Mark L. Kahn mainly investigates Cell biology, Receptor, Platelet, Molecular biology and Platelet activation. His Cell biology study combines topics in areas such as PDPN, Podoplanin, Immunology, Endothelium and Protease-activated receptor. The study incorporates disciplines such as Endothelial stem cell and Signal transduction in addition to Receptor.
His work in GPVI and Platelet membrane glycoprotein are all subfields of Platelet research. His study in the fields of Convulxin under the domain of GPVI overlaps with other disciplines such as Linker for Activation of T cells. His Molecular biology research is multidisciplinary, relying on both Secretion, A549 cell, Gene expression and Transfection.
The scientist’s investigation covers issues in Cell biology, Platelet, Receptor, GPVI and Signal transduction. The concepts of his Cell biology study are interwoven with issues in Endothelial stem cell, Biochemistry, Lymphatic system and Protease-activated receptor, Thrombin. Mark L. Kahn has researched Protease-activated receptor in several fields, including Inflammation and Thrombin receptor.
His Platelet research includes themes of Collagen receptor and Integrin. His GPVI research is multidisciplinary, incorporating elements of Immune receptor, Calmodulin and Fc receptor. His studies deal with areas such as Function and Phosphorylation as well as Signal transduction.
Mark L. Kahn focuses on Cell biology, Lymphatic system, Pathology, Cancer research and Transcription factor. His work carried out in the field of Cell biology brings together such families of science as Receptor, Stimulation and FOXC2. While the research belongs to areas of Receptor, Mark L. Kahn spends his time largely on the problem of Zebrafish, intersecting his research to questions surrounding CXCR4 and Chemokine.
His Lymphatic system study combines topics in areas such as Endothelial stem cell, Vascular endothelial growth factor C, Lung and Lymphangiogenesis. His biological study spans a wide range of topics, including Hemostasis, Wound healing and Platelet activation, Platelet, Thrombin. His Pathology study combines topics from a wide range of disciplines, such as Cerebral cavernous malformations, Lung injury, Immune system and Mutation.
Mark L. Kahn mainly focuses on Pathology, Cell biology, Lymphatic system, Protein kinase A and Lymph. His studies in Pathology integrate themes in fields like Mutation and Familial cerebral cavernous malformation. His research in Cell biology is mostly concerned with Hippo signaling pathway.
The Lymphatic system study combines topics in areas such as Hennekam syndrome, Lung injury and Cell polarity. His study in Protein kinase A is interdisciplinary in nature, drawing from both Lesion, Myosin light-chain kinase, Hindbrain, Somatic cell and Phenotype. His study in the field of Lymphatic Endothelium also crosses realms of PIEZO1.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
A dual thrombin receptor system for platelet activation
Mark L. Kahn;Yao-Wu Zheng;Wei Huang;Violeta Bigornia.
Protease-activated receptors 1 and 4 mediate activation of human platelets by thrombin
Mark L. Kahn;Mayumi Nakanishi-Matsui;Michael J. Shapiro;Hiroaki Ishihara.
Journal of Clinical Investigation (1999)
Protease-activated receptor 3 is a second thrombin receptor in humans.
Hiroaki Ishihara;Andrew J. Connolly;Dewan Zeng;Mark L. Kahn.
Role of the thrombin receptor in development and evidence for a second receptor
Andrew J. Connolly;Hiroaki Ishihara;Mark L. Kahn;Robert V. Farese.
Molecular cloning, expression and potential functions of the human proteinase-activated receptor-2
Stephan K. Böhm;Wuyi Kong;Dieter Brömme;Steven P. Smeekens.
Biochemical Journal (1996)
Regulation of Blood and Lymphatic Vascular Separation by Signaling Proteins SLP-76 and Syk
Farhad Abtahian;Anastasia Guerriero;Eric Sebzda;Min-Min Lu.
Platelets regulate lymphatic vascular development through CLEC-2–SLP-76 signaling
Cara C. Bertozzi;Alec A. Schmaier;Patricia Mericko;Paul R. Hess.
Delayed Onset of Inflammation in Protease-Activated Receptor-2-Deficient Mice
Jonathan R. Lindner;Mark L. Kahn;Shaun R. Coughlin;Gilberto R. Sambrano.
Journal of Immunology (2000)
Klf2 Is an Essential Regulator of Vascular Hemodynamic Forces In Vivo
John S. Lee;Qing Yu;Jordan T. Shin;Eric Sebzda.
Developmental Cell (2006)
Protease activated receptors: theme and variations.
Peter J O'Brien;Marina Molino;Mark Kahn;Lawrence F Brass.
If you think any of the details on this page are incorrect, let us know.
We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below: