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Mus musculus (House mouse)

Homo sapiens (Human)

Rattus norvegicus (Rat)

Danio rerio (Zebrafish)

Gallus gallus domesticus (Chicken)

Research Area

Cancer Research

Neuroscience

Immunology and Microbiology

Cell Biology

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Fig.2.B showing Immunocytochemistry in a Rattus norvegicus (Rat) sample from the publication: A Strategy for Magnetic and Electric Stimulation to Enhance Proliferation and Differentiation of NPCs Seeded over PLA Electrospun Membranes.

Fig.2.A showing Immunocytochemistry in a Rattus norvegicus (Rat) sample from the publication: A Strategy for Magnetic and Electric Stimulation to Enhance Proliferation and Differentiation of NPCs Seeded over PLA Electrospun Membranes.

Fig.5.B showing Immunohistochemistry in a Rattus norvegicus (Rat) sample from the publication: A new murine ileostomy model: recycling stool prevents intestinal atrophy in the distal side of ileostomy.

Fig.5.A showing Immunohistochemistry in a Rattus norvegicus (Rat) sample from the publication: A new murine ileostomy model: recycling stool prevents intestinal atrophy in the distal side of ileostomy.

Fig.6.B showing Immunohistochemistry in a Rattus norvegicus (Rat) sample from the publication: A new murine ileostomy model: recycling stool prevents intestinal atrophy in the distal side of ileostomy.

Fig.6.A showing Immunohistochemistry in a Rattus norvegicus (Rat) sample from the publication: A new murine ileostomy model: recycling stool prevents intestinal atrophy in the distal side of ileostomy.

Fig.5.C,D showing Immunohistochemistry in a Homo sapiens (Human) sample from the publication: WDHD1 Leads to Cisplatin Resistance by Promoting MAPRE2 Ubiquitination in Lung Adenocarcinoma.

Fig.4.E showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: Truncated PPM1D impairs stem cell response to genotoxic stress and promotes growth of APC-deficient tumors in the mouse colon.

Fig.3.F showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Truncated PPM1D impairs stem cell response to genotoxic stress and promotes growth of APC-deficient tumors in the mouse colon.

Fig.4.B showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Dietary intake of genistein suppresses hepatocellular carcinoma through AMPK-mediated apoptosis and anti-inflammation.

Fig.7.F showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Utrophin Compensates dystrophin Loss during Mouse Spermatogenesis.

Fig.3.A showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: ERK5 signalling rescues intestinal epithelial turnover and tumour cell proliferation upon ERK1/2 abrogation.

Fig.5.A showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: ERK5 signalling rescues intestinal epithelial turnover and tumour cell proliferation upon ERK1/2 abrogation.

Fig.4.C showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: ERK5 signalling rescues intestinal epithelial turnover and tumour cell proliferation upon ERK1/2 abrogation.

Fig.4.A showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: The TLX-miR-219 cascade regulates neural stem cell proliferation in neurodevelopment and schizophrenia iPSC model.

Fig.6.D showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: The TLX-miR-219 cascade regulates neural stem cell proliferation in neurodevelopment and schizophrenia iPSC model.

Fig.3.E showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: The TLX-miR-219 cascade regulates neural stem cell proliferation in neurodevelopment and schizophrenia iPSC model.

Fig.6.F showing Immunohistochemistry in a Homo sapiens (Human) sample from the publication: SD-208, a novel protein kinase D inhibitor, blocks prostate cancer cell proliferation and tumor growth in vivo by inducing G2/M cell cycle arrest.

18 images found

Spint1 disruption in mouse pancreas leads to glucose intolerance and impaired insulin production involving HEPSIN/MAFA.

In Nature Communications on 3 December 2024 by Lin, H. H., Yu, I. S., et al.

