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muc13  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology muc13
    Lack of effect of Compound-1 on <t>MUC13</t> localization in MVID model mice. Immunostaining for MUC13 and ACTG1 in jejunal tissues of control, MYO5BΔIEC, and MYO5B(G519R) mice treated with Compound-1 or vehicle. In control jejunum and distal colon, MUC13 (red) is localized to the apical tips of microvilli above actin filaments (green). Both MYO5B loss-of-function mouse tissues demonstrate strong MUC13 immunostaining in cytoplasm of jejunal and colonic epithelial cells. The mislocalization of MUC13 is not remarkably altered by Compound-1 treatments in MYO5BΔIEC or MYO5B(G519R) mice. Scale bars = 20 µm. MYO5B, myosin Vb; MVID, microvillus inclusion disease.
    Muc13, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+muc13/pmc11684887-59-70-72?v=Santa+Cruz+Biotechnology
    Average 92 stars, based on 21 article reviews
    muc13 - by Bioz Stars, 2026-08
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    Images

    1) Product Images from "Alterations in cellular metabolic pathway and epithelial cell maturation induced by MYO5B defects are partially reversible by LPAR5 activation"

    Article Title: Alterations in cellular metabolic pathway and epithelial cell maturation induced by MYO5B defects are partially reversible by LPAR5 activation

    Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

    doi: 10.1152/ajpgi.00091.2024

    Lack of effect of Compound-1 on MUC13 localization in MVID model mice. Immunostaining for MUC13 and ACTG1 in jejunal tissues of control, MYO5BΔIEC, and MYO5B(G519R) mice treated with Compound-1 or vehicle. In control jejunum and distal colon, MUC13 (red) is localized to the apical tips of microvilli above actin filaments (green). Both MYO5B loss-of-function mouse tissues demonstrate strong MUC13 immunostaining in cytoplasm of jejunal and colonic epithelial cells. The mislocalization of MUC13 is not remarkably altered by Compound-1 treatments in MYO5BΔIEC or MYO5B(G519R) mice. Scale bars = 20 µm. MYO5B, myosin Vb; MVID, microvillus inclusion disease.
    Figure Legend Snippet: Lack of effect of Compound-1 on MUC13 localization in MVID model mice. Immunostaining for MUC13 and ACTG1 in jejunal tissues of control, MYO5BΔIEC, and MYO5B(G519R) mice treated with Compound-1 or vehicle. In control jejunum and distal colon, MUC13 (red) is localized to the apical tips of microvilli above actin filaments (green). Both MYO5B loss-of-function mouse tissues demonstrate strong MUC13 immunostaining in cytoplasm of jejunal and colonic epithelial cells. The mislocalization of MUC13 is not remarkably altered by Compound-1 treatments in MYO5BΔIEC or MYO5B(G519R) mice. Scale bars = 20 µm. MYO5B, myosin Vb; MVID, microvillus inclusion disease.

    Techniques Used: Immunostaining, Control



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    Image Search Results


    A Alcian blue-periodic acid Schiff (AB-PAS) staining of intestinal mucus in mice with or without NP treatment. Scale bars indicate 100 µm (upper) and 50 µm (lower). Data were shown as mea n ± SEM ( n = 12). B IHC stain of intestinal MUC-13 in NP-treated mice. Scale bars indicate 100 µm (upper) and 50 µm (lower). Data were shown as mea n ± SEM ( n = 12) (*** p value < 0.001). C MUC13 expression in NP-treated enterocyte-like differentiated Caco-2 cells for 48 h by ICC stain (Scale bars indicate 20 µm), qPCR, and Western blot. Data are presented as means ± SD ( n = 3). Significant difference was shown by different letters (* p < 0.05; *** p < 0.001). D Western blot analysis of MUC-13 levels in goblet-like LS174T cells treated with NP for 48 h. E Heatmap predicting various intestinal miRNAs suppressing MUC-13 in NP-exposed mice. Validation of miR-700-5p interference on MUC-13 in enterocyte-like differentiated Caco-2 cells by ( F ) qPCR. G ICC stain (Scale bars indicate 20 µm), and ( H ) Western blot. Data are presented as means ± SD ( n = 3). Significant difference was shown by different letters (*** p < 0.001). I Schematic of NP im p act on MUC-13 and mucus secretion in the gut.

