Product Citations: 864

Fig.3.C showing Immunohistochemistry-immunofluorescence from the publication: Acute stress induces severe neural inflammation and overactivation of glucocorticoid signaling in interleukin-18-deficient mice.
Fig.3.A showing Immunocytochemistry-immunofluorescence from the publication: Disruption of rack1 suppresses SHH-type medulloblastoma formation in mice.
Fig.7.E showing Immunocytochemistry in a Homo sapiens (Human) sample from the publication: RNAi Screening Identifies that TEX10 Promotes the Proliferation of Colorectal Cancer Cells by Increasing NF-κB Activation.
Fig.3.E showing Immunocytochemistry-immunofluorescence in a Homo sapiens (Human) sample from the publication: A new patient-derived iPSC model for dystroglycanopathies validates a compound that increases glycosylation of α-dystroglycan.
Fig.3.F showing Immunocytochemistry-immunofluorescence in a Homo sapiens (Human) sample from the publication: A new patient-derived iPSC model for dystroglycanopathies validates a compound that increases glycosylation of α-dystroglycan.
Fig.3.F showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration.
Fig.2.D showing Western Blotting in a Mus musculus (House mouse) sample from the publication: ABL kinase inhibition sensitizes primary lung adenocarcinomas to chemotherapy by promoting tumor cell differentiation.
Fig.2.C showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: ABL kinase inhibition sensitizes primary lung adenocarcinomas to chemotherapy by promoting tumor cell differentiation.
Fig.3.E showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Deficiency in intestinal epithelial O-GlcNAcylation predisposes to gut inflammation.
Fig.3.C showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: Estrogen Action in the Epithelial Cells of the Mouse Vagina Regulates Neutrophil Infiltration and Vaginal Tissue Integrity.
Fig.1.A showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: Estrogen Action in the Epithelial Cells of the Mouse Vagina Regulates Neutrophil Infiltration and Vaginal Tissue Integrity.
Fig.5.D showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: hnRNP I regulates neonatal immune adaptation and prevents colitis and colorectal cancer.
Fig.5.C showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: hnRNP I regulates neonatal immune adaptation and prevents colitis and colorectal cancer.
Fig.2.A showing Immunocytochemistry-immunofluorescence in a Pan troglodytes (Common chimpanzee) sample from the publication: 2D and 3D Stem Cell Models of Primate Cortical Development Identify Species-Specific Differences in Progenitor Behavior Contributing to Brain Size.
Fig.4.B showing Immunocytochemistry-immunofluorescence in a Pan troglodytes (Common chimpanzee) sample from the publication: 2D and 3D Stem Cell Models of Primate Cortical Development Identify Species-Specific Differences in Progenitor Behavior Contributing to Brain Size.
Fig.3.E,F showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: Inhibition of the JAK2/STAT3 pathway reduces gastric cancer growth in vitro and in vivo.
Fig.1.A showing Flow cytometry/Cell sorting from the publication: Novel application of Ki67 to quantify antigen-specific in vitro lymphoproliferation.
Fig.5.A showing Flow cytometry/Cell sorting from the publication: Novel application of Ki67 to quantify antigen-specific in vitro lymphoproliferation.
18 images found

Gas1-high quiescent neural stem cells are multipotent and produce oligodendrocytes during aging and after demyelinating injury.

In PLoS Biology on 1 April 2025 by Ding, C., Pan, Z., et al.

Quiescent neural stem cells (qNSCs) in the adult mouse subventricular zone (SVZ) normally have limited capacity to generate glia. Gliogenic domains are present in both dorsal and ventral SVZ, with the ventral region featuring a subpopulation of Gli1+ qNSCs. In dorsal SVZ, however, the molecular identity and developmental origin of oligodendrogenic qNSCs remains elusive. Here, through single-cell analysis and lineage tracing, we identify an undefined subpopulation of Gas1high qNSCs in dorsal SVZ, distinct from Gli1+ qNSCs. These cells originate from embryonic Gas1high dorsal radial glia, and persist into the aged SVZ. Remarkably, they are multipotent and more gliogenic than Gas1low/- qNSCs, continuously generating oligodendrocytes in the adult and aged brain, and can be mobilized for myelin repair upon demyelination. Together, our study uncovers a subpopulation of dorsally derived, multipotent long-term qNSCs in the adult and aged SVZ with enhanced gliogenic potential, shedding light on the heterogeneity and plasticity of NSCs in normal, aging, and disease conditions.
Copyright: © 2025 Ding et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

  • Neuroscience
  • Stem Cells and Developmental Biology
Show More
Show Less

Deciphering shared molecular dysregulation across Parkinson's disease variants using a multi-modal network-based data integration and analysis.

In NPJ Parkinson's Disease on 31 March 2025 by Žagare, A., Balaur, I., et al.

Parkinson's disease (PD) is a progressive neurodegenerative disorder with no effective treatment. Advances in neuroscience and systems biomedicine now enable the use of complex patient-specific in vitro disease models and cutting-edge computational tools for data integration, enhancing our understanding of complex PD mechanisms. To explore common biomedical features across monogenic PD forms, we developed a knowledge graph (KG) by integrating previously published high-content imaging and RNA sequencing data of PD patient-specific midbrain organoids harbouring LRRK2-G2019S, SNCA triplication, GBA-N370S or MIRO1-R272Q mutations with publicly available biological data. Furthermore, we generated a single-cell RNA sequencing dataset of midbrain organoids derived from idiopathic PD patients (IPD) to stratify IPD patients within the spectrum of monogenic forms of PD. Despite the high degree of PD heterogeneity, we found that common transcriptomic dysregulation in monogenic PD forms is reflected in glial cells of IPD patient midbrain organoids. In addition, dysregulation in ROBO signalling might be involved in shared pathophysiology between monogenic PD and IPD cases.
© 2025. The Author(s).

