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1دورية أكاديمية
المؤلفون: Kayo Yoshida, Megumi Hada, Masami Hayashi, Akane Kizu, Kohei Kitada, Kiyomi Eguchi-Kasai, Toshiaki Kokubo, Takeshi Teramura, Hiromi Hashizume Suzuki, Hitomi Watanabe, Gen Kondoh, Aiko Nagamatsu, Premkumar Saganti, Masafumi Muratani, Francis A. Cucinotta, Takashi Morita
المصدر: International Journal of Molecular Sciences, Vol 25, Iss 6, p 3283 (2024)
مصطلحات موضوعية: International Space Station, space radiation, mouse ES cells, RNA sequencing, gene expression, p53-related genes, Biology (General), QH301-705.5, Chemistry, QD1-999
وصف الملف: electronic resource
العلاقة: https://www.mdpi.com/1422-0067/25/6/3283Test; https://doaj.org/toc/1661-6596Test; https://doaj.org/toc/1422-0067Test
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المؤلفون: Masanori Goto, Bing Xin, Lingtong Meng, Takako Ooshio, Masahiro Yamamoto, Yuji Nishikawa, Hiroki Tanaka, Yusuke Mizukami, Yang Liu, Yuki Kamikokura, Yoko Okada
المصدر: Cancer Science
مصطلحات موضوعية: 0301 basic medicine, Heterozygote, Cancer Research, Carcinoma, Hepatocellular, Carcinogenesis, Cellular differentiation, Cre recombinase, Biology, Cholangiocarcinoma, Proto-Oncogene Proteins c-myc, Proto-Oncogene Proteins p21(ras), Mice, 03 medical and health sciences, 0302 clinical medicine, medicine, Animals, HRAS, Progenitor cell, oncogenes and tumor‐suppressor genes, characteristics of cancer cells, Mice, Knockout, gene‐manipulated animal models, Calcium-Binding Proteins, Homozygote, Liver Neoplasms, Transdifferentiation, p53‐related genes, Original Articles, General Medicine, Cell Dedifferentiation, medicine.disease, Phenotype, experimental animal models and genetically engineered animals, Gene Expression Regulation, Neoplastic, cell differentiation, 030104 developmental biology, Bile Duct Neoplasms, Oncology, animal model for carcinogenesis, 030220 oncology & carcinogenesis, Hepatocellular carcinoma, Cell Transdifferentiation, Knockout mouse, Cancer research, Original Article, Tumor Suppressor Protein p53
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::94d422ad4a0c2de305662b975e9fb0ceTest
https://doi.org/10.1111/cas.14996Test -
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المؤلفون: Laura Sancillo, Rosa Alba Rana, Francesca Masiello, Fabrizio Martelli, Giovanni Barosi, Maria Zingariello, Judith D. Goldberg, Xiaochun Li, Fiorella Ciaffoni, Margherita Massa, Anna Rita Migliaccio, Barbara Ghinassi, Emanuela D'Amore
المساهمون: Zingariello, M, Martelli, F, Ciaffoni, F, Masiello, F, Ghinassi, B, D'Amore, E, Massa, M, Barosi, G, Sancillo, L, Li, X, Goldberg, Jd, Rana, Ra, Franco Migliaccio, Anna Rita
المصدر: Blood. 121:3345-3363
مصطلحات موضوعية: Adult, Male, Vascular Endothelial Growth Factor A, Hematopoiesis and Stem Cells, Blotting, Western, Immunology, Spleen, Biology, Real-Time Polymerase Chain Reaction, Primary myelofibrosis (PMF) is characterized by fibrosis, ineffective hematopoiesis in marrow, and hematopoiesis in extramedullary sites and is associated with abnormal megakaryocyte (MK) development and increased transforming growth factor (TGF)-β1 release. To clarify the role of TGF-β1 in the pathogenesis of this disease, the TGF-β1 signaling pathway of marrow and spleen of the Gata1(low) mouse model of myelofibrosis (MF) was profiled and the consequences of inhibition of TGF-β1 signaling on disease manifestations determined. The expression of 20 genes in marrow and 36 genes in spleen of Gata1(low) mice was altered. David-pathway analyses identified alterations of TGF-β1, Hedgehog, and p53 signaling in marrow and spleen and of mammalian target of rapamycin (mTOR) in spleen only and predicted that these alterations would induce consequences consistent with the Gata1(low) phenotype (increased apoptosis and G1 arrest both in