Mouse models of myeloproliferative neoplasms: JAK of all grades
In 2005, several groups identified a single gain-of-function point mutation in the JAK2 kinase that was present in the majority of patients with myeloproliferative neoplasms (MPNs). Since this discovery, much effort has been dedicated to understanding the molecular consequences of the JAK2V617F muta...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
The Company of Biologists
2011-05-01
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| Series: | Disease Models & Mechanisms |
| Online Access: | http://dmm.biologists.org/content/4/3/311 |
| _version_ | 1818313333858631680 |
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| author | Juan Li David G. Kent Edwin Chen Anthony R. Green |
| author_facet | Juan Li David G. Kent Edwin Chen Anthony R. Green |
| author_sort | Juan Li |
| collection | DOAJ |
| description | In 2005, several groups identified a single gain-of-function point mutation in the JAK2 kinase that was present in the majority of patients with myeloproliferative neoplasms (MPNs). Since this discovery, much effort has been dedicated to understanding the molecular consequences of the JAK2V617F mutation in the haematopoietic system. Three waves of mouse models have been produced recently (bone marrow transplantation, transgenic and targeted knock-in), which have facilitated the understanding of the molecular pathogenesis of JAK2V617F-positive MPNs, providing potential platforms for designing and validating novel therapies in humans. This Commentary briefly summarises the first two types of mouse models and then focuses on the more recently generated knock-in models. |
| first_indexed | 2024-12-13T08:32:05Z |
| format | Article |
| id | doaj.art-1473835664054d78b6cbee62dedd101a |
| institution | Directory Open Access Journal |
| issn | 1754-8403 1754-8411 |
| language | English |
| last_indexed | 2024-12-13T08:32:05Z |
| publishDate | 2011-05-01 |
| publisher | The Company of Biologists |
| record_format | Article |
| series | Disease Models & Mechanisms |
| spelling | doaj.art-1473835664054d78b6cbee62dedd101a2022-12-21T23:53:44ZengThe Company of BiologistsDisease Models & Mechanisms1754-84031754-84112011-05-014331131710.1242/dmm.006817006817Mouse models of myeloproliferative neoplasms: JAK of all gradesJuan LiDavid G. KentEdwin ChenAnthony R. GreenIn 2005, several groups identified a single gain-of-function point mutation in the JAK2 kinase that was present in the majority of patients with myeloproliferative neoplasms (MPNs). Since this discovery, much effort has been dedicated to understanding the molecular consequences of the JAK2V617F mutation in the haematopoietic system. Three waves of mouse models have been produced recently (bone marrow transplantation, transgenic and targeted knock-in), which have facilitated the understanding of the molecular pathogenesis of JAK2V617F-positive MPNs, providing potential platforms for designing and validating novel therapies in humans. This Commentary briefly summarises the first two types of mouse models and then focuses on the more recently generated knock-in models.http://dmm.biologists.org/content/4/3/311 |
| spellingShingle | Juan Li David G. Kent Edwin Chen Anthony R. Green Mouse models of myeloproliferative neoplasms: JAK of all grades Disease Models & Mechanisms |
| title | Mouse models of myeloproliferative neoplasms: JAK of all grades |
| title_full | Mouse models of myeloproliferative neoplasms: JAK of all grades |
| title_fullStr | Mouse models of myeloproliferative neoplasms: JAK of all grades |
| title_full_unstemmed | Mouse models of myeloproliferative neoplasms: JAK of all grades |
| title_short | Mouse models of myeloproliferative neoplasms: JAK of all grades |
| title_sort | mouse models of myeloproliferative neoplasms jak of all grades |
| url | http://dmm.biologists.org/content/4/3/311 |
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