  • IHC-IF
  • Homo sapiens (Human)
  • Neuroscience
Show More
Show Less

Astrocyte-secreted cues promote neural maturation and augment activity in human forebrain organoids.

In Nature Communications on 23 March 2025 by Zheng, H., Feng, Y., et al.

Brain organoids have been proposed as suitable human brain model candidates for a variety of applications. However, the lack of appropriate maturation limits the transferability of such functional tools. Here, we present a method to facilitate neuronal maturation by integrating astrocyte-secreted factors into hPSC-derived 2D and 3D neural culture systems. We demonstrate that protein- and nutrient-enriched astrocyte-conditioned medium (ACM) accelerates neuronal differentiation with enlarged neuronal layer and the overproduction of deep-layer cortical neurons. We captured the elevated changes in the functional activity of neuronal networks within ACM-treated organoids using comprehensive electrophysiological recordings. Furthermore, astrocyte-secreted cues can induce lipid droplet accumulation in neural cultures, offering protective effects in neural differentiation to withstand cellular stress. Together, these data indicate the potential of astrocyte secretions to promote neural maturation.
© 2025. The Author(s).

  • IHC
  • Homo sapiens (Human)
  • Neuroscience
Show More
Show Less

Outer radial glia promotes white matter regeneration after neonatal brain injury.

In Cell Reports Medicine on 18 March 2025 by Jinnou, H., Rosko, L. M., et al.

The developing gyrencephalic brain contains a large population of neural stem cells in the ventricular zone and outer subventricular zone (OSVZ), the latter populated by outer radial glia (oRG). The role of oRG during postnatal development is not well understood. We show that oRG cells increase proliferative capacity and contribute to oligodendrocyte precursor cell (OPC) production following brain injury in human infants and neonatal piglets, whose brains resemble the human brain in structure and development. RNA sequencing revealed oRG-specific transcriptional responses to injury in piglets and showed that the activating transcription factor 5 (ATF5) pathway positively regulates oRG proliferation. Intranasal activation of ATF5 using salubrinal enhanced OSVZ-derived oligodendrogenesis in the injured periventricular white matter and improved functional recovery. These results reveal a key role for postnatal oRG in brain injury recovery and identify ATF5 as a potential therapeutic target for treating white matter injury in infants.
Copyright © 2025 The Author(s). Published by Elsevier Inc. All rights reserved.

  • Neuroscience
Show More
Show Less

Shaping early neural development by timed elevated tissue oxygen tension: Insights from multiomic analysis on human cerebral organoids.

In Science Advances on 14 March 2025 by Liu, Y. H., Chung, M. T., et al.

Oxygen plays a critical role in early neural development in brains, particularly before establishment of complete vasculature; however, it has seldom been investigated due to technical limitations. This study uses an in vitro human cerebral organoid model with multiomic analysis, integrating advanced microscopies and single-cell RNA sequencing, to monitor tissue oxygen tension during neural development. Results reveal a key period between weeks 4 and 6 with elevated intra-organoid oxygen tension, altered energy homeostasis, and rapid neurogenesis within the organoids. The timed oxygen tension elevation can be suppressed by hypoxia treatment or silencing of neuroglobin gene. This study provides insights into the role of oxygen in early neurogenesis from functional, genotypic, phenotypic, and proteomic aspects. These findings highlight the significance of the timed tissue oxygen tension elevation in neurogenesis and provide insights into the role of neuroglobin in neural development, with potential implications for understanding neurodegenerative diseases and therapeutic strategies.

Show More
Show Less
View this product on CiteAb
Acute stress induces severe neural inflammation and overactivation of glucocorticoid signaling in interleukin-18-deficient mice.

In Transl Psychiatry on 23 September 2022 by Yamanishi, K., Doe, N., et al.

Fig.3.C
Fig.3.C showing Immunohistochemistry-immunofluorescence from the publication: Acute stress induces severe neural inflammation and overactivation of glucocorticoid signaling in interleukin-18-deficient mice.
  • IHC-IF
The assessment of glucocorticoid signaling and neurogenesis mediated by a single stress.A The serum corticosterone level in each group is shown. B The ratio of glucocorticoid receptors and phosphorylated glucocorticoid receptors in stressed Il18−/− mice was increased compared with that in other g... more
The assessment of glucocorticoid signaling and neurogenesis mediated by a single stress.A The serum corticosterone level in each group is shown. B The ratio of glucocorticoid receptors and phosphorylated glucocorticoid receptors in stressed Il18−/− mice was increased compared with that in other groups. C Immunofluorescence staining of Ki67 and doublecortin (DCX) is shown, and the graphs indicate the density of Ki67- and DCX-positive cells in each group. (red; Ki67, DCX; green, blue; DAPI) *p < 0.05, ***p < 0.001. (A; n = 12, B; n = 6, C; n = 4 per group). less

Collected and cropped from Transl Psychiatry by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 18

Disruption of rack1 suppresses SHH-type medulloblastoma formation in mice.

In CNS Neurosci Ther on 1 December 2021 by Liu, F., Shao, J., et al.