SPINT1, a membrane-anchored serine protease inhibitor, regulates cascades of pericellular proteolysis while its tissue-specific functions remain incompletely characterized. In this study, we generate Spint1-lacZ knock-in mice and observe Spint1 expression in embryonic pancreatic epithelium. Pancreas-specific Spint1 disruption significantly diminishes islet size and mass, causing glucose intolerance and downregulation of MAFA and insulin. Mechanistically, the serine protease HEPSIN interacts with SPINT1 in β cells, and Hepsin silencing counteracts the downregulation of Mafa and Ins1 caused by Spint1 depletion. Furthermore, we demonstrate a potential interaction between HEPSIN and GLP1R in β cells. Spint1 silencing or Hepsin overexpression reduces GLP1R-related cyclic AMP levels and Mafa expression. Spint1-disrupted mice also exhibit a significant reduction in Exendin-4-induced insulin secretion. Moreover, SPINT1 expression increases in islets of prediabetic humans compared to non-prediabetic groups. The results unveil a role for SPINT1 in β cells, modulating glucose homeostasis and insulin production via HEPSIN/MAFA signaling.
© 2024. The Author(s).

Overexpression of NUDT16L1 sustains proper function of mitochondria and leads to ferroptosis insensitivity in colorectal cancer.

In Redox Biology on 1 November 2024 by Lin, Y. S., Tsai, Y. C., et al.

Cancer research is continuously exploring new avenues to improve treatments, and ferroptosis induction has emerged as a promising approach. However, the lack of comprehensive analysis of the ferroptosis sensitivity in different cancer types has limited its clinical application. Moreover, identifying the key regulator that influences the ferroptosis sensitivity during cancer progression remains a major challenge. In this study, we shed light on the role of ferroptosis in colorectal cancer and identified a novel ferroptosis repressor, NUDT16L1, that contributes to the ferroptosis insensitivity in this cancer type. Mechanistically, NUDT16L1 promotes ferroptosis insensitivity in colon cancer by enhancing the expression of key ferroptosis repressor and mitochondrial genes through direct binding to NAD-capped RNAs and the indirect action of MALAT1. Our findings also reveal that NUDT16L1 localizes to the mitochondria to maintain its proper function by preventing mitochondrial DNA leakage after treatment of ferroptosis inducer in colon cancer cells. Importantly, our orthotopic injection and Nudt16l1 transgenic mouse models of colon cancer demonstrated the critical role of NUDT16L1 in promoting tumor growth. Moreover, clinical specimens revealed that NUDT16L1 was overexpressed in colorectal cancer, indicating its potential as a therapeutic target. Finally, our study shows the therapeutic potential of a NUDT16L1 inhibitor in vitro, in vivo and ex vivo. Taken together, these findings provide new insights into the crucial role of NUDT16L1 in colorectal cancer and highlight its potential as a promising therapeutic target.
Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.

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Truncated PPM1D impairs stem cell response to genotoxic stress and promotes growth of APC-deficient tumors in the mouse colon.

In Cell Death Dis on 28 October 2019 by Burocziova, M., Burdová, K., et al.

Fig.4.E

Fig.4.E showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: Truncated PPM1D impairs stem cell response to genotoxic stress and promotes growth of APC-deficient tumors in the mouse colon.

Truncation of PPM1D promotes growth of APC-induced colon tumors.a Wild-type Ppm1d+/+, Ppm1dT/+, Apcmin, and ApcminPpm1dT/+ mice were sacrificed at 16 weeks and the number of intestinal polyps was scored (p = 0.044). Numbers indicate numbers of animals of each genotype. b Wild-type Ppm1d+/+, Ppm1d... more

Truncation of PPM1D promotes growth of APC-induced colon tumors.a Wild-type Ppm1d+/+, Ppm1dT/+, Apcmin, and ApcminPpm1dT/+ mice were sacrificed at 16 weeks and the number of intestinal polyps was scored (p = 0.044). Numbers indicate numbers of animals of each genotype. b Wild-type Ppm1d+/+, Ppm1dT/+, Apcmin, and ApcminPpm1dT/+ mice were sacrificed at 16 weeks and tumor formation in colon was scored. Proportion of animals developing tumor(s) is shown, N indicates number of animals of each genotype. Statistical significance was determined by two tailed Fisher’s exact test (***p < 0.001, **p < 0.01, *p < 0.05). c Proportion of animals with multiple tumors in mice from b was scored. N indicates number of animals that developed at least one tumor. Statistical significance was determined by two tailed Fisher’s exact test (***p < 0.001, **p < 0.01, *p < 0.05). d Volume of the colon tumors developed in mice with indicated genotypes. In case of multiplicity, the largest tumor was quantified. Line indicates mean. e Representative sections of colon tumors from 16 weeks old Apcmin, ApcminPpm1dT/+ mice stained for Ki-67. Scale bars 50 and 25 μm. f Kaplan–Meier survival plot of mice of indicated genotypes over a period of 50 weeks. Statistical significance was determined by log rank test as follows Apcmin vs. ApcminPpm1dT/+p = 0.019; Apcmin vs. ApcminTp53+/−p = 0.008; ApcminPpm1dT/+ vs. ApcminTp53+/−p = 0.717; Ppm1d+/+ vs. Ppm1dT/+p = 0.014). Numbers of animals per group are shown less

