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rabbit anti human nicd  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc rabbit anti human nicd
    Characterisation of W and F organoids. a. Brightfield microscopy of W and F organoids revealed no observable phenotypic differences. Scale bars represent 500μm. b. Western blot validation showing loss of FBXW7 protein in F organoids. c. Immunofluorescence of W and F organoids with DAPI nuclear stain (blue), F-actin (red), FBXW7 (orange). Scale bars represent 100μm. d. FBXW7 targets the phosphorylated substrates and ubiquitinates these substrates for proteasomal degradation. This included phosphorylated cJun, phosphorylated CCNE1, phosphosylated cMyc, and notch intracellular domain <t>(NICD).</t> The non-phosphorylated substrates were affected to varying degrees. While upregulation of cJun, was observed, there was no change in the quantities of CCNE1, cMYC and NOTCH. e. Volcano plot from bulk RNAseq of F vs W organoids revealed minimal differential expression of genes. Only HLA-DQB1 was found to be significantly downregulated, and GSTM1 significantly upregulated in F organoids. All experiments were performed with N = 3 biological replicates.
    Rabbit Anti Human Nicd, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1119 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti human nicd/product/Cell Signaling Technology Inc
    Average 97 stars, based on 1119 article reviews
    rabbit anti human nicd - by Bioz Stars, 2026-03
    97/100 stars

    Images

    1) Product Images from "Mutational order and epistasis determine the consequences of FBXW7 mutations during colorectal cancer evolution"

    Article Title: Mutational order and epistasis determine the consequences of FBXW7 mutations during colorectal cancer evolution

    Journal: bioRxiv

    doi: 10.1101/2023.08.25.554836

    Characterisation of W and F organoids. a. Brightfield microscopy of W and F organoids revealed no observable phenotypic differences. Scale bars represent 500μm. b. Western blot validation showing loss of FBXW7 protein in F organoids. c. Immunofluorescence of W and F organoids with DAPI nuclear stain (blue), F-actin (red), FBXW7 (orange). Scale bars represent 100μm. d. FBXW7 targets the phosphorylated substrates and ubiquitinates these substrates for proteasomal degradation. This included phosphorylated cJun, phosphorylated CCNE1, phosphosylated cMyc, and notch intracellular domain (NICD). The non-phosphorylated substrates were affected to varying degrees. While upregulation of cJun, was observed, there was no change in the quantities of CCNE1, cMYC and NOTCH. e. Volcano plot from bulk RNAseq of F vs W organoids revealed minimal differential expression of genes. Only HLA-DQB1 was found to be significantly downregulated, and GSTM1 significantly upregulated in F organoids. All experiments were performed with N = 3 biological replicates.
    Figure Legend Snippet: Characterisation of W and F organoids. a. Brightfield microscopy of W and F organoids revealed no observable phenotypic differences. Scale bars represent 500μm. b. Western blot validation showing loss of FBXW7 protein in F organoids. c. Immunofluorescence of W and F organoids with DAPI nuclear stain (blue), F-actin (red), FBXW7 (orange). Scale bars represent 100μm. d. FBXW7 targets the phosphorylated substrates and ubiquitinates these substrates for proteasomal degradation. This included phosphorylated cJun, phosphorylated CCNE1, phosphosylated cMyc, and notch intracellular domain (NICD). The non-phosphorylated substrates were affected to varying degrees. While upregulation of cJun, was observed, there was no change in the quantities of CCNE1, cMYC and NOTCH. e. Volcano plot from bulk RNAseq of F vs W organoids revealed minimal differential expression of genes. Only HLA-DQB1 was found to be significantly downregulated, and GSTM1 significantly upregulated in F organoids. All experiments were performed with N = 3 biological replicates.

    Techniques Used: Microscopy, Western Blot, Biomarker Discovery, Immunofluorescence, Staining, Quantitative Proteomics



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    Characterisation of W and F organoids. a. Brightfield microscopy of W and F organoids revealed no observable phenotypic differences. Scale bars represent 500μm. b. Western blot validation showing loss of FBXW7 protein in F organoids. c. Immunofluorescence of W and F organoids with DAPI nuclear stain (blue), F-actin (red), FBXW7 (orange). Scale bars represent 100μm. d. FBXW7 targets the phosphorylated substrates and ubiquitinates these substrates for proteasomal degradation. This included phosphorylated cJun, phosphorylated CCNE1, phosphosylated cMyc, and notch intracellular domain <t>(NICD).</t> The non-phosphorylated substrates were affected to varying degrees. While upregulation of cJun, was observed, there was no change in the quantities of CCNE1, cMYC and NOTCH. e. Volcano plot from bulk RNAseq of F vs W organoids revealed minimal differential expression of genes. Only HLA-DQB1 was found to be significantly downregulated, and GSTM1 significantly upregulated in F organoids. All experiments were performed with N = 3 biological replicates.
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    Image Search Results