Fig.3.A
Fig.3.A showing Immunocytochemistry-immunofluorescence from the publication: Disruption of rack1 suppresses SHH-type medulloblastoma formation in mice.
  • ICC-IF
Loss of Rack1 suppresses the proliferation of MB tumor cells. (A) Schematic diagram showing the proliferation of granular neurons was evaluated by BrdU administration and incorporation assay. (B and C) Proliferating granular neurons were immunolabeled with anti‐BrdU and anti‐Ki67 antibodies, resp... more
Loss of Rack1 suppresses the proliferation of MB tumor cells. (A) Schematic diagram showing the proliferation of granular neurons was evaluated by BrdU administration and incorporation assay. (B and C) Proliferating granular neurons were immunolabeled with anti‐BrdU and anti‐Ki67 antibodies, respectively. (D and E) Quantitative analysis of proliferating granular neurons shows significantly decreased percentage of BrdU+(C) and Ki67+(E) cells in rescue mice compared with SHH‐MB tumor mice. **p < 0.01, ***p < 0.001, n ≥ 3. (F) Quantitative RT‐PCR (qRT‐PCR) analysis shows significantly downregulated expression of E2f7, ccnd3, ccne2, cckn2c and cdk4 in rescue mice compared to SHH‐MB tumor mice. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, n.s., not significant, n ≥ 3 less

Collected and cropped from CNS Neurosci Ther by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 18

RNAi Screening Identifies that TEX10 Promotes the Proliferation of Colorectal Cancer Cells by Increasing NF-κB Activation.

In Adv Sci (Weinh) on 1 September 2020 by Wang, Z., Sheng, C., et al.

Fig.7.E
Fig.7.E showing Immunocytochemistry in a Homo sapiens (Human) sample from the publication: RNAi Screening Identifies that TEX10 Promotes the Proliferation of Colorectal Cancer Cells by Increasing NF-κB Activation.
  • ICC
  • Homo sapiens (Human)
TEX10 knockdown decreases the growth of CRC in vivo. A) Subcutaneous injection of TEX10 knockdown and shNC HCT116 cells into nude mice to establish a xenograft model (n = 7). Tumor volumes recorded at the indicated times are shown. B) Tumor images and C) tumor weights on day 20 are shown. D) H&E ... more
TEX10 knockdown decreases the growth of CRC in vivo. A) Subcutaneous injection of TEX10 knockdown and shNC HCT116 cells into nude mice to establish a xenograft model (n = 7). Tumor volumes recorded at the indicated times are shown. B) Tumor images and C) tumor weights on day 20 are shown. D) H&E and TEX10 IHC staining analyses of HCT116 xenograft tumors. E) Ki‐67 IHC staining analyses and F) quantification of the proliferation index (Ki‐67 staining) in HCT116 xenograft tumors. G) qPCR analysis of TNFAIP8, SAT1, IL6ST, and TEX10 mRNA expression in tumors derived from subcutaneously implanted HCT116 cells infected with TEX10 shRNAs (sh1 and sh2) or shNC. H) A proposed model of the process by which TEX10 promotes proliferation in CRC by increasing NF‐κB activation. *P < 0.05, **P < 0.01, and ***P < 0.001 (one‐way ANOVA with Bonferroni's post‐test). less

Collected and cropped from Adv Sci (Weinh) by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 18

A new patient-derived iPSC model for dystroglycanopathies validates a compound that increases glycosylation of α-dystroglycan.

In EMBO Rep on 5 November 2019 by Kim, J., Lana, B., et al.

Fig.3.E
Fig.3.E showing Immunocytochemistry-immunofluorescence in a Homo sapiens (Human) sample from the publication: A new patient-derived iPSC model for dystroglycanopathies validates a compound that increases glycosylation of α-dystroglycan.
  • ICC-IF
  • Homo sapiens (Human)
Characterization of NSCs and cortical neurons derived from FKRP‐ and CRISPR/Cas9 corrected‐iPSCsA, BRepresentative images of NSCs derived from FKRP‐ and corrected‐iPSC lines expressing SOX1, SOX2, and nestin.C, DQuantification of percentage of SOX1+ (C) and SOX2+ (D) cells in culture. The efficie... more
Characterization of NSCs and cortical neurons derived from FKRP‐ and CRISPR/Cas9 corrected‐iPSCsA, BRepresentative images of NSCs derived from FKRP‐ and corrected‐iPSC lines expressing SOX1, SOX2, and nestin.C, DQuantification of percentage of SOX1+ (C) and SOX2+ (D) cells in culture. The efficiency of neural induction is more than 99% in FKRP‐ and corrected‐iPSC (5D17, 5D23, and 3B17) lines. Data are mean ± s.d. n = 4 technical replicates.E, FFKRP‐ and corrected‐NSC lines can be further differentiated to cortical neural progenitor cells, expressing PAX6, OTX2, and vimentin.G–IQuantification of percentage of PAX6+ (G) and OTX2+ (H) cells in culture. About 91‐98% of cells derived from FKRP, 5D17, 5D23, and 3B17 NSC lines express PAX6 (G). About 93‐96% of cells derived from FKRP, 5D17, 5D23, and 3B17 NSC lines express OTX2 (H). Of the OTX2+ population, about 60‐67% cells are also Ki67+ cycling progenitors (I). Data are mean ± s.d. n = 4 technical replicates.J, KGlutamatergic projection neurons derived from FKRP and corrected (5D17, 5D23, and 3B17) progenitor cells. The vast majority of neurons contain vGlut1+ punctae in their neurites (labeled by Tuj1). Right panels are enlarged images from the insets of left panels.Data information: Scale bars, 50 μm. less

Collected and cropped from EMBO Rep by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 18

A new patient-derived iPSC model for dystroglycanopathies validates a compound that increases glycosylation of α-dystroglycan.

In EMBO Rep on 5 November 2019 by Kim, J., Lana, B., et al.