    Journal: Nature Communications

    Article Title: Polystyrene nanoplastics disrupt the intestinal microenvironment by altering bacteria-host interactions through extracellular vesicle-delivered microRNAs

    doi: 10.1038/s41467-025-59884-y

    Figure Lengend Snippet: A Alcian blue-periodic acid Schiff (AB-PAS) staining of intestinal mucus in mice with or without NP treatment. Scale bars indicate 100 µm (upper) and 50 µm (lower). Data were shown as mea n ± SEM ( n = 12). B IHC stain of intestinal MUC-13 in NP-treated mice. Scale bars indicate 100 µm (upper) and 50 µm (lower). Data were shown as mea n ± SEM ( n = 12) (*** p value < 0.001). C MUC13 expression in NP-treated enterocyte-like differentiated Caco-2 cells for 48 h by ICC stain (Scale bars indicate 20 µm), qPCR, and Western blot. Data are presented as means ± SD ( n = 3). Significant difference was shown by different letters (* p < 0.05; *** p < 0.001). D Western blot analysis of MUC-13 levels in goblet-like LS174T cells treated with NP for 48 h. E Heatmap predicting various intestinal miRNAs suppressing MUC-13 in NP-exposed mice. Validation of miR-700-5p interference on MUC-13 in enterocyte-like differentiated Caco-2 cells by ( F ) qPCR. G ICC stain (Scale bars indicate 20 µm), and ( H ) Western blot. Data are presented as means ± SD ( n = 3). Significant difference was shown by different letters (*** p < 0.001). I Schematic of NP im p act on MUC-13 and mucus secretion in the gut.

    Article Snippet: For Western blot, the primary antibodies for beta-actin (SC-47778, Santa Cruz, Dallas, Texas, USA), MUC13 (bs-10074R, Bioss, Boston, Massachusetts, USA), GAPDH (GTX100118, GENETEX, Texas, USA), ZO-1 (ab96587, Abcam, Bristol, UK), and OCC (ab216327, Abcam, Bristol, UK) were used to evaluated protein level.

    Techniques: Staining, Expressing, Western Blot, Biomarker Discovery

    A The effects of NP treatment (1 × 10 10 particles/mL) on the growth of various lactic acid bacteria ( L. paracasei, L. acidophilus , and P. acidiloctici ) , Lachnospiraceae sp. (TSD-26; ATCC), and Ruminococcaceae sp. (TSD-27; ATCC). B Schematic of experimental process by interactions between bacterial EV and cell-derived EV. C Impact of Lachnospiraceae sp.-derived EV without or with NP treatment (1 × 10 10 particles/mL) for 18 h on the growth of different bacterial species ( L. paracasei , L. acidophilus , P. acidiloctici , and Ruminococcaceae sp.). D The impact of Ruminococcaceae sp.-derived EV without or with NP treatment (1 × 10 10 particles/mL) for 44 h on the growth of different bacterial species ( L. paracasei , L. acidophilus , P. acidiloctici , and Lachnospiraceae sp.). E Impact of goblet-like LS174T cells without or with NP treatment (10 6 particles/mL) for 48 h on the growth of different bacterial species ( L. paracasei, L. acidophilus, P. acidiloctici , and Lachnospiraceae sp. and Ruminococcaceae sp.). F Western blot of MUC13 inhibition by Lachnospiraceae sp.-derived EV. Data were shown as mea n ± SD ( n = 3) (* p value < 0.05). G Schematic representation summarizing the proposed mechanisms of NP-induced modulation of gut microbiota via EV. NP are taken up by Lachnospiraceae , whose EV suppress MUC13 expression in goblet cells. Concurrently, NP-modified EV from goblet cells promote the growth of Ruminococcaceae , collectively contributing to gut microbiota imbalance and potential intestinal barrier dysfunction.

