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pan tissue single cell transcriptomic data  (Human Protein Atlas)

 
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    Human Protein Atlas pan tissue single cell transcriptomic data
    Platelet-Driven CAF Activation and ECM Barriers in the Tumor Microenvironment. A. Expression levels of TGFB1 and PDGFB were assessed <t>using</t> <t>pan-tissue</t> <t>single-cell</t> RNA-sequencing data from the Human Protein Atlas. Normalized counts (nCPM) were aggregated at the cell-type level. Among all surveyed human cell types, platelets showed the highest expression of TGFB1 and were among the top expressors of PDGFB, highlighting their distinct capacity as a concentrated source of these exclusion-related factors. B. Activated platelets engage CAFs via CLEC-2–podoplanin interaction and release TGF-β, PDGF, and SDF-1, inducing fibroblast, epithelial cell, and MSC differentiation into CAFs. MSCs activate platelets via PAF, forming a feedback loop. CAFs (α-SMA/FAP + ) remodel the ECM and promote desmoplasia, creating a barrier to T cell infiltration and sustaining immune suppression in the TME. Abbreviations: CAF: Cancer-Associated Fibroblast, CLEC-2: C-type Lectin-like Receptor 2, PDPN: Podoplanin, TGF-β: Transforming Growth Factor Beta, PDGF: Platelet-Derived Growth Factor, SDF-1: Stromal Cell-Derived Factor 1, MSC: Mesenchymal Stem Cell, PAF: Platelet-Activating Factor, α-SMA: Alpha-Smooth Muscle Actin, FAP: Fibroblast Activation Protein, ECM: Extracellular Matrix, TME: Tumor Microenvironment
    Pan Tissue Single Cell Transcriptomic Data, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pan tissue single cell transcriptomic data/product/Human Protein Atlas
    Average 86 stars, based on 1 article reviews
    pan tissue single cell transcriptomic data - by Bioz Stars, 2026-05
    86/100 stars

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    1) Product Images from "Platelets in the tumor microenvironment: potential mediators of immune exclusion and resistance to immune checkpoint inhibitor therapy"

    Article Title: Platelets in the tumor microenvironment: potential mediators of immune exclusion and resistance to immune checkpoint inhibitor therapy

    Journal: Cellular Oncology (Dordrecht, Netherlands)

    doi: 10.1007/s13402-025-01129-7

    Platelet-Driven CAF Activation and ECM Barriers in the Tumor Microenvironment. A. Expression levels of TGFB1 and PDGFB were assessed using pan-tissue single-cell RNA-sequencing data from the Human Protein Atlas. Normalized counts (nCPM) were aggregated at the cell-type level. Among all surveyed human cell types, platelets showed the highest expression of TGFB1 and were among the top expressors of PDGFB, highlighting their distinct capacity as a concentrated source of these exclusion-related factors. B. Activated platelets engage CAFs via CLEC-2–podoplanin interaction and release TGF-β, PDGF, and SDF-1, inducing fibroblast, epithelial cell, and MSC differentiation into CAFs. MSCs activate platelets via PAF, forming a feedback loop. CAFs (α-SMA/FAP + ) remodel the ECM and promote desmoplasia, creating a barrier to T cell infiltration and sustaining immune suppression in the TME. Abbreviations: CAF: Cancer-Associated Fibroblast, CLEC-2: C-type Lectin-like Receptor 2, PDPN: Podoplanin, TGF-β: Transforming Growth Factor Beta, PDGF: Platelet-Derived Growth Factor, SDF-1: Stromal Cell-Derived Factor 1, MSC: Mesenchymal Stem Cell, PAF: Platelet-Activating Factor, α-SMA: Alpha-Smooth Muscle Actin, FAP: Fibroblast Activation Protein, ECM: Extracellular Matrix, TME: Tumor Microenvironment
    Figure Legend Snippet: Platelet-Driven CAF Activation and ECM Barriers in the Tumor Microenvironment. A. Expression levels of TGFB1 and PDGFB were assessed using pan-tissue single-cell RNA-sequencing data from the Human Protein Atlas. Normalized counts (nCPM) were aggregated at the cell-type level. Among all surveyed human cell types, platelets showed the highest expression of TGFB1 and were among the top expressors of PDGFB, highlighting their distinct capacity as a concentrated source of these exclusion-related factors. B. Activated platelets engage CAFs via CLEC-2–podoplanin interaction and release TGF-β, PDGF, and SDF-1, inducing fibroblast, epithelial cell, and MSC differentiation into CAFs. MSCs activate platelets via PAF, forming a feedback loop. CAFs (α-SMA/FAP + ) remodel the ECM and promote desmoplasia, creating a barrier to T cell infiltration and sustaining immune suppression in the TME. Abbreviations: CAF: Cancer-Associated Fibroblast, CLEC-2: C-type Lectin-like Receptor 2, PDPN: Podoplanin, TGF-β: Transforming Growth Factor Beta, PDGF: Platelet-Derived Growth Factor, SDF-1: Stromal Cell-Derived Factor 1, MSC: Mesenchymal Stem Cell, PAF: Platelet-Activating Factor, α-SMA: Alpha-Smooth Muscle Actin, FAP: Fibroblast Activation Protein, ECM: Extracellular Matrix, TME: Tumor Microenvironment

