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258 results for “TGF-β”
Comparing the effect of TGF-β receptor inhibition on human mesenchymal stem/stromal cells derived from endometrium, bone marrow and adipose tissues
<p><strong>Figure S1: Differences between bmMSC donors. A)</strong> Graph showing two groups of bmMSCs with and without effect of A83-01 treatment on % SUSD2<sup>+</sup> cells. <strong>B)</strong> Graph showing no difference in the number of cells following A83-01 treatment in the two groups of donor cells from <strong>A</strong>. Plots are median for n=3 biological samples per treatment group.</p>
Oncogenic calreticulin induces TGF-β expression and Treg expansion in the bone marrow microenvironment as a mechanism of immune escape
<p>This repository contains all necessary scRNA-seq inputs to reproduce the results described in "Oncogenic calreticulin induces TGF-β expression and Treg expansion in the bone marrow microenvironment as a mechanism of immune escape" by Schmidt et al. (Cancer Research 2024). </p> <p>Content:</p> <ol> <li>"MPN_calreticulin_bm.R" --> R script containing all code</li> <li>"cells_table.RDS" --> cells table containing, cell_id, UMAP coordinates, complexity, cell type annotation and metadata</li> <li>"normalized_matrix.RDS" --> quality control filtered, log2-normalized and centered expression matrix</li> <li>"reference_signatures.RDS" --> all external signatures used for this study</li> <li>"EV2_*", "EV5_*", "MPN2_*", "MPN5_*", --> cellranger outputs</li> </ol>
TGF-β neutralization attenuates tumor residency of activated T cells to enhance systemic immunity in mice
<p>Deep TCR sequencing was performed using the TCR Profiling Kit from MiLaboratories (Mouse α/β TCR RNA; Kit MiLaboratories; TMMR-001). Deep TCR sequencing was analyzed using the MiXCR software from MiLaboratories per manufacturer's recommendations. The files correspond to the TCR-beta sequences.<br>The files are named as follows:</p> <p> </p> <table> <tbody> <tr> <td>file_name</td> <td>cell type sequenced</td> <td>tissue of origin</td> <td>treatment</td> <td>mouse_id</td> </tr> <tr> <td>21BA1dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>bintrafusp alpha</td> <td>1</td> </tr> <tr> <td>23BA2dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>bintrafusp alpha</td> <td>2</td> </tr> <tr> <td>25BA3dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>bintrafusp alpha</td> <td>3</td> </tr> <tr> <td>27BA4dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>bintrafusp alpha</td> <td>4</td> </tr> <tr> <td>29BA5dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>bintrafusp alpha</td> <td>5</td> </tr> <tr> <td>22BA1SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>bintrafusp alpha</td> <td>1</td> </tr> <tr> <td>24BA2SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>bintrafusp alpha</td> <td>2</td> </tr> <tr> <td>26BA3SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>bintrafusp alpha</td> <td>3</td> </tr> <tr> <td>28BA4SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>bintrafusp alpha</td> <td>4</td> </tr> <tr> <td>30BA5SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>bintrafusp alpha</td> <td>5</td> </tr> <tr> <td>31CON1dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>control</td> <td>6</td> </tr> <tr> <td>33CON2dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>control</td> <td>7</td> </tr> <tr> <td>35CON3dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>control</td> <td>8</td> </tr> <tr> <td>37CON4dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>control</td> <td>9</td> </tr> <tr> <td>39CON5dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>control</td> <td>10</td> </tr> <tr> <td>32CON1SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>control</td> <td>6</td> </tr> <tr> <td>34CON2SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>control</td> <td>7</td> </tr> <tr> <td>36CON3SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>control</td> <td>8</td> </tr> <tr> <td>38CON4SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>control</td> <td>9</td> </tr> <tr> <td>40CON5SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>control</td> <td>10</td> </tr> <tr> <td>1aPDL11dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>anti-PDL1 antibody</td> <td>11</td> </tr> <tr> <td>3aPDL12dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>anti-PDL1 antibody</td> <td>12</td> </tr> <tr> <td>5aPDL13dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>anti-PDL1 