Fig.3.F
Fig.3.F showing Immunocytochemistry-immunofluorescence in a Homo sapiens (Human) sample from the publication: A new patient-derived iPSC model for dystroglycanopathies validates a compound that increases glycosylation of α-dystroglycan.
  • ICC-IF
  • Homo sapiens (Human)
Characterization of NSCs and cortical neurons derived from FKRP‐ and CRISPR/Cas9 corrected‐iPSCsA, BRepresentative images of NSCs derived from FKRP‐ and corrected‐iPSC lines expressing SOX1, SOX2, and nestin.C, DQuantification of percentage of SOX1+ (C) and SOX2+ (D) cells in culture. The efficie... more
Characterization of NSCs and cortical neurons derived from FKRP‐ and CRISPR/Cas9 corrected‐iPSCsA, BRepresentative images of NSCs derived from FKRP‐ and corrected‐iPSC lines expressing SOX1, SOX2, and nestin.C, DQuantification of percentage of SOX1+ (C) and SOX2+ (D) cells in culture. The efficiency of neural induction is more than 99% in FKRP‐ and corrected‐iPSC (5D17, 5D23, and 3B17) lines. Data are mean ± s.d. n = 4 technical replicates.E, FFKRP‐ and corrected‐NSC lines can be further differentiated to cortical neural progenitor cells, expressing PAX6, OTX2, and vimentin.G–IQuantification of percentage of PAX6+ (G) and OTX2+ (H) cells in culture. About 91‐98% of cells derived from FKRP, 5D17, 5D23, and 3B17 NSC lines express PAX6 (G). About 93‐96% of cells derived from FKRP, 5D17, 5D23, and 3B17 NSC lines express OTX2 (H). Of the OTX2+ population, about 60‐67% cells are also Ki67+ cycling progenitors (I). Data are mean ± s.d. n = 4 technical replicates.J, KGlutamatergic projection neurons derived from FKRP and corrected (5D17, 5D23, and 3B17) progenitor cells. The vast majority of neurons contain vGlut1+ punctae in their neurites (labeled by Tuj1). Right panels are enlarged images from the insets of left panels.Data information: Scale bars, 50 μm. less

Collected and cropped from EMBO Rep by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 18

BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration.

In Nat Commun on 10 October 2019 by Liu, M., Sun, T., et al.

Fig.3.F
Fig.3.F showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: BRG1 attenuates colonic inflammation and tumorigenesis through autophagy-dependent oxidative stress sequestration.
  • IHC
  • Mus musculus (House mouse)
Brg1 loss promotes the inflammation-associated CRC. a Scheme of AOM alone treatment protocol. Representative images of H&E-stained colonic sections from Brg1F/F and Brg1IEC-AKO mice at 7 months of age (n = 10 per genotype). b RT-qPCR analysis of the relative mRNA levels of the indicated genes in ... more
Brg1 loss promotes the inflammation-associated CRC. a Scheme of AOM alone treatment protocol. Representative images of H&E-stained colonic sections from Brg1F/F and Brg1IEC-AKO mice at 7 months of age (n = 10 per genotype). b RT-qPCR analysis of the relative mRNA levels of the indicated genes in whole colonic homogenates from 7-month-old mice (n = 5 per genotype). cBrg1F/F and Brg1IEC-AKO mice were injected with AOM on day 0 (2 months of age) and treated with 1% DSS during three 4-day cycles as indicated. Body weight changes are recorded as indicated (n = 10 per genotype). d Twelve weeks after the AOM injection, the mice were sacrificed to examine the tumor burden (n = 10 per genotype). e Representative images of colons and the overall grading of the tumors in each genotype (χ2 test) are shown (n = 10 per genotype). f Representative images of Ki67 and cleaved caspase-3 staining in the tumors from 20-week-old AOM/1% DSS-treated Brg1F/F and Brg1IEC-AKO are shown (n = 4 per genotype). The data represent the mean ± S.E.M., and statistical significance was determined by a two-tailed Student’s t-test unless otherwise indicated. *p < 0.05, **p < 0.01, and ***p < 0.01. Scale bars: 100 μm (a), 50 μm (bottom e, f), 1 cm (d, upper e). N.S., not significant less

Collected and cropped from Nat Commun by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 18

ABL kinase inhibition sensitizes primary lung adenocarcinomas to chemotherapy by promoting tumor cell differentiation.

In Oncotarget on 8 March 2019 by Khatri, A., Gu, J. J., et al.

Fig.2.D
Fig.2.D showing Western Blotting in a Mus musculus (House mouse) sample from the publication: ABL kinase inhibition sensitizes primary lung adenocarcinomas to chemotherapy by promoting tumor cell differentiation.
  • WB
  • Mus musculus (House mouse)
Inhibition of ABL kinases in the presence of docetaxel decreases cell proliferation and increases cell death in KrasG12D/+; p53−/− driven lung tumorsTreatments began 10 weeks after Adeno-Cre infection of Rosa26-fGFP; LSL-KrasG12D/+; p53fl/fl mice. Mouse lungs were harvested at 12 weeks after Aden... more
Inhibition of ABL kinases in the presence of docetaxel decreases cell proliferation and increases cell death in KrasG12D/+; p53−/− driven lung tumorsTreatments began 10 weeks after Adeno-Cre infection of Rosa26-fGFP; LSL-KrasG12D/+; p53fl/fl mice. Mouse lungs were harvested at 12 weeks after Adeno-Cre infection. A. IHC for Ki67+ cells in sections of mouse lungs from mice treated with vehicle control, docetaxel, GNF5, or combination (docetaxel+GNF5) treatment showing a decrease in Ki67 staining, particularly in the combination therapy group. Scale bar = 50 μm. B. Quantification of IHC staining for Ki67 (n = 5-7 tumors per group). C. Immunofluorescence staining for Ki67 showing a decrease in the percentage of Ki67+ (red) tumor cells (labeled with farnesylated GFP, green) in mice treated with combination therapy of GNF5 and docetaxel compared to vehicle treated mice. Scale bar = 150 μm. D. Immunoblotting of lysates showed a decrease in Ki67 expression and increase in cleaved caspase 3 expression in mice given combination therapy compared to control mice and a corresponding decrease in pERK and cyclin D1, which are downstream targets of oncogenic Kras. Phospho-CrkL is a marker for ABL kinase activity while GAPD is a loading control. Graphs depict means and S.E.M. less

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

View on PubMed®

Image 1 of 18

ABL kinase inhibition sensitizes primary lung adenocarcinomas to chemotherapy by promoting tumor cell differentiation.