marrow and spleen and increased osteoblast differentiation and reduced ubiquitin-mediated proteolysis in marrow only). Inhibition of TGF-β1 signaling normalized the expression of p53-related genes, restoring hematopoiesis and MK development and reducing fibrosis, neovascularization, and osteogenesis in marrow. It also normalized p53/mTOR/Hedgehog-related genes in spleen, reducing extramedullary hematopoiesis. These data identify altered expression signatures of TGF-β1 signaling that may be responsible for MF in Gata1(low) mice and may represent additional targets for therapeutic intervention in PMF, Biochemistry, Transforming Growth Factor beta1, Mice, Bone Marrow, Fibrosis, Biomarkers, Tumor, medicine, Animals, Humans, GATA1 Transcription Factor, RNA, Messenger, RNA, Small Interfering, Myelofibrosis, PI3K/AKT/mTOR pathway, Oligonucleotide Array Sequence Analysis, Ineffective Hematopoiesis, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, TOR Serine-Threonine Kinases, Cell Biology, Hematology, Middle Aged, Flow Cytometry, medicine.disease, Chemokine CXCL12, Extramedullary hematopoiesis, Disease Models, Animal, Haematopoiesis, medicine.anatomical_structure, Primary Myelofibrosis, Case-Control Studies, Cancer research, Cytokines, Bone marrow, Signal Transduction
وصف الملف: STAMPA
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2c708320f0f269d9717c1cd36e3eb8bcTest
https://doi.org/10.1182/blood-2012-06-439661Test -
4دورية أكاديميةCharacterization of the TGF-β1 signaling abnormalities in the Gata1low mouse model of myelofibrosis.
المؤلفون: Zingariello, M, Martelli, F, Ciaffoni, F, Masiello, F, Ghinassi, B, D'Amore, E, Massa, M, Barosi, G, Sancillo, L, Li, X, Goldberg, Jd, Rana, Ra, FRANCO MIGLIACCIO, ANNA RITA
المساهمون: Zingariello, M, Martelli, F, Ciaffoni, F, Masiello, F, Ghinassi, B, D'Amore, E, Massa, M, Barosi, G, Sancillo, L, Li, X, Goldberg, Jd, Rana, Ra, Franco Migliaccio, Anna Rita
مصطلحات موضوعية: Primary myelofibrosis (PMF) is characterized by fibrosis, ineffective hematopoiesis in marrow, and hematopoiesis in extramedullary sites and is associated with abnormal megakaryocyte (MK) development and increased transforming growth factor (TGF)-β1 release. To clarify the role of TGF-β1 in the pathogenesis of this disease, the TGF-β1 signaling pathway of marrow and spleen of the Gata1(low) mouse model of myelofibrosis (MF) was profiled and the consequences of inhibition of TGF-β1 signaling on disease manifestations determined. The expression of 20 genes in marrow and 36 genes in spleen of Gata1(low) mice was altered. David-pathway analyses identified alterations of TGF-β1, Hedgehog, and p53 signaling in marrow and spleen and of mammalian target of rapamycin (mTOR) in spleen only and predicted that these alterations would induce consequences consistent with the Gata1(low) phenotype (increased apoptosis and G1 arrest both in marrow and spleen and increased osteoblast differentiation and reduced ubiquitin-mediated proteolysis in marrow only). Inhibition of TGF-β1 signaling normalized the expression of p53-related genes, restoring hematopoiesis and MK development and reducing fibrosis, neovascularization, and osteogenesis in marrow. It also normalized p53/mTOR/Hedgehog-related genes in spleen, reducing extramedullary hematopoiesis. These data identify altered expression signatures of TGF-β1 signaling that may be responsible for MF in Gata1(low) mice and may represent additional targets for therapeutic intervention in PMF
وصف الملف: STAMPA
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/23462118; info:eu-repo/semantics/altIdentifier/wos/WOS:000321831600010; ispartofbook:Blood; volume:121; firstpage:3345; lastpage:3363; numberofpages:19; journal:BLOOD; http://hdl.handle.net/11585/466967Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-84879390119