Collected and cropped from Cell Death Dis by CiteAb, provided under a CC-BY license

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Truncated PPM1D impairs stem cell response to genotoxic stress and promotes growth of APC-deficient tumors in the mouse colon.

In Cell Death Dis on 28 October 2019 by Burocziova, M., Burdová, K., et al.

Fig.3.F

Fig.3.F showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Truncated PPM1D impairs stem cell response to genotoxic stress and promotes growth of APC-deficient tumors in the mouse colon.

Truncation of PPM1D impairs response to ionizing radiation in the mouse colon.a Expression of Cdkn1a in colon mucosa 6 and 12 h after exposure of mice of indicated genotypes to 3 Gy of IR was measured by RT-qPCR and normalized to GAPDH (n ≥ 3). b) Expression of PUMA in the colon mucosa 48 h after... more

Truncation of PPM1D impairs response to ionizing radiation in the mouse colon.a Expression of Cdkn1a in colon mucosa 6 and 12 h after exposure of mice of indicated genotypes to 3 Gy of IR was measured by RT-qPCR and normalized to GAPDH (n ≥ 3). b) Expression of PUMA in the colon mucosa 48 h after exposure to 3 Gy of IR was measured by RT-qPCR and normalized to GAPDH (n ≥ 3). c LGR5-EGFP-positive ICS cells were sorted from colon of wt Ppm1d+/+, and Ppm1dT/+ mice exposed or not to 3 Gy of IR and expression of Cdkn1a was measured by RT-qPCR and normalized to GAPDH (n = 3). d Levels of p21 were determined in the mouse colon 48 h after exposure to 3 Gy of IR by immuno-histochemistry. The percentage of p21-positive cells per crypt was scored (n ≥ 4). At least 90 crypts were counted for each group. Representative images are shown. Scale bar 25 µm. e Apoptotic cells were detected in colon epithelia of mice of indicated genotypes 48 h after exposure to IR (3 Gy) by TUNEL apoptosis assay (n = 5). At least 90 crypts were counted for each group. Representative images are shown. Scale bar 50 µm. f Levels of a proliferation marker Ki-67 were determined in the mouse colon 48 h after exposure to 3 Gy of IR by immuno-histochemistry (n ≥ 4). At least 90 crypts were counted for each group. Representative images are shown. Scale bar 50 µm less

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ERK5 signalling rescues intestinal epithelial turnover and tumour cell proliferation upon ERK1/2 abrogation.

In Nat Commun on 17 May 2016 by de Jong, P. R., Taniguchi, K., et al.

Fig.3.A

Fig.3.A showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: ERK5 signalling rescues intestinal epithelial turnover and tumour cell proliferation upon ERK1/2 abrogation.

Abrogation of ERK1/2IEC results in enhanced ERK5 signalling.(a,b) Ki67 staining of paraffin-embedded ileum sections from fl/fl and ΔIEC mice, 10 days after tamoxifen treatment. Nuclear staining with Hoechst. Sections were analysed by confocal fluorescent imaging; scale bar, 100 μm (a). Enumeratio... more