In Oncotarget on 8 March 2019 by Khatri, A., Gu, J. J., et al.

Fig.2.C
Fig.2.C showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: ABL kinase inhibition sensitizes primary lung adenocarcinomas to chemotherapy by promoting tumor cell differentiation.
  • IHC-IF
  • Mus musculus (House mouse)
Inhibition of ABL kinases in the presence of docetaxel decreases cell proliferation and increases cell death in KrasG12D/+; p53−/− driven lung tumorsTreatments began 10 weeks after Adeno-Cre infection of Rosa26-fGFP; LSL-KrasG12D/+; p53fl/fl mice. Mouse lungs were harvested at 12 weeks after Aden... more
Inhibition of ABL kinases in the presence of docetaxel decreases cell proliferation and increases cell death in KrasG12D/+; p53−/− driven lung tumorsTreatments began 10 weeks after Adeno-Cre infection of Rosa26-fGFP; LSL-KrasG12D/+; p53fl/fl mice. Mouse lungs were harvested at 12 weeks after Adeno-Cre infection. A. IHC for Ki67+ cells in sections of mouse lungs from mice treated with vehicle control, docetaxel, GNF5, or combination (docetaxel+GNF5) treatment showing a decrease in Ki67 staining, particularly in the combination therapy group. Scale bar = 50 μm. B. Quantification of IHC staining for Ki67 (n = 5-7 tumors per group). C. Immunofluorescence staining for Ki67 showing a decrease in the percentage of Ki67+ (red) tumor cells (labeled with farnesylated GFP, green) in mice treated with combination therapy of GNF5 and docetaxel compared to vehicle treated mice. Scale bar = 150 μm. D. Immunoblotting of lysates showed a decrease in Ki67 expression and increase in cleaved caspase 3 expression in mice given combination therapy compared to control mice and a corresponding decrease in pERK and cyclin D1, which are downstream targets of oncogenic Kras. Phospho-CrkL is a marker for ABL kinase activity while GAPD is a loading control. Graphs depict means and S.E.M. less

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

View on PubMed®

Image 1 of 18

Deficiency in intestinal epithelial O-GlcNAcylation predisposes to gut inflammation.

In EMBO Mol Med on 1 August 2018 by Zhao, M., Xiong, X., et al.

Fig.3.E
Fig.3.E showing Immunohistochemistry-immunofluorescence in a Mus musculus (House mouse) sample from the publication: Deficiency in intestinal epithelial O-GlcNAcylation predisposes to gut inflammation.
  • IHC-IF
  • Mus musculus (House mouse)
IEC‐specific loss of OGT disrupts intestinal proliferative/apoptotic homeostasisARepresentative images of the H&E staining of ileum and colon of 10‐week‐old male wild‐type and Vil‐Ogt KO mice. Scale bars = 100 μm.BCombined scores of the mucosal injury in 10‐week‐old male wild‐type and Vil‐Ogt KO ... more
IEC‐specific loss of OGT disrupts intestinal proliferative/apoptotic homeostasisARepresentative images of the H&E staining of ileum and colon of 10‐week‐old male wild‐type and Vil‐Ogt KO mice. Scale bars = 100 μm.BCombined scores of the mucosal injury in 10‐week‐old male wild‐type and Vil‐Ogt KO mice (n = 11, ileum: P < 0.0001, colon: P = 0.0012).CRepresentative images of MPO, F4/80, and CD4 immunohistochemistry in the ileum tissue of male wild‐type and Vil‐Ogt KO mice. Scale bars = 50 μm.DRT–qPCR of inflammatory markers in jejunum, ileum, and colon (n = 5, jejunum: Il6 P = 0.029, Ifng P = 0.0009; ileum: Tnfa P = 0.0094, Ifng P = 0.0066; colon: Tnfa P = 0.028).EImmunofluorescent staining of Ki‐67 in ileal tissues (n = 5). Scale bars = 50 μm.F, GTUNEL staining (F) and immunostaining of Cleaved‐CASPASE3 (G) in the ileum. Quantification of the numbers of positive cells is shown at the right. (TUNEL WT n = 9, KO n = 6, P = 0.0003; Cleaved Cas3 WT = 8, KO = 7, P < 0.0001).HNumbers of survived organoids per 1000 isolated ileal crypts (WT n = 4, KO n = 23, P < 0.0001).Data information: Data are represented as mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001 by two‐tailed t‐test. less

Collected and cropped from EMBO Mol Med by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 18

Estrogen Action in the Epithelial Cells of the Mouse Vagina Regulates Neutrophil Infiltration and Vaginal Tissue Integrity.

In Sci Rep on 26 July 2018 by Li, S., Herrera, G. G., et al.