    Journal: Nature Communications

    Article Title: Polystyrene nanoplastics disrupt the intestinal microenvironment by altering bacteria-host interactions through extracellular vesicle-delivered microRNAs

    doi: 10.1038/s41467-025-59884-y

    Figure Lengend Snippet: A The effects of NP treatment (1 × 10 10 particles/mL) on the growth of various lactic acid bacteria ( L. paracasei, L. acidophilus , and P. acidiloctici ) , Lachnospiraceae sp. (TSD-26; ATCC), and Ruminococcaceae sp. (TSD-27; ATCC). B Schematic of experimental process by interactions between bacterial EV and cell-derived EV. C Impact of Lachnospiraceae sp.-derived EV without or with NP treatment (1 × 10 10 particles/mL) for 18 h on the growth of different bacterial species ( L. paracasei , L. acidophilus , P. acidiloctici , and Ruminococcaceae sp.). D The impact of Ruminococcaceae sp.-derived EV without or with NP treatment (1 × 10 10 particles/mL) for 44 h on the growth of different bacterial species ( L. paracasei , L. acidophilus , P. acidiloctici , and Lachnospiraceae sp.). E Impact of goblet-like LS174T cells without or with NP treatment (10 6 particles/mL) for 48 h on the growth of different bacterial species ( L. paracasei, L. acidophilus, P. acidiloctici , and Lachnospiraceae sp. and Ruminococcaceae sp.). F Western blot of MUC13 inhibition by Lachnospiraceae sp.-derived EV. Data were shown as mea n ± SD ( n = 3) (* p value < 0.05). G Schematic representation summarizing the proposed mechanisms of NP-induced modulation of gut microbiota via EV. NP are taken up by Lachnospiraceae , whose EV suppress MUC13 expression in goblet cells. Concurrently, NP-modified EV from goblet cells promote the growth of Ruminococcaceae , collectively contributing to gut microbiota imbalance and potential intestinal barrier dysfunction.

    Article Snippet: For Western blot, the primary antibodies for beta-actin (SC-47778, Santa Cruz, Dallas, Texas, USA), MUC13 (bs-10074R, Bioss, Boston, Massachusetts, USA), GAPDH (GTX100118, GENETEX, Texas, USA), ZO-1 (ab96587, Abcam, Bristol, UK), and OCC (ab216327, Abcam, Bristol, UK) were used to evaluated protein level.

    Techniques: Bacteria, Derivative Assay, Western Blot, Inhibition, Expressing, Modification

    Lack of effect of Compound-1 on MUC13 localization in MVID model mice. Immunostaining for MUC13 and ACTG1 in jejunal tissues of control, MYO5BΔIEC, and MYO5B(G519R) mice treated with Compound-1 or vehicle. In control jejunum and distal colon, MUC13 (red) is localized to the apical tips of microvilli above actin filaments (green). Both MYO5B loss-of-function mouse tissues demonstrate strong MUC13 immunostaining in cytoplasm of jejunal and colonic epithelial cells. The mislocalization of MUC13 is not remarkably altered by Compound-1 treatments in MYO5BΔIEC or MYO5B(G519R) mice. Scale bars = 20 µm. MYO5B, myosin Vb; MVID, microvillus inclusion disease.

    Journal: American Journal of Physiology - Gastrointestinal and Liver Physiology

    Article Title: Alterations in cellular metabolic pathway and epithelial cell maturation induced by MYO5B defects are partially reversible by LPAR5 activation

    doi: 10.1152/ajpgi.00091.2024

    Figure Lengend Snippet: Lack of effect of Compound-1 on MUC13 localization in MVID model mice. Immunostaining for MUC13 and ACTG1 in jejunal tissues of control, MYO5BΔIEC, and MYO5B(G519R) mice treated with Compound-1 or vehicle. In control jejunum and distal colon, MUC13 (red) is localized to the apical tips of microvilli above actin filaments (green). Both MYO5B loss-of-function mouse tissues demonstrate strong MUC13 immunostaining in cytoplasm of jejunal and colonic epithelial cells. The mislocalization of MUC13 is not remarkably altered by Compound-1 treatments in MYO5BΔIEC or MYO5B(G519R) mice. Scale bars = 20 µm. MYO5B, myosin Vb; MVID, microvillus inclusion disease.