Abrogation of ERK1/2IEC results in enhanced ERK5 signalling.(a,b) Ki67 staining of paraffin-embedded ileum sections from fl/fl and ΔIEC mice, 10 days after tamoxifen treatment. Nuclear staining with Hoechst. Sections were analysed by confocal fluorescent imaging; scale bar, 100 μm (a). Enumeration of the number of Ki67-positive cells per crypt (b). Data are mean±s.e.m. of 10 crypts (n=3 per group). **P<0.001 (Student's t-test). (c) Immunoblotting for indicated proteins with IEC lysates isolated from fl/fl and ΔIEC mice as in a. (d) Immunoblotting for indicated proteins with IEC lysates as in a. (e) HCT116 cells were treated with the specific MEK1/2 inhibitor, PD0325901, for 0, 1, 2, 4 or 6 h and analysed by immunoblotting for indicated proteins. (f) HCT116 cells were treated with PD0325901 (0, 1, 10 and 100 nM) for 6 h and analysed by immunoblotting for indicated proteins. As control, some cells were co-treated with the specific ERK5 inhibitor, XMD8-92 (10 μM). (g) DLD-1 cells were treated as in e, and cell lysates analysed by immunoblotting. (h) DLD-1 cells were treated as in f, and lysates were analysed by immunoblotting. (i) Caco2 cells were treated as in e, and lysates were analysed by immunoblotting. (j) Caco2 cells were treated as in f, and analysed by immunoblotting. All data are representative of two to three experiments. less

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The TLX-miR-219 cascade regulates neural stem cell proliferation in neurodevelopment and schizophrenia iPSC model.

In Nat Commun on 11 March 2016 by Murai, K., Sun, G., et al.

Fig.6.D

Fig.6.D showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: The TLX-miR-219 cascade regulates neural stem cell proliferation in neurodevelopment and schizophrenia iPSC model.

The Dpi peptide regulates NSC proliferation and differentiation.(a–c) Expression of the Dpi peptide inhibits NSC proliferation and promotes neuronal differentiation, and this effect could be reversed by the miR-219 inhibitor, TuD-miR-219. Mouse embryonic NSCs were transduced with virus expressing... more

The Dpi peptide regulates NSC proliferation and differentiation.(a–c) Expression of the Dpi peptide inhibits NSC proliferation and promotes neuronal differentiation, and this effect could be reversed by the miR-219 inhibitor, TuD-miR-219. Mouse embryonic NSCs were transduced with virus expressing the Dpi peptide or a control peptide (C), in the absence or presence of TuD-miR-219. The virus-transduced cells were labelled with a GFP reporter. Cell proliferation was determined by the percentage of GFP+BrdU+ cells (BrdU+GFP+/GFP+; b) and neuronal differentiation was determined by the percentage of GFP+Tuj1+ cells (Tuj1+GFP+/GFP+; c). n=7 (b); n=5 (c). ‘n' represents experimental repeats. (d–g) Expression of Dpi inhibited NSC proliferation (d,e), but promoted neuronal differentiation (f,g) in mouse brains. E13.5 mouse brains were electroporated in utero with vectors expressing: (1) a control peptide and RFP reporter (C); (2) Dpi peptide and RFP reporter (Dpi); (3) TuD-miR-219 plus control peptide and RFP reporter (TuD-miR-219+C); or (4) TuD-miR-219 plus Dpi and RFP reporter (TuD-miR-219+Dpi). The electroporated cells were labelled with RFP, proliferating cells were labelled with Ki67 (e) and neuronal cells were labelled with DCX (f). The percentage of RFP+Ki67+ cells (e) or RFP+ cells that migrated to the CP (g) out of total RFP+ cells is shown. n=3 mice per group for panels (e,g). *P<0.05, **P<0.01 and ***P<0.001 by Student's t-test for panels (b,c,e,g). Scale bar, 100 μm for panel (a); 50 μm for panel (d); and 200 μm for panel (f). less

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The TLX-miR-219 cascade regulates neural stem cell proliferation in neurodevelopment and schizophrenia iPSC model.

In Nat Commun on 11 March 2016 by Murai, K., Sun, G., et al.

Fig.3.E

Fig.3.E showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: The TLX-miR-219 cascade regulates neural stem cell proliferation in neurodevelopment and schizophrenia iPSC model.