antibody</td> <td>13</td> </tr> <tr> <td>7aPDL14dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>anti-PDL1 antibody</td> <td>14</td> </tr> <tr> <td>9aPDL15dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>anti-PDL1 antibody</td> <td>15</td> </tr> <tr> <td>2aPDL11SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>anti-PDL1 antibody</td> <td>11</td> </tr> <tr> <td>4aPDL12SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>anti-PDL1 antibody</td> <td>12</td> </tr> <tr> <td>6aPDL13SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>anti-PDL1 antibody</td> <td>13</td> </tr> <tr> <td>8aPDL14SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>anti-PDL1 antibody</td> <td>14</td> </tr> <tr> <td>10aPDL15SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>anti-PDL1 antibody</td> <td>15</td> </tr> <tr> <td>11aTGFB1dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>anti-TGF-beta antibody</td> <td>16</td> </tr> <tr> <td>13aTGFB2dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>anti-TGF-beta antibody</td> <td>17</td> </tr> <tr> <td>15aTGFB3dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>anti-TGF-beta antibody</td> <td>18</td> </tr> <tr> <td>17aTGFB4dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>anti-TGF-beta antibody</td> <td>19</td> </tr> <tr> <td>19aTGFB5dLN.clones_TRB.tsv</td> <td>T cells</td> <td>tumor-draining lymph node</td> <td>anti-TGF-beta antibody</td> <td>20</td> </tr> <tr> <td>12aTGFB1SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>anti-TGF-beta antibody</td> <td>16</td> </tr> <tr> <td>14aTGFB2SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>anti-TGF-beta antibody</td> <td>17</td> </tr> <tr> <td>16aTGFB3SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>anti-TGF-beta antibody</td> <td>18</td> </tr> <tr> <td>18aTGFB4SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>anti-TGF-beta antibody</td> <td>19</td> </tr> <tr> <td>20aTGFB5SP.clones_TRB.tsv</td> <td>T cells</td> <td>spleen</td> <td>anti-TGF-beta antibody</td> <td>20</td> </tr> </tbody> </table>
Research on the Relationship of Ions Content with TNF-α and TGF-β Expression in BALF of Silica-induced Rats
<p>All data of this article.</p>
Data from: Cruzipain activates latent TGF-β from host cells during T. cruzi invasion
Several studies indicate that the activity of cruzipain, the main lysosomal cysteine peptidase of Trypanosoma cruzi, contributes to parasite infectivity. In addition, the parasitic invasion process of mammalian host cells is described to be dependent on the activation of the host TGF-β signaling pathway by T. cruzi. Here, we tested the hypothesis that cruzipain could be an important activator of latent TGF-β and thereby trigger TGF-β-mediated events crucial for the development of Chagas disease. We found that live epimastigotes of T. cruzi, parasite lysates and purified cruzipain were able to activate latent TGF-β in vitro. This activation could be inhibited by the cysteine peptidase inhibitor Z-Phe-Ala-FMK. Moreover, transfected parasites overexpressing chagasin, a potent endogenous cruzipain inhibitor, prevented latent TGF-β activation. We also observed that T. cruzi invasion, as well as parasite intracellular growth, were inhibited by the administration of Z-Phe-Ala-FMK or anti-TGF-β neutralizing antibody to Vero cell cultures. We further demonstrated that addition of purified cruzipain enhanced the invasive activity of trypomastigotes and that this effect could be completely inhibited by addition of a neutralizing anti-TGF-β antibody. Taken together, these results demonstrate that the activities of cruzipain and TGF-β in the process of cell invasion are functionally linked. Our data suggest that cruzipain inhibition is an interesting chemotherapeutic approach for Chagas disease not only because of its trypanocidal activity, but also due to the inhibitory effect on TGF-β activation.
Study of TGF-β Receptor Inhibitor Galunisertib (LY2157299) and Enzalutamide in Metastatic Castration-resistant Prostate Cancer
ClinicalTrials.gov study NCT02452008. IPD Sharing: Not stated. Countries: 1. Publications: 1.
The EFFECTS of GAMBIR CATECHIN (UNCARIA GAMBIR ROXB) SUPPLEMENTATION on COGNITIVE FUNCTION, EXPRESSION of APP, MAPT, BDNF, IL-10, TGF-Β GENES, and PLASMA MDA LEVELS in the ELDERLY.
ClinicalTrials.gov study NCT06604390. IPD Sharing: NO. Countries: 2. Publications: 4.
SMAD2, SMAD3 AND TGF-β GENE EXPRESSION IN URGE URINARY INCONTINENCE
ClinicalTrials.gov study NCT04525105. IPD Sharing: UNDECIDED. Countries: 1. Publications: 1.