    Techniques Used: Activation Assay, Expressing, RNA Sequencing, Derivative Assay



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    pan tissue single cell transcriptomic data  (Human Protein Atlas)
    86
    Human Protein Atlas pan tissue single cell transcriptomic data
    Platelet-Driven CAF Activation and ECM Barriers in the Tumor Microenvironment. A. Expression levels of TGFB1 and PDGFB were assessed <t>using</t> <t>pan-tissue</t> <t>single-cell</t> RNA-sequencing data from the Human Protein Atlas. Normalized counts (nCPM) were aggregated at the cell-type level. Among all surveyed human cell types, platelets showed the highest expression of TGFB1 and were among the top expressors of PDGFB, highlighting their distinct capacity as a concentrated source of these exclusion-related factors. B. Activated platelets engage CAFs via CLEC-2–podoplanin interaction and release TGF-β, PDGF, and SDF-1, inducing fibroblast, epithelial cell, and MSC differentiation into CAFs. MSCs activate platelets via PAF, forming a feedback loop. CAFs (α-SMA/FAP + ) remodel the ECM and promote desmoplasia, creating a barrier to T cell infiltration and sustaining immune suppression in the TME. Abbreviations: CAF: Cancer-Associated Fibroblast, CLEC-2: C-type Lectin-like Receptor 2, PDPN: Podoplanin, TGF-β: Transforming Growth Factor Beta, PDGF: Platelet-Derived Growth Factor, SDF-1: Stromal Cell-Derived Factor 1, MSC: Mesenchymal Stem Cell, PAF: Platelet-Activating Factor, α-SMA: Alpha-Smooth Muscle Actin, FAP: Fibroblast Activation Protein, ECM: Extracellular Matrix, TME: Tumor Microenvironment
    Pan Tissue Single Cell Transcriptomic Data, supplied by Human Protein Atlas, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pan tissue single cell transcriptomic data/product/Human Protein Atlas
    Average 86 stars, based on 1 article reviews
    pan tissue single cell transcriptomic data - by Bioz Stars, 2026-05
    86/100 stars
    		  Buy from Supplier

    Image Search Results


    Platelet-Driven CAF Activation and ECM Barriers in the Tumor Microenvironment. A. Expression levels of TGFB1 and PDGFB were assessed using pan-tissue single-cell RNA-sequencing data from the Human Protein Atlas. Normalized counts (nCPM) were aggregated at the cell-type level. Among all surveyed human cell types, platelets showed the highest expression of TGFB1 and were among the top expressors of PDGFB, highlighting their distinct capacity as a concentrated source of these exclusion-related factors. B. Activated platelets engage CAFs via CLEC-2–podoplanin interaction and release TGF-β, PDGF, and SDF-1, inducing fibroblast, epithelial cell, and MSC differentiation into CAFs. MSCs activate platelets via PAF, forming a feedback loop. CAFs (α-SMA/FAP + ) remodel the ECM and promote desmoplasia, creating a barrier to T cell infiltration and sustaining immune suppression in the TME. Abbreviations: CAF: Cancer-Associated Fibroblast, CLEC-2: C-type Lectin-like Receptor 2, PDPN: Podoplanin, TGF-β: Transforming Growth Factor Beta, PDGF: Platelet-Derived Growth Factor, SDF-1: Stromal Cell-Derived Factor 1, MSC: Mesenchymal Stem Cell, PAF: Platelet-Activating Factor, α-SMA: Alpha-Smooth Muscle Actin, FAP: Fibroblast Activation Protein, ECM: Extracellular Matrix, TME: Tumor Microenvironment

    Journal: Cellular Oncology (Dordrecht, Netherlands)

    Article Title: Platelets in the tumor microenvironment: potential mediators of immune exclusion and resistance to immune checkpoint inhibitor therapy

    doi: 10.1007/s13402-025-01129-7

    Figure Lengend Snippet: Platelet-Driven CAF Activation and ECM Barriers in the Tumor Microenvironment. A. Expression levels of TGFB1 and PDGFB were assessed using pan-tissue single-cell RNA-sequencing data from the Human Protein Atlas. Normalized counts (nCPM) were aggregated at the cell-type level. Among all surveyed human cell types, platelets showed the highest expression of TGFB1 and were among the top expressors of PDGFB, highlighting their distinct capacity as a concentrated source of these exclusion-related factors. B. Activated platelets engage CAFs via CLEC-2–podoplanin interaction and release TGF-β, PDGF, and SDF-1, inducing fibroblast, epithelial cell, and MSC differentiation into CAFs. MSCs activate platelets via PAF, forming a feedback loop. CAFs (α-SMA/FAP + ) remodel the ECM and promote desmoplasia, creating a barrier to T cell infiltration and sustaining immune suppression in the TME. Abbreviations: CAF: Cancer-Associated Fibroblast, CLEC-2: C-type Lectin-like Receptor 2, PDPN: Podoplanin, TGF-β: Transforming Growth Factor Beta, PDGF: Platelet-Derived Growth Factor, SDF-1: Stromal Cell-Derived Factor 1, MSC: Mesenchymal Stem Cell, PAF: Platelet-Activating Factor, α-SMA: Alpha-Smooth Muscle Actin, FAP: Fibroblast Activation Protein, ECM: Extracellular Matrix, TME: Tumor Microenvironment

    Article Snippet: Our analysis of pan-tissue single-cell transcriptomic data from the Human Protein Atlas identifies platelets as a dominant cellular source of TGF-β and among the highest expressors of PDGFB across human cell types (Fig. A), providing a strong molecular basis for their impact on CAF activation and differentiation.

    Techniques: Activation Assay, Expressing, RNA Sequencing, Derivative Assay