    Characterisation of W and F organoids. a. Brightfield microscopy of W and F organoids revealed no observable phenotypic differences. Scale bars represent 500μm. b. Western blot validation showing loss of FBXW7 protein in F organoids. c. Immunofluorescence of W and F organoids with DAPI nuclear stain (blue), F-actin (red), FBXW7 (orange). Scale bars represent 100μm. d. FBXW7 targets the phosphorylated substrates and ubiquitinates these substrates for proteasomal degradation. This included phosphorylated cJun, phosphorylated CCNE1, phosphosylated cMyc, and notch intracellular domain (NICD). The non-phosphorylated substrates were affected to varying degrees. While upregulation of cJun, was observed, there was no change in the quantities of CCNE1, cMYC and NOTCH. e. Volcano plot from bulk RNAseq of F vs W organoids revealed minimal differential expression of genes. Only HLA-DQB1 was found to be significantly downregulated, and GSTM1 significantly upregulated in F organoids. All experiments were performed with N = 3 biological replicates.

    Journal: bioRxiv

    Article Title: Mutational order and epistasis determine the consequences of FBXW7 mutations during colorectal cancer evolution

    doi: 10.1101/2023.08.25.554836

    Figure Lengend Snippet: Characterisation of W and F organoids. a. Brightfield microscopy of W and F organoids revealed no observable phenotypic differences. Scale bars represent 500μm. b. Western blot validation showing loss of FBXW7 protein in F organoids. c. Immunofluorescence of W and F organoids with DAPI nuclear stain (blue), F-actin (red), FBXW7 (orange). Scale bars represent 100μm. d. FBXW7 targets the phosphorylated substrates and ubiquitinates these substrates for proteasomal degradation. This included phosphorylated cJun, phosphorylated CCNE1, phosphosylated cMyc, and notch intracellular domain (NICD). The non-phosphorylated substrates were affected to varying degrees. While upregulation of cJun, was observed, there was no change in the quantities of CCNE1, cMYC and NOTCH. e. Volcano plot from bulk RNAseq of F vs W organoids revealed minimal differential expression of genes. Only HLA-DQB1 was found to be significantly downregulated, and GSTM1 significantly upregulated in F organoids. All experiments were performed with N = 3 biological replicates.

    Article Snippet: Rabbit anti-human FBXW7 antibody (1:2500, BS-8394R, Bioss, USA), rabbit anti-human phosphor-CJUN antibody (1:2500, PA5-40193, Invitrogen, USA), rabbit anti-human CJUN antibody (1:2500, ab40766, Abcam, USA), rabbit anti-human phosphor-CCNE1 antibody (1:2500, ab52195, Abcam, USA), rabbit anti-human CCNE1 antibody (1:2500, ab33911, Abcam, USA), rabbit anti-human phosphor-CMYC (1:2500, ab185655 and ab185656, Abcam, USA), rabbit anti-human CMYC (1:2500, ab32072, Abcam, USA), rabbit anti-human NICD (1:2500, #4147, Cell signalling technologies, USA), rabbit anti-human NOTCH1 (1:2500, ab52627, Abcam, USA), and rabbit anti-human GAPDH (1:2500, ab52627, Abcam, USA) was used.

    Techniques: Microscopy, Western Blot, Biomarker Discovery, Immunofluorescence, Staining, Quantitative Proteomics

    Primary and secondary antibodies used for Immunoblotting

    Journal: Molecular Neurodegeneration

    Article Title: Anti-malaria drug artesunate prevents development of amyloid-β pathology in mice by upregulating PICALM at the blood-brain barrier

    doi: 10.1186/s13024-023-00597-5

    Figure Lengend Snippet: Primary and secondary antibodies used for Immunoblotting

    Article Snippet: Rabbit anti-human N-terminal sequence of the cleaved NICD, cross-reacts with mouse NICD (Millipore Sigma, 07-1232, 1:1000) , HRP-conjugated donkey anti-rabbit (Invitrogen, A16023,1:3000).

    Techniques: Sequencing

    Artesunate does not alter the levels of Aβ processing proteins and Aβ clearance enzymes in Picalm +/− ; 5XFAD mice. A amyloid precursor protein (APP) abundance in cortex, B APP C-terminal fragment (APP-CTF) abundance in cortex. C β-secretase (BACE1) abundance in cortex, D soluble APP-β (sAPPβ) levels in cerebrospinal fluid (CSF), E γ–secretase activity as determined by the production of Notch intracellular domain (NICD) fragment from Notch protein, indicated by NICD abundance in cortex, F neprilysin abundance in cortex, and G insulin degrading enzyme (IDE) abundance in cortex of Picalm +/− ; 5X FAD mice treated with artesunate or vehicle as in Fig. A. The relative abundance of proteins was normalized by the house-keeping gene glyceraldehyde 3-phosphate dehydrogenase (GAPDH) protein. Single points per mouse indicated by circles, with boxes representing mean ± SD. A-E , G n = 8 per group; F n = 7–8 per group. ns = non-significant by two-tailed t-test. Full blots for A-C, E-G shown in supp. Fig.

