Hisamaru Hirai mostly deals with Cell biology, Molecular biology, Cancer research, Immunology and Haematopoiesis. His Cell biology study which covers Cellular differentiation that intersects with Marginal zone. His studies in Molecular biology integrate themes in fields like Gene, Chromosomal translocation, Binding domain, Alternative splicing and Runt.
His Cancer research research incorporates themes from Tyrosine kinase, Tyrosine phosphorylation, Tumor suppressor gene, Leukemia and Acute lymphocytic leukemia. In his study, Cardiology is strongly linked to Internal medicine, which falls under the umbrella field of Immunology. His Haematopoiesis research is multidisciplinary, relying on both Myeloid, Cytokine, Bone marrow and Progenitor cell.
His scientific interests lie mostly in Molecular biology, Cancer research, Cell biology, Immunology and Internal medicine. Hisamaru Hirai works mostly in the field of Molecular biology, limiting it down to topics relating to Gene and, in certain cases, DNA. Hisamaru Hirai interconnects Chronic myelogenous leukemia, Leukemia, Haematopoiesis and ABL in the investigation of issues within Cancer research.
His Haematopoiesis study combines topics from a wide range of disciplines, such as Myeloid and Progenitor cell. Many of his studies on Cell biology apply to Cellular differentiation as well. His Immunology study frequently links to related topics such as Stem cell.
Hisamaru Hirai mainly investigates Internal medicine, Cell biology, Transplantation, Cancer research and Haematopoiesis. His Internal medicine study incorporates themes from Gastroenterology and Surgery. His Cell biology study focuses on RUNX1 in particular.
His Cancer research research is multidisciplinary, incorporating perspectives in Cellular differentiation, CD135, Receptor tyrosine kinase, Progenitor cell and Chronic myelogenous leukemia. Hisamaru Hirai has researched Haematopoiesis in several fields, including Immunology, Myeloid, Cytokine, K562 cells and Transformation. His work carried out in the field of Transcription factor brings together such families of science as Molecular biology, Leukemia and Signal transduction.
His primary scientific interests are in Cancer research, Haematopoiesis, Cell biology, RUNX1 and Transcription factor. His work deals with themes such as Progenitor cell, Tyrosine kinase and Cytokine, which intersect with Cancer research. Haematopoiesis is frequently linked to Leukemia in his study.
Hisamaru Hirai specializes in Cell biology, namely Lymphocyte homing receptor. His Corepressor research is multidisciplinary, incorporating elements of Carcinogenesis, Molecular biology, Transcriptional regulation and DNA-binding protein. Myeloid is a subfield of Immunology that Hisamaru Hirai explores.
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Hematopoietic stem cells differentiate into vascular cells that participate in the pathogenesis of atherosclerosis
Masataka Sata;Akio Saiura;Atsushi Kunisato;Akihiro Tojo.
Nature Medicine (2002)
Eph Receptors and Ligands Comprise Two Major Specificity Subclasses and Are Reciprocally Compartmentalized during Embryogenesis
Nicholas W Gale;Sacha J Holland;David M Valenzuela;Ann Flenniken.
Neuron (1996)
AML-1 is required for megakaryocytic maturation and lymphocytic differentiation, but not for maintenance of hematopoietic stem cells in adult hematopoiesis.
Motoshi Ichikawa;Takashi Asai;Toshiki Saito;Go Yamamoto.
Nature Medicine (2004)
Notch2 is preferentially expressed in mature B cells and indispensable for marginal zone B lineage development.
Toshiki Saito;Shigeru Chiba;Motoshi Ichikawa;Atsushi Kunisato.
Immunity (2003)
A novel putative tyrosine kinase receptor encoded by the eph gene
Hisamaru Hirai;Yoshiro Maru;Koichi Hagiwara;Junji Nishida.
Science (1987)
Notch1 but Not Notch2 Is Essential for Generating Hematopoietic Stem Cells from Endothelial Cells
Keiki Kumano;Shigeru Chiba;Atsushi Kunisato;Masataka Sata.
Immunity (2003)
Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia.
K. Mitani;S. Ogawa;T. Tanaka;H. Miyoshi.
The EMBO Journal (1994)
Gain-of-function of mutated C-CBL tumour suppressor in myeloid neoplasms.
Masashi Sanada;Takahiro Suzuki;Lee-Yung Shih;Makoto Otsu.
Nature (2009)
The oncoprotein Evi-1 represses TGF-Beta signalling by inhibiting Smad3
Mineo Kurokawa;Kinuko Mitani;Kenji Irie;Tomohiro Matsuyama.
Nature (1998)
Cardiovascular anomaly, impaired actin bundling and resistance to Src-induced transformation in mice lacking p130Cas.
Hiroaki Honda;Hideaki Oda;Tetsuya Nakamoto;Zen-ichiro Honda.
Nature Genetics (1998)
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