Fig.3.C
Fig.3.C showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: Estrogen Action in the Epithelial Cells of the Mouse Vagina Regulates Neutrophil Infiltration and Vaginal Tissue Integrity.
  • IHC
  • Mus musculus (House mouse)
Increased number of leukocytes in the absence of epithelial ESR1. (A) H&E staining of vaginal smears from Esr1f/f and Wnt7acre/+; Esr1f/f animals at each stage of estrous cycle. Scale bars = 20 µm. n = 3–4 mice/genotype. (B) Quantification of leukocyte levels through estrous cycle (arbitrary unit... more
Increased number of leukocytes in the absence of epithelial ESR1. (A) H&E staining of vaginal smears from Esr1f/f and Wnt7acre/+; Esr1f/f animals at each stage of estrous cycle. Scale bars = 20 µm. n = 3–4 mice/genotype. (B) Quantification of leukocyte levels through estrous cycle (arbitrary unit). + = less than 10% of cells within the microscopic field are leukocytes, ++ = 10–60% of cells within the microscopic field are leucocytes, +++ = more than 60% of cells within the microscopic field are leukocytes. Data presented as mean ± SEM. *p < 0.05 compared to Esr1f/f at the similar time-point, Mann-Whitney test. n = 6 mice/genotype. (C) Histological staining of vaginal tissue in Wnt7acre/+; Esr1f/f compared to Esr1f/f animals at 0.5 dpc. Ki67 IHC staining of the vaginal lumen at the top two panels and high magnification of H&E staining of Wnt7acre/+; Esr1f/f vaginal epithelium at the bottom. Arrows denote multinucleated cells within the semen portion in the vaginal lumen and in the epithelial cell layer. n = 4–6 mice/genotype. Scale bar = 10 µm. less

Collected and cropped from Sci Rep by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 18

Estrogen Action in the Epithelial Cells of the Mouse Vagina Regulates Neutrophil Infiltration and Vaginal Tissue Integrity.

In Sci Rep on 26 July 2018 by Li, S., Herrera, G. G., et al.

Fig.1.A
Fig.1.A showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: Estrogen Action in the Epithelial Cells of the Mouse Vagina Regulates Neutrophil Infiltration and Vaginal Tissue Integrity.
  • IHC
  • Mus musculus (House mouse)
Loss of tissue integrity and leukocyte infiltration after mating in the absence of vaginal epithelial ESR1. Immunohistochemical (IHC) staining of ESR1, H&E, Ki67 IHC, Masson’s Trichrome (MT), and Periodic Acid-Schiff (PAS) staining in (A) the upper vaginal tract and (B) the lower vaginal tract, r... more
Loss of tissue integrity and leukocyte infiltration after mating in the absence of vaginal epithelial ESR1. Immunohistochemical (IHC) staining of ESR1, H&E, Ki67 IHC, Masson’s Trichrome (MT), and Periodic Acid-Schiff (PAS) staining in (A) the upper vaginal tract and (B) the lower vaginal tract, respectively, at 0.5 dpc in Esr1f/f and Wnt7acre/+; Esr1f/f animals. Black arrows indicate a site of cell infiltration from stromal and epithelial layers into the vaginal lumen. Yellow arrowheads indicate the distinct cornified layer in Esr1f/f tissues. Black arrowheads denote the PAS-positive cell on the apical side of Wnt7acre/+; Esr1f/f vaginal lumen. Insets are negative control without primary antibodies. Scale bars = 100 µm. n = 4–6 mice/genotype. less

Collected and cropped from Sci Rep by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 18

hnRNP I regulates neonatal immune adaptation and prevents colitis and colorectal cancer.

In PLoS Genet on 1 March 2017 by Jin, Z., Liang, F., et al.

Fig.5.D
Fig.5.D showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: hnRNP I regulates neonatal immune adaptation and prevents colitis and colorectal cancer.
  • IHC
  • Mus musculus (House mouse)
The IEC-specific hnRNPI knockout mice develop severe inflammation at P14.(A) and (B) HE–stained sections show the severely inflamed colonic epithelium in the knockout mice at P14 (B). (C) and (D) Immunohistochemical staining with an anti-Ki67 antibody shows hyperproliferation of the colonic epith... more
The IEC-specific hnRNPI knockout mice develop severe inflammation at P14.(A) and (B) HE–stained sections show the severely inflamed colonic epithelium in the knockout mice at P14 (B). (C) and (D) Immunohistochemical staining with an anti-Ki67 antibody shows hyperproliferation of the colonic epithelium in the knockout mice. (E) and (F) Immunofluorescence staining with an anti-ZO1 antibody shows impaired tight junctions in the colonic epithelium of the knockout mice. (G) and (H) FISH with a universal eubacterial probe shows bacteria infiltration in the colonic epithelium of the knockout mice (arrowhead in H). Nuclei were counterstained with DAPI in E to H. (I) to (N) Immunohistochemical staining with indicated antibodies shows increased number of inflammatory cells in the lamina propria of the knockout mice. (I) and (J) show CD4 positive T-cells, (K) and (L) show macrophages, (M) and (N) show neutrophils. WT, wild-type; KO, knockout. Scale bars, 50 μm. less

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

View on PubMed®

Image 1 of 18

hnRNP I regulates neonatal immune adaptation and prevents colitis and colorectal cancer.

In PLoS Genet on 1 March 2017 by Jin, Z., Liang, F., et al.