    Journal: Molecular Neurodegeneration

    Article Title: Anti-malaria drug artesunate prevents development of amyloid-β pathology in mice by upregulating PICALM at the blood-brain barrier

    doi: 10.1186/s13024-023-00597-5

    Figure Lengend Snippet: Artesunate does not alter the levels of Aβ processing proteins and Aβ clearance enzymes in Picalm +/− ; 5XFAD mice. A amyloid precursor protein (APP) abundance in cortex, B APP C-terminal fragment (APP-CTF) abundance in cortex. C β-secretase (BACE1) abundance in cortex, D soluble APP-β (sAPPβ) levels in cerebrospinal fluid (CSF), E γ–secretase activity as determined by the production of Notch intracellular domain (NICD) fragment from Notch protein, indicated by NICD abundance in cortex, F neprilysin abundance in cortex, and G insulin degrading enzyme (IDE) abundance in cortex of Picalm +/− ; 5X FAD mice treated with artesunate or vehicle as in Fig. A. The relative abundance of proteins was normalized by the house-keeping gene glyceraldehyde 3-phosphate dehydrogenase (GAPDH) protein. Single points per mouse indicated by circles, with boxes representing mean ± SD. A-E , G n = 8 per group; F n = 7–8 per group. ns = non-significant by two-tailed t-test. Full blots for A-C, E-G shown in supp. Fig.

    Article Snippet: Rabbit anti-human N-terminal sequence of the cleaved NICD, cross-reacts with mouse NICD (Millipore Sigma, 07-1232, 1:1000) , HRP-conjugated donkey anti-rabbit (Invitrogen, A16023,1:3000).

    Techniques: Activity Assay, Two Tailed Test

    Identification of NICD expression in each group of cells by immunofluorescence staining.

    Journal: Computational Intelligence and Neuroscience

    Article Title: Targeting Inhibition of Notch1 Signaling Pathway on the Study of Human Gastric Cancer Stem Cells with Chemosensitization

    doi: 10.1155/2022/1098394

    Figure Lengend Snippet: Identification of NICD expression in each group of cells by immunofluorescence staining.

    Article Snippet: Rabbit anti-human NICD polyclonal antibody, rabbit anti-glial fibrillary acidic protein (GFAP) polyclonal antibody, rhodamine-labeled anti-rabbit IgG antibody, and rhodamine-labeled anti-mouse IgG antibody were purchased from Millipore.

    Techniques: Expressing, Immunofluorescence, Staining

    The expression of nestin and GFAP in each group (mean ± SD; n = 3).

    Journal: Computational Intelligence and Neuroscience

    Article Title: Targeting Inhibition of Notch1 Signaling Pathway on the Study of Human Gastric Cancer Stem Cells with Chemosensitization

    doi: 10.1155/2022/1098394

    Figure Lengend Snippet: The expression of nestin and GFAP in each group (mean ± SD; n = 3).

    Article Snippet: Rabbit anti-human NICD polyclonal antibody, rabbit anti-glial fibrillary acidic protein (GFAP) polyclonal antibody, rhodamine-labeled anti-rabbit IgG antibody, and rhodamine-labeled anti-mouse IgG antibody were purchased from Millipore.

    Techniques: Expressing, Immunofluorescence

    Overexpression of NICD enhanced the formation of xenograft tumor in SCID mice.

    Journal: Computational Intelligence and Neuroscience

    Article Title: Targeting Inhibition of Notch1 Signaling Pathway on the Study of Human Gastric Cancer Stem Cells with Chemosensitization

    doi: 10.1155/2022/1098394

    Figure Lengend Snippet: Overexpression of NICD enhanced the formation of xenograft tumor in SCID mice.

    Article Snippet: Rabbit anti-human NICD polyclonal antibody, rabbit anti-glial fibrillary acidic protein (GFAP) polyclonal antibody, rhodamine-labeled anti-rabbit IgG antibody, and rhodamine-labeled anti-mouse IgG antibody were purchased from Millipore.

    Techniques: Over Expression

    Journal: Cell Reports

    Article Title: The onset of circulation triggers a metabolic switch required for endothelial to hematopoietic transition

    doi: 10.1016/j.celrep.2021.110103

    Figure Lengend Snippet:

    Article Snippet: Rabbit anti-human/rat/mouse NICD - Cleaved Notch1 (Val1744), clone D3B8 , Cell Signaling Technology , Cat# 4147; RRID: AB_2153348.

    Techniques: Blocking Assay, Virus, Recombinant, Modification, Reverse Transcription, TaqMan Assay, DNA Library Preparation, Gene Expression, Control, RNA Sequencing, Mutagenesis, Knock-Out, Software, Membrane