    Article Snippet: The primary antibodies against NDUFB8 (1:1,000, Abcam ab192878), HMGCS2 (1:50, Abcam ab137043), NHE3 (1:200, Novus NBP1-82574), SGLT1 (0.5 μg/mL, own) , LAMP1 (1:100, Santa Cruz sc-19992), PHH3 (1:50, Novus NBP3-08511IR, DyLight 750), Ki67 (1:100, Cell Signaling 11882S, Alexa Fluor 488), DCLK1 (1:2,000, Abcam ab202755 Alexa Fluor 647), PCNA (1:50, Santa Cruz sc-56 Alexa Fluor 647), β-catenin/CTNNB1 (12F7) (1:100, Novus NBP1-54467R, DyLight 550), villin (1:50, Santa Cruz sc-58897 Alexa Fluor 488), MUC13 (1:100, Santa Cruz, sc-390115 Alexa Fluor 546), and ACTG1 (1:100, Santa Cruz sc-65638 Alexa Fluor 546 or Alexa Fluor 790) were diluted in Dako antibody diluent with background reducing compound (S3022) and incubated on sections for 1 h at room temperature or overnight at 4°C.

    Techniques: Immunostaining, Control

    Journal: iScience

    Article Title: Bidirectional signals generated by Siglec-7 and its crucial ligand tri-sialylated T to escape of cancer cells from immune surveillance

    doi: 10.1016/j.isci.2024.111139

    Figure Lengend Snippet:

    Article Snippet: Rabbit Anti-MUC13 , IMGENEX , Cat# IMG-6250A, RRID: AB_1930301.

    Techniques: Blocking Assay, Plasmid Preparation, Purification, Control, Staining, Recombinant, Membrane, Mutagenesis, Cytotoxicity Assay, Cloning, Expressing, Sequencing, Software

    Journal: iScience

    Article Title: Bidirectional signals generated by Siglec-7 and its crucial ligand tri-sialylated T to escape of cancer cells from immune surveillance

    doi: 10.1016/j.isci.2024.111139

    Figure Lengend Snippet:

    Article Snippet: The antibodies were Anti-β-Actin antibody (1:5000, Sigma), Anti-AKT (1:1000, Cell Signaling Technology), Anti- p -AKT (S473) (1:1000, Cell Signaling Technology), Anti-phospho ERK1/2 (1:1000, Cell Signaling Technology), Anti-p44/42 MAPK (ERK1/2) (1:1000, Cell Signaling Technology), Anti-rabbit IgG-HRP (1:1000, Cell Signaling Technology), Goat TrueBlot anti-goat Ig HRP (1:2000, ebioscience), Anti-Mouse IgG HRP-Linked Whole Ab (1:2000, GE HealthCare), Anti-MUC13 (1:1000, IMGENEX), Anti- p -Tyr (4G10) HEP conjugate (1:5000, Millipore), Anti-SHP-1 (1:1000, Millipore), Anti-Siglec-7/CD328 antibody (1:1000, R&D), Anti-PODXL (3D3) (1:1000, Santa Cruz), Anti- p -Tyr (PY20) HRP conjugate (1:2000, BD), Rat anti-PDPN (NZ-1) (1:1000, AngioBio Co), Anti-Rat IgG-HRP (1:2000, Cosmo bio), ABC standard kit Elite (5 μL/mL each, Vector) for immunoblotting, Anti-rabbit IgG Fab2 Alexa 555 (1:400, Cell Signaling Technology), Anti-mouse IgG Fab2 Alexa 647 (1:400, Cell Signaling Technology), Anti-mouse IgG Alexa 488 (1:400, Invitrogen), Phalloidin Alexa 647 (1:400, Invitrogen), DAPI (1:500, Sigma) for immunocyte chemistry.

    Techniques: Blocking Assay, Plasmid Preparation, Purification, Control, Staining, Recombinant, Membrane, Mutagenesis, Cytotoxicity Assay, Cloning, Expressing, Sequencing, Software