Fig.5.C
Fig.5.C showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: hnRNP I regulates neonatal immune adaptation and prevents colitis and colorectal cancer.
  • IHC
  • Mus musculus (House mouse)
The IEC-specific hnRNPI knockout mice develop severe inflammation at P14.(A) and (B) HE–stained sections show the severely inflamed colonic epithelium in the knockout mice at P14 (B). (C) and (D) Immunohistochemical staining with an anti-Ki67 antibody shows hyperproliferation of the colonic epith... more
The IEC-specific hnRNPI knockout mice develop severe inflammation at P14.(A) and (B) HE–stained sections show the severely inflamed colonic epithelium in the knockout mice at P14 (B). (C) and (D) Immunohistochemical staining with an anti-Ki67 antibody shows hyperproliferation of the colonic epithelium in the knockout mice. (E) and (F) Immunofluorescence staining with an anti-ZO1 antibody shows impaired tight junctions in the colonic epithelium of the knockout mice. (G) and (H) FISH with a universal eubacterial probe shows bacteria infiltration in the colonic epithelium of the knockout mice (arrowhead in H). Nuclei were counterstained with DAPI in E to H. (I) to (N) Immunohistochemical staining with indicated antibodies shows increased number of inflammatory cells in the lamina propria of the knockout mice. (I) and (J) show CD4 positive T-cells, (K) and (L) show macrophages, (M) and (N) show neutrophils. WT, wild-type; KO, knockout. Scale bars, 50 μm. less

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

View on PubMed®

Image 1 of 18

2D and 3D Stem Cell Models of Primate Cortical Development Identify Species-Specific Differences in Progenitor Behavior Contributing to Brain Size.

In Cell Stem Cell on 7 April 2016 by Otani, T., Marchetto, M. C., et al.

Fig.2.A
Fig.2.A showing Immunocytochemistry-immunofluorescence in a Pan troglodytes (Common chimpanzee) sample from the publication: 2D and 3D Stem Cell Models of Primate Cortical Development Identify Species-Specific Differences in Progenitor Behavior Contributing to Brain Size.
  • ICC-IF
  • Pan troglodytes (Common chimpanzee)
Timing of Cortical Neurogenesis Is Independent of Neuronal Lamination and 3D Organization(A) Chimpanzee cerebral cortex organoids (scale bar, 200 μm). Organoids develop in vivo-like organization of VZ, with PAX6+/Ki67+ polarized (apical aPKC localization) progenitor cells within the VZ, apical mi... more
Timing of Cortical Neurogenesis Is Independent of Neuronal Lamination and 3D Organization(A) Chimpanzee cerebral cortex organoids (scale bar, 200 μm). Organoids develop in vivo-like organization of VZ, with PAX6+/Ki67+ polarized (apical aPKC localization) progenitor cells within the VZ, apical mitoses (pH3+ cells), and IPCs at the outer margin of the VZ. Antibodies as indicated in each panel. Scale bar, 100 μm(B) Human, chimpanzee, and macaque cortical organoids undergo sequential production of TBR1+ deep-layer neurons and SATB2+ upper-layer neurons (yellow arrowheads indicate initial SATB2+ neurons generated). As organoids developed for longer periods, cortical neurons migrated to form cortical plate-like structures (yellow bracket) with some separation of layers of TBR1+ and SATB2+ neurons. Scale bars, 50 μm.(C) Scatterplots of positions of TBR1+ and SATB2+ neurons relative to the ventricular surface in human day 80, chimpanzee day 80, and macaque day 60 cortical organoids. Red lines represent median positions. less

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

View on PubMed®

Image 1 of 18

2D and 3D Stem Cell Models of Primate Cortical Development Identify Species-Specific Differences in Progenitor Behavior Contributing to Brain Size.

In Cell Stem Cell on 7 April 2016 by Otani, T., Marchetto, M. C., et al.

Fig.4.B
Fig.4.B showing Immunocytochemistry-immunofluorescence in a Pan troglodytes (Common chimpanzee) sample from the publication: 2D and 3D Stem Cell Models of Primate Cortical Development Identify Species-Specific Differences in Progenitor Behavior Contributing to Brain Size.
  • ICC-IF
  • Pan troglodytes (Common chimpanzee)
Clonal Analysis Reveals Marked Differences between Human and Macaque Cortical Progenitor Cell Dynamics over Developmental Time(A) Single cortical progenitor cells were labeled with low-titer, replication-incompetent lentiviruses at clonal resolution (see Supplemental Experimental Procedures for f... more
Clonal Analysis Reveals Marked Differences between Human and Macaque Cortical Progenitor Cell Dynamics over Developmental Time(A) Single cortical progenitor cells were labeled with low-titer, replication-incompetent lentiviruses at clonal resolution (see Supplemental Experimental Procedures for further details). Following infection at days 20, 30, or 40, progenitor cells were cultured for 2, 6, or 10 days, fixed, and immunostained for analysis.(B) Representative immunofluorescence images of clones derived from a single progenitor cell after 2, 6, or 10 day chase periods (panels as labeled) and immunostained for Ki67 (cycling progenitor cells) and βIII-tubulin (postmitotic neurons). Scale bar, 100 μm.(C) Human and macaque clone size distributions for each developmental stage (days 20, 30, and 40) at each time point postlabeling (2, 6, and 10 days). Red horizontal bars represent medians, and vertical bars indicate the interval between the first and third quartiles of the clonal distribution. Data for each species are combined from four human pluripotent cell lines (two ESCs and two iPSCs) and from three macaque ESC lines. Total number of clones analyzed for each line is as follows: HS1, n = 440; HS2, n = 43; HS3, n = 201; HS4, n = 93; MF1, n = 247; MF2, n = 469; MN1, n = 303.(D) Human and macaque average clone sizes for time points shown in (C). Significant differences between the average sizes of human and macaque clones at day 30 + 10 (p = 0.0437), day 40 + 6 (p = 0.0154), and day 40 + 10 (p = 0.205 × 10−2) are labeled. Error bars, SD. less

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

View on PubMed®

Image 1 of 18

Inhibition of the JAK2/STAT3 pathway reduces gastric cancer growth in vitro and in vivo.