Data from: Cruzipain activates latent TGF-β from host cells during T. cruzi invasion
Open the record for dataset details and reuse information.
Data from: Evolutionary suppression of erythropoiesis via the modulation of TGF-β signaling in an Antarctic icefish
The Antarctic icefish, a family (Channichthyidae) of teleosts within the perciform suborder Notothenioidei, are the only known vertebrates without oxygen-transporting haemoglobins and that are largely devoid of circulating erythrocytes. To elucidate the evo-devo mechanisms underpinning the suppressed erythropoiesis in the icefish, we conducted comparative studies on the transcriptomes and microRNAomes of the primary haematopoietic tissues between an icefish (Chionodraco hamatus) and two red-blooded notothenioids (Trematomus bernacchii and Gymnodraco acuticeps). We identified substantial remodelling of the haematopoietic programs in the icefish through which erythropoiesis is selectively suppressed. Experimental verification showed that erythropoietic suppression in the icefish may be attributable to the upregulation of TGF-β signalling, which coincides with reductions in multiple transcription factors essential for erythropoiesis and the upregulation of hundreds of microRNAs, the majority (> 80%) of which potentially target erythropoiesis regulating factors. Of the six microRNAs selected for verification, three miRNAs (miR-152, miR-1388 and miR-16b) demonstrated suppressive functions on GATA1 and ALAS2, which are two factors important for erythroid differentiation, resulting in reduced numbers of erythroids in microinjected zebra fish embryos. Codon substitution analyses of the genes of the TGF-β superfamily revealed signs of positive selection in TGF-β1 and endoglin in the lineages leading to Antarctic notothenioids. Both genes are previously known to function in erythropoietic suppression. These findings implied a general trend of erythropoietic suppression in the cold-adapted notothenioid lineages through evolutionary modulation of the multi-functional TGF-β signalling pathway. This trend is more pronounced in the haemoglobin-less icefish, which may pre-emptively hinder the otherwise defective erythroids from production.
Data from: Evolutionary suppression of erythropoiesis via the modulation of TGF-β signaling in an Antarctic icefish
Open the record for dataset details and reuse information.
TEM1/endosialin/CD248 promotes pathologic scarring and TGF-β activity through its receptor stability in dermal fibroblasts
GEO Series GSE207284. Mus musculus. 12 samples. Type: Expression profiling by high throughput sequencing.
Remodeling of the tumor microenvironment via blockade of LAIR-1 and TGF-β signaling
GEO Series GSE195686. Homo sapiens; Mus musculus. 18 samples. Type: Expression profiling by high throughput sequencing.
TGF-β signaling activated by cancer-associated fibroblasts determines the histological signature of lung adenocarcinoma
GEO Series GSE169029. Homo sapiens. 4 samples. Type: Expression profiling by high throughput sequencing.
TGF-β/Nodal signaling boosts glucose uptake during mesendoderm differentiation by inducing a transmembrane micropeptide
GEO Series GSE157073. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
The atypical KRASQ22K mutation directs TGF-β response towards partial epithelial-to-mesenchymal transition in patient-derived colorectal cancer tumoroids
GEO Series GSE270815. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.
Molecular Signature of CAID Syndrome: Noncanonical Roles of SGO1 in Regulation of TGF-β Signaling and Epigenomics. [ATAC-seq]
GEO Series GSE110576. Homo sapiens. 12 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
miRNA profiles in head and neck natural epithelial - mesenchymal phenotype cell line pair, and in TGF-β induced EMT models
GEO Series GSE38459. Mus musculus; Human alphaherpesvirus 1; Human betaherpesvirus 5; Murid betaherpesvirus 1; Human immunodeficiency virus 1; Homo sapiens; Murid gammaherpesvirus 4; Betapolyomavirus hominis; human gammaherpesvirus 4; JC polyomavirus; Human gammaherpesvirus 8; Mus musculus cytomegalovirus 2; Betapolyomavirus macacae; Rattus norvegicus; Human alphaherpesvirus 2; Merkel cell polyomavirus. 3 samples. Type: Non-coding RNA profiling by array.
TMPRSS2:ERG gene fusion variants induce TGF-β signaling and epithelial to mesenchymal transition in human prostate cancer cells
GEO Series GSE78032. Homo sapiens. 12 samples. Type: Expression profiling by array.
Neoplastic pancreas cells enter a quasi-mesenchymal state with increased oncogenic potential following transient TGF-β exposure
GEO Series GSE101659. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
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The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
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