Rabbit polyclonal, STAT5 , Santa Cruz , Cat#sc-836; RRID:AB_632445.

    Techniques: Western Blot, Activation Assay, Expressing, Staining

    KEY RESOURCES TABLE

    Journal: Cell reports

    Article Title: The Janus kinase 1 is critical for pancreatic cancer initiation and progression

    doi: 10.1016/j.celrep.2024.114202

    Figure Lengend Snippet: KEY RESOURCES TABLE

    Article Snippet: Rabbit polyclonal, STAT5 , Santa Cruz , Cat#sc-836; RRID:AB_632445.

    Techniques: Recombinant, Transduction, Polymer, Virus, Western Blot, Software