In PLoS One on 9 May 2014 by Judd, L. M., Menheniott, T. R., et al.

Fig.3.E,F
Fig.3.E,F showing Immunohistochemistry in a Mus musculus (House mouse) sample from the publication: Inhibition of the JAK2/STAT3 pathway reduces gastric cancer growth in vitro and in vivo.
  • IHC
  • Mus musculus (House mouse)
Treatment of gp130757FF mice with WP1066 reduces tumour size.gp130757FF mice (8 weeks old) were treated i.p with 10 mg/kg of WP1066 or DMSO twice with a gap of one day between doses, followed by doses of 20 mg/kg every 2 days for 2 weeks. Antral tumours in 8 week untreated mice (A) and 10 week DM... more
Treatment of gp130757FF mice with WP1066 reduces tumour size.gp130757FF mice (8 weeks old) were treated i.p with 10 mg/kg of WP1066 or DMSO twice with a gap of one day between doses, followed by doses of 20 mg/kg every 2 days for 2 weeks. Antral tumours in 8 week untreated mice (A) and 10 week DMSO-treated vehicle controls (B) were no different in mean area, however WP1066 treatment resulted in ∼50% smaller tumours (C). This was confirmed by quantitative morphometry (D) where antral tumours were significantly smaller in WP1066 mice compared to 10 w.o. DMSO controls and 8 w.o. untreated mice (n = 7–10; p<0.05). The effect of WP1066 on cell proliferation was assessed by staining sections with an antibody for Ki-67. There was a significant decrease in the number of Ki-67 positive cells per gland in the WP1066 treated mice (F) compared to controls (E) and quantified graphically (G). The number of apoptotic cells quantified after caspase 3 staining of antral sections of a DMSO control (H) and WP1066 (I) mouse, and was quantified by counting stained cells/mm2 of gastric mucosa (J). less

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

View on PubMed®

Image 1 of 18

Novel application of Ki67 to quantify antigen-specific in vitro lymphoproliferation.

In J Immunol Methods on 31 October 2010 by Soares, A., Govender, L., et al.

Fig.1.A
Fig.1.A showing Flow cytometry/Cell sorting from the publication: Novel application of Ki67 to quantify antigen-specific in vitro lymphoproliferation.
  • FC/FACS
Ki67 as a specific marker of in vitro lymphoproliferation. Whole blood from healthy donors was incubated with the indicated antigens and Ki67 expression quantified on a daily basis over 6 days. (A) Representative example showing the frequencies of Ki67 expression by CD4+ T cells after incubation ... more
Ki67 as a specific marker of in vitro lymphoproliferation. Whole blood from healthy donors was incubated with the indicated antigens and Ki67 expression quantified on a daily basis over 6 days. (A) Representative example showing the frequencies of Ki67 expression by CD4+ T cells after incubation of whole blood with medium only (unstim.), PPD or αCD3/αCD28 over 6 days. Dotplots were gated on live, CD3+ CD4+ lymphocytes. Ki67+ CD4+ T cell frequencies after (B) PPD stimulation or (C) αCD3/αCD28 stimulation in 4 donors. Data are expressed as a percentage of the maximum response. The frequency of Ki67+ CD4+ T cells is indicated in each plot. (D) Frequencies of Ki67 expressing CD4+ T cells in whole blood from 15 donors after 6-day culture with medium only (unstim.) or PPD. (E) Frequencies of Ki67+ CD4+ T cells in PBMC from 14 donors. Differences were calculated using the Wilcoxon matched pairs test. less

Collected and cropped from J Immunol Methods by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 18

Novel application of Ki67 to quantify antigen-specific in vitro lymphoproliferation.

In J Immunol Methods on 31 October 2010 by Soares, A., Govender, L., et al.

Fig.5.A
Fig.5.A showing Flow cytometry/Cell sorting from the publication: Novel application of Ki67 to quantify antigen-specific in vitro lymphoproliferation.
  • FC/FACS
Monitoring of vaccine-induced T cell proliferation. (A) Dotplots showing Ki67 expression by CD4+ T cells from a representative 18 month old toddler before (pre-TT) and after TT vaccination (post-TT). Dotplots are gated on live, CD3+ lymphocytes. Values in each dotplot represent the frequency of K... more
Monitoring of vaccine-induced T cell proliferation. (A) Dotplots showing Ki67 expression by CD4+ T cells from a representative 18 month old toddler before (pre-TT) and after TT vaccination (post-TT). Dotplots are gated on live, CD3+ lymphocytes. Values in each dotplot represent the frequency of Ki67+ T cells within the CD3+ CD8− T cell population. Frequencies of (B) TT-specific and (C) BCG-specific CD4+ T cells pre- and post-TT vaccination in 11 toddlers. CD4+ T cells are defined as CD3+ CD8− T cells (see Data analysis). (D) Relative increase in TT-specific or BCG-specific CD4+ T cells pre- and post-TT. The lines represent the medians. (E) Dotplots depicting frequencies of Ki67+ CD4+ T cells in whole blood directly ex vivo or after culture in the absence of antigen (unstim.) for 6 days. Values in each dotplot represent the frequency of Ki67+ T cells within the CD3+ CD8− T cell population. (F) Frequencies of Ki67+ CD4+ T cells directly ex vivo or after culture for 6 days with medium (n = 11). CD4+ T cells are defined as CD3+ CD8− T cells (see Data analysis). Differences were calculated using the Wilcoxon matched pairs test. less

Collected and cropped from J Immunol Methods by CiteAb, provided under a CC-BY license

View on PubMed®

Image 1 of 18