miR-219 inhibits NSC proliferation and promotes neuronal differentiation.(a,b) Overexpressing miR-219 in NSCs inhibited cell proliferation (a) and promoted neuronal differentiation (b). BrdU or Tuj1 staining is shown in red and Dapi counterstaining is shown in blue. (c,d) Quantification of BrdU+ ... more

miR-219 inhibits NSC proliferation and promotes neuronal differentiation.(a,b) Overexpressing miR-219 in NSCs inhibited cell proliferation (a) and promoted neuronal differentiation (b). BrdU or Tuj1 staining is shown in red and Dapi counterstaining is shown in blue. (c,d) Quantification of BrdU+ cells (c) and Tuj1+ cells (d) in control RNA (C) and miR-219-treated NSCs. n=5; *P<0.001 by Student's t-test for both panels. ‘n' represents experimental repeats. (e) In utero electroporation of miR-219 decreased NSC proliferation in the VZ/SVZ of embryonic brains. Electroporated cells were labelled with RFP and proliferating cells were labelled with Ki67. (f) The percentage of RFP+Ki67+ cells out of total RFP+ cells in control RNA or miR-219-electroporated brains. n=3 mice per group. *P<0.01 by Student's t-test. (g) Electroporation of miR-219 induced precocious outward cell migration. The electroporated brains were stained for neuronal marker doublecortin (DCX). Transfected cells were labelled with RFP. (h) The percentage of electroporated cells (RFP+) that migrated to the CP. n=3 mice per group. *P<0.01 by Student's t-test. (i) Higher magnification images of RFP+DCX+ cells at the CP of brains electroporated with control RNA or miR-219. Scale bar, 50 μm for panels (a,b,e); 100 μm for panel (g); and 25 μm for panel (i). (j) The percentage of Tbr1+RFP+ cells out of total RFP+ cells in control RNA or miR-219-electroporated brains. n=3 mice per group. *P<0.01 by Student's t-test. less

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SD-208, a novel protein kinase D inhibitor, blocks prostate cancer cell proliferation and tumor growth in vivo by inducing G2/M cell cycle arrest.

In PLoS One on 10 March 2015 by Tandon, M., Salamoun, J. M., et al.

Fig.6.F

Fig.6.F showing Immunohistochemistry in a Homo sapiens (Human) sample from the publication: SD-208, a novel protein kinase D inhibitor, blocks prostate cancer cell proliferation and tumor growth in vivo by inducing G2/M cell cycle arrest.

SD-208 inhibited the growth of PC3 tumor xenografts in vivo.A-D. Effects of SD-208 on the growth of PC3 tumor xenograft. PC3 cells (1.4 X 106) were injected s.c. to both flanks of nude mice. Once tumors were palpable, mice were randomized into two groups (5 mice/group) and were administered 0.2 m... more

SD-208 inhibited the growth of PC3 tumor xenografts in vivo.A-D. Effects of SD-208 on the growth of PC3 tumor xenograft. PC3 cells (1.4 X 106) were injected s.c. to both flanks of nude mice. Once tumors were palpable, mice were randomized into two groups (5 mice/group) and were administered 0.2 ml twice daily doses of vehicle [1% (w/v) methylcellulose] or SD-208 (60 mg/kg) by oral gavage. Tumor volume (C) and mouse weight (D) were measured every 2 to 3 days. Twenty-four days after treatment, mice were euthanized by CO2 inhalation, and tumors were excised. Images of representative mice (A) and dissected tumors (B) are shown. All animal studies were conducted in accordance with the Institutional Animal Care and Use Committee (IACUC). Statistical significance was determined using the unpaired t-test. **, p<0.01; ***, p<0.001. E, Analysis of apoptotic marker cleaved caspase-3 by IHC. Quantification of in situ cleaved caspase-3-positive cells as described in Materials and Methods. Representative images of cleaved caspase-3 staining (x200) are shown. F, Analysis of proliferative marker Ki67 by IHC. Quantification of Ki-67-positive cells or proliferation index as described in Materials and Methods. Representative images of Ki-67 staining (x200) are shown. G. Analysis of PKD-regulated biomarkers in PC3 tumor xenografts. Cell lysates were prepared from tumor explants obtained from vehicle and SD-208-treated mice. Levels of PKD-regulated proteins were analyzed by Western blotting analysis. The densitometry data represents ‘fold change’ as compared with vehicle control after normalization with GAPDH as loading control. H. Effect of SD-208 on the PKD2 activity in PC3 tumor xenografts. Cell lysates from tumor explants obtained from vehicle and SD-208-treated mice were immunoprecipitated with PKD2 antibody followed by in vitro kinase assay as described in Material and Methods. The experiment was repeated three times and data are the mean ± S.E. of all three independent experiments with triplicate determinations at each data point in each experiment. less

Collected and cropped from PLoS One by CiteAb, provided under a CC-BY license

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