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polyclonal rabbit igg  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc polyclonal rabbit igg
    Polyclonal Rabbit Igg, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1225 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/phospho+stat5+polyclonal+antibody/Phospho-Stat5+(Tyr694)+Antibody/pmc12620314-23-10-15
    Average 96 stars, based on 1225 article reviews
    polyclonal rabbit igg - by Bioz Stars, 2026-09
    96/100 stars

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    other:

    Article Title: AC-73 and Syrosingopine Inhibit SARS-CoV-2 Entry into Megakaryocytes by Targeting CD147 and MCT4
    Article Snippet: Antibodies used were: JAK2 monoclonal antibody (Jak2 (D2E12)XP #3230 Cell Signaling Technology, Danvers, MA, USA); MPL polyclonal antibody (TpoR/MPL (AF1016) R&D, Minneapolis, MN, USA); phospho-STAT5 polyclonal antibody (phospho-Stat5 (Tyr694) #9351 Cell Signaling Technology, Danvers, MA, USA); phospho-STAT3 polyclonal antibody (phospho-Stat3 (Ser727) #9134 Cell Signaling Technology, Danvers, MA, USA); phospho-ERK1/2 polyclonal antibody (phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) #9101 Cell Signaling Technology, Danvers, MA, USA); total ERK1/2 polyclonal antibody (p44/42 MAP Kinase antibody #9102 Cell Signaling Technology, Danvers, MA, USA), CD147 monoclonal antibody (EMMPRIN/CD147 (B5) sc-46700, Santa Cruz Biotechnology, CA, USA); MCT4 monoclonal antibody (MCT4 (F-10) sc-376101, Santa Cruz, CA, USA).

    Article Title: AC-73 and Syrosingopine Inhibit SARS-CoV-2 Entry into Megakaryocytes by Targeting CD147 and MCT4.
    Article Snippet: Antibodies used were: JAK2 monoclonal antibody (Jak2 (D2E12)XP #3230 Cell Signaling Technology, Danvers, MA, USA); MPL polyclonal antibody (TpoR/MPL (AF1016) R&D, Minneapolis, MN, USA); phospho-STAT5 polyclonal antibody (phospho-Stat5 (Tyr694) #9351 Cell Signaling Technology, Danvers, MA, USA); phospho-STAT3 polyclonal antibody (phospho-Stat3 (Ser727) #9134 Cell Signaling Technology, Danvers, MA, USA); phosphoERK1/2 polyclonal antibody (phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) #9101 Cell Signaling Technology, Danvers, MA, USA); total ERK1/2 polyclonal antibody (p44/42 MAP Kinase antibody #9102 Cell Signaling Technology, Danvers, MA, USA), CD147 monoclonal antibody (EMMPRIN/CD147 (B5) sc-46700, Santa Cruz Biotechnology, CA, USA); MCT4 monoclonal antibody (MCT4 (F-10) sc-376101, Santa Cruz, CA, USA).



