{"entity": "researcher", "timestamp": "2026-08-20T21:46:01.317Z", "family": "Hamidi", "given": "Anahita", "initials": "A", "orcid": "0000-0002-5445-2446", "affiliations": ["Department of Medical Biochemistry and Microbiology, Science for Life Laboratory, Uppsala University, Box 582, SE-751 23 Uppsala, Sweden."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/c9d2a9063065410385248b810cc9790f.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/c9d2a9063065410385248b810cc9790f"}}, "publications": [{"entity": "publication", "iuid": "de71697736f74b5fb891aa0a05150ea3", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/de71697736f74b5fb891aa0a05150ea3.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/de71697736f74b5fb891aa0a05150ea3"}}, "title": "The type II TGF-\u03b2 receptor phosphorylates Tyr182 in the type I receptor to activate downstream Src signaling.", "authors": [{"family": "Yakymovych", "given": "Ihor", "initials": "I", "orcid": "0000-0003-1860-5369", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/465de9e47634452fac8adf60f4b71f3e.json"}}, {"family": "Yakymovych", "given": "Mariya", "initials": "M"}, {"family": "Hamidi", "given": "Anahita", "initials": "A", "orcid": "0000-0002-5445-2446", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c9d2a9063065410385248b810cc9790f.json"}}, {"family": "Landstr\u00f6m", "given": "Mar\u00e9ne", "initials": "M", "orcid": "0000-0001-6737-7230", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8cbb0a1e30bf44a2a267e6a3090acf01.json"}}, {"family": "Heldin", "given": "Carl-Henrik", "initials": "CH", "orcid": "0000-0002-9508-896X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/5bca6678f5eb4baf853fca6ed5f9b726.json"}}], "type": "journal article", "published": "2022-11-15", "journal": {"title": "Sci Signal", "issn": "1937-9145", "volume": "15", "issue": "760", "pages": "eabp9521", "issn-l": "1945-0877"}, "abstract": "Transforming growth factor-\u03b2 (TGF-\u03b2) signaling has important roles during embryonic development and in tissue homeostasis. TGF-\u03b2 ligands exert cellular effects by binding to type I (T\u03b2RI) and type II (T\u03b2RII) receptors and inducing both SMAD-dependent and SMAD-independent intracellular signaling pathways, the latter of which includes the activation of the tyrosine kinase Src. We investigated the mechanism by which TGF-\u03b2 stimulation activates Src in human and mouse cells. Before TGF-\u03b2 stimulation, inactive Src was complexed with T\u03b2RII. Upon TGF-\u03b21 stimulation, T\u03b2RII associated with and phosphorylated T\u03b2RI at Tyr182. Binding of Src to T\u03b2RI involved the interaction of the Src SH2 domain with phosphorylated Tyr182 and the interaction of the Src SH3 domain with a proline-rich region in T\u03b2RI and led to the activation of Src kinase activity and Src autophosphorylation. TGF-\u03b21-induced Src activation required the kinase activities of T\u03b2RII and Src but not that of T\u03b2RI. Activated Src also phosphorylated T\u03b2RI on several tyrosine residues, which may stabilize the binding of Src to the receptor. Src activation was required for the ability of TGF-\u03b2 to induce fibronectin production and migration in human breast carcinoma cells and to induce \u03b1-smooth muscle actin and actin reorganization in mouse fibroblasts. Thus, TGF-\u03b2 induces Src activation by stimulating a direct interaction with T\u03b2RI that depends on tyrosine phosphorylation of T\u03b2RI by T\u03b2RII.", "doi": "10.1126/scisignal.abp9521", "pmid": "36378749", "labels": [], "xrefs": [], "notes": [], "created": "2026-08-20T11:59:45.050Z", "modified": "2026-08-20T11:59:45.226Z"}, {"entity": "publication", "iuid": "d449f0a4fad642e59027b725b02ef124", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/d449f0a4fad642e59027b725b02ef124.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/d449f0a4fad642e59027b725b02ef124"}}, "title": "Platelet-Derived PDGFB Promotes Recruitment of Cancer-Associated Fibroblasts, Deposition of Extracellular Matrix and Tgf\u03b2 Signaling in the Tumor Microenvironment.", "authors": [{"family": "Zhang", "given": "Yanyu", "initials": "Y", "orcid": "0000-0001-9939-1838", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/33cec15d087243bcb0a9b6ff967a8a05.json"}}, {"family": "Manouchehri Doulabi", "given": "Ehsan", "initials": "E", "orcid": "0000-0003-1639-2267", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/ad12164c3f004575b93f26cf83df40eb.json"}}, {"family": "Herre", "given": "Melanie", "initials": "M"}, {"family": "Cedervall", "given": "Jessica", "initials": "J"}, {"family": "Qiao", "given": "Qi", "initials": "Q"}, {"family": "Miao", "given": "Zuoxiu", "initials": "Z"}, {"family": "Hamidi", "given": "Anahita", "initials": "A", "orcid": "0000-0002-5445-2446", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c9d2a9063065410385248b810cc9790f.json"}}, {"family": "Hellman", "given": "Lars", "initials": "L", "orcid": "0000-0003-1459-3815", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/d8880fe8eb1847faba04190c7f9a76cf.json"}}, {"family": "Kamali-Moghaddam", "given": "Masood", "initials": "M", "orcid": "0000-0002-1303-2218", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/70fceb2370d74e39a8c26d17963981cc.json"}}, {"family": "Olsson", "given": "Anna-Karin", "initials": "AK"}], "type": "journal