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    (A) The GH/IGF-1 axis required for postnatal skeletal growth. At the onset of growth spurt, growth hormone releasing hormone (GHRH) from the hypothalamus causes the release of growth hormone (GH) from the anterior pituitary. Circulating GH binds to its receptor (GHR) in liver and other peripheral tissues to induce the synthesis and secretion of IGF-1, which then acts in an endocrine, paracrine, and/or autocrine manner to induce skeletal growth. (B) Expression levels of Ghr (growth hormone receptor), Igf-1 , Igfals (IGF binding protein acid labile subunit), and Igfbp3 (IGF binding protein 3) transcripts in the liver of WT and KO mice. Sample size of male mice (WT, n = 8; KO, n = 8) and Female mice (WT, n = 8; KO, n = 8). (C) Immunoblot analysis of growth hormone receptor (GH-R) protein levels in the liver of WT ( n = 7) and KO ( n = 7) mice. (D) Quantification of the immunoblot results as shown in C. (E) Reduced hepatic GH-induced signaling in KO (-/-) mice relative to WT (+/+) controls. Immunoblot analysis of phospho-JAK2 (Tyr1008), total JAK2, <t>phospho-STAT5</t> <t>(Y694),</t> and total STAT5 in liver lysates from mice injected with recombinant GH. (F) Quantification of the immunoblot results as shown in E. All data are presented as mean ± S.E.M. ** P < 0.01; *** P < 0.001; **** P < 0.0001 (One-way ANOVA with Tukey’s multiple comparisons test for data in B and two-tailed student’s t -test for data in D and F).
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    (A) The GH/IGF-1 axis required for postnatal skeletal growth. At the onset of growth spurt, growth hormone releasing hormone (GHRH) from the hypothalamus causes the release of growth hormone (GH) from the anterior pituitary. Circulating GH binds to its receptor (GHR) in liver and other peripheral tissues to induce the synthesis and secretion of IGF-1, which then acts in an endocrine, paracrine, and/or autocrine manner to induce skeletal growth. (B) Expression levels of Ghr (growth hormone receptor), Igf-1 , Igfals (IGF binding protein acid labile subunit), and Igfbp3 (IGF binding protein 3) transcripts in the liver of WT and KO mice. Sample size of male mice (WT, n = 8; KO, n = 8) and Female mice (WT, n = 8; KO, n = 8). (C) Immunoblot analysis of growth hormone receptor (GH-R) protein levels in the liver of WT ( n = 7) and KO ( n = 7) mice. (D) Quantification of the immunoblot results as shown in C. (E) Reduced hepatic GH-induced signaling in KO (-/-) mice relative to WT (+/+) controls. Immunoblot analysis of phospho-JAK2 (Tyr1008), total JAK2, phospho-STAT5 (Y694), and total STAT5 in liver lysates from mice injected with recombinant GH. (F) Quantification of the immunoblot results as shown in E. All data are presented as mean ± S.E.M. ** P < 0.01; *** P < 0.001; **** P < 0.0001 (One-way ANOVA with Tukey’s multiple comparisons test for data in B and two-tailed student’s t -test for data in D and F).

    Journal: bioRxiv

    Article Title: Tmem263 deletion disrupts the GH/IGF-1 axis and causes dwarfism and impairs skeletal acquisition

    doi: 10.1101/2023.08.02.551694

    Figure Lengend Snippet: (A) The GH/IGF-1 axis required for postnatal skeletal growth. At the onset of growth spurt, growth hormone releasing hormone (GHRH) from the hypothalamus causes the release of growth hormone (GH) from the anterior pituitary. Circulating GH binds to its receptor (GHR) in liver and other peripheral tissues to induce the synthesis and secretion of IGF-1, which then acts in an endocrine, paracrine, and/or autocrine manner to induce skeletal growth. (B) Expression levels of Ghr (growth hormone receptor), Igf-1 , Igfals (IGF binding protein acid labile subunit), and Igfbp3 (IGF binding protein 3) transcripts in the liver of WT and KO mice. Sample size of male mice (WT, n = 8; KO, n = 8) and Female mice (WT, n = 8; KO, n = 8). (C) Immunoblot analysis of growth hormone receptor (GH-R) protein levels in the liver of WT ( n = 7) and KO ( n = 7) mice. (D) Quantification of the immunoblot results as shown in C. (E) Reduced hepatic GH-induced signaling in KO (-/-) mice relative to WT (+/+) controls. Immunoblot analysis of phospho-JAK2 (Tyr1008), total JAK2, phospho-STAT5 (Y694), and total STAT5 in liver lysates from mice injected with recombinant GH. (F) Quantification of the immunoblot results as shown in E. All data are presented as mean ± S.E.M. ** P < 0.01; *** P < 0.001; **** P < 0.0001 (One-way ANOVA with Tukey’s multiple comparisons test for data in B and two-tailed student’s t -test for data in D and F).

    Article Snippet: Rabbit polyclonal antibody against phospho-STAT5 (Y694) was obtained from Cell Signaling Technology (CST#9351).

    Techniques: Expressing, Binding Assay, Western Blot, Injection, Recombinant, Two Tailed Test