article", "published": "2022-04-12", "journal": {"title": "Cancers (Basel)", "issn": "2072-6694", "volume": "14", "issue": "8", "issn-l": "2072-6694"}, "abstract": "Platelets constitute a major reservoir of platelet-derived growth factor B (PDGFB) and are continuously activated in the tumor microenvironment, exposing tumors to the plethora of growth factors contained in platelet granules. To address the specific role of platelet-derived PDGFB in the tumor microenvironment, we have created a mouse model with conditional knockout of PDGFB in platelets (pl-PDGFB KO). Lack of PDGFB in platelets resulted in 10-fold lower PDGFB concentration in the tumor microenvironment, fewer cancer-associated fibroblasts and reduced deposition of the extracellular matrix (ECM) molecules fibronectin and collagen I in the orthotopic RIP1-Tag2 model for pancreatic neuroendocrine cancer. Myosin light chain phosphorylation, promoting cell contraction and, consequently, the mechano-induced release of active transforming growth factor (TGF) \u03b2 from extracellular compartments, was reduced in tumors from pl-PDGFB KO mice. In agreement, TGF\u03b2 signaling, measured as phosphorylated Smad2, was significantly hampered in tumors from mice lacking PDGFB in their platelets, providing a plausible explanation for the reduced deposition of extracellular matrix. These findings indicate a major contribution of platelet-derived PDGFB to a malignant transformation of the tumor microenvironment and address for the first time the role of PDGFB released specifically from platelets in the remodeling of the ECM in tumors.", "doi": "10.3390/cancers14081947", "pmid": "35454853", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9024906"}, {"db": "pii", "key": "cancers14081947"}], "notes": [], "created": "2026-08-20T13:39:45.836Z", "modified": "2026-08-20T13:39:46.014Z"}, {"entity": "publication", "iuid": "55d83db8aeb940cd98680d07ccfc7c8c", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/55d83db8aeb940cd98680d07ccfc7c8c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/55d83db8aeb940cd98680d07ccfc7c8c"}}, "title": "Platelet-Specific PDGFB Ablation Impairs Tumor Vessel Integrity and Promotes Metastasis.", "authors": [{"family": "Zhang", "given": "Yanyu", "initials": "Y"}, {"family": "Cedervall", "given": "Jessica", "initials": "J"}, {"family": "Hamidi", "given": "Anahita", "initials": "A", "orcid": "0000-0002-5445-2446", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/c9d2a9063065410385248b810cc9790f.json"}}, {"family": "Herre", "given": "Melanie", "initials": "M"}, {"family": "Viitaniemi", "given": "Kati", "initials": "K"}, {"family": "D'Amico", "given": "Gabriela", "initials": "G"}, {"family": "Miao", "given": "Zuoxiu", "initials": "Z"}, {"family": "Unnithan", "given": "Ragaseema Valsala Madhavan", "initials": "RVM", "orcid": "0000-0002-5915-1685", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/20e313b8a02d4930984e90e55b657b2f.json"}}, {"family": "Vaccaro", "given": "Alessandra", "initials": "A"}, {"family": "van Hooren", "given": "Luuk", "initials": "L"}, {"family": "Georganaki", "given": "Maria", "initials": "M"}, {"family": "Thulin", "given": "\u00c5sa", "initials": "\u00c5"}, {"family": "Qiao", "given": "Qi", "initials": "Q"}, {"family": "Andrae", "given": "Johanna", "initials": "J"}, {"family": "Siegbahn", "given": "Agneta", "initials": "A"}, {"family": "Heldin", "given": "Carl-Henrik", "initials": "CH"}, {"family": "Alitalo", "given": "Kari", "initials": "K"}, {"family": "Betsholtz", "given": "Christer", "initials": "C"}, {"family": "Dimberg", "given": "Anna", "initials": "A"}, {"family": "Olsson", "given": "Anna-Karin", "initials": "AK"}], "type": "journal article", "published": "2020-08-15", "journal": {"title": "Cancer Res.", "issn": "1538-7445", "volume": "80", "issue": "16", "pages": "3345-3358", "issn-l": "0008-5472"}, "abstract": "Platelet-derived growth factor B (PDGFB) plays a crucial role in recruitment of PDGF receptor \u03b2-positive pericytes to blood vessels. The endothelium is an essential source of PDGFB in this process. Platelets constitute a major reservoir of PDGFB and are continuously activated in the tumor microenvironment, exposing tumors to the plethora of growth factors contained in platelet granules. Here, we show that tumor vascular function, as well as pericyte coverage is significantly impaired in mice with conditional knockout of PDGFB in platelets. A lack of PDGFB in platelets led to enhanced hypoxia and epithelial-to-mesenchymal transition in the primary tumors, elevated levels of circulating tumor cells, and increased spontaneous metastasis to the liver or lungs in two mouse models. These findings establish a previously unknown role for platelet-derived PDGFB, whereby it promotes and maintains vascular integrity in the tumor microenvironment by contributing to the recruitment of pericytes. SIGNIFICANCE: Conditional knockout of PDGFB in platelets demonstrates its previously unknown role in the maintenance of tumor vascular integrity and host protection against metastasis.", "doi": "10.1158/0008-5472.CAN-19-3533", "pmid": "32586981", "labels": [], "xrefs": [{"db": "pii", "key": "0008-5472.CAN-19-3533"}], "notes": [], "created": "2026-08-20T12:10:59.347Z", "modified": "2026-08-20T12:10:59.440Z"}]}