JAK2V617F homozygosity drives a phenotypic switch in myeloproliferative neoplasms, but is insufficient to sustain disease
- Submitting institution
-
University of Salford, The
- Unit of assessment
- 3 - Allied Health Professions, Dentistry, Nursing and Pharmacy
- Output identifier
- 33628
- Type
- D - Journal article
- DOI
-
10.1182/blood-2013-06-510222
- Title of journal
- Blood
- Article number
- -
- First page
- 3139
- Volume
- 123
- Issue
- 20
- ISSN
- 0006-4971
- Open access status
- Out of scope for open access requirements
- Month of publication
- April
- Year of publication
- 2014
- URL
-
-
- Supplementary information
-
-
- Request cross-referral to
- -
- Output has been delayed by COVID-19
- No
- COVID-19 affected output statement
- -
- Forensic science
- No
- Criminology
- No
- Interdisciplinary
- No
- Number of additional authors
-
16
- Research group(s)
-
B - Biomedical Research
- Citation count
- 44
- Proposed double-weighted
- No
- Reserve for an output with double weighting
- No
- Additional information
- -
- Author contribution statement
- My work was mainly focused on apoptosis and proliferation analysis of CD71+, erythroid precursor cells from wild type and knock-in mouse. Once those ex-vivo experimental systems were established I isolated erythroid tissue with FACS and then analysed for Annexin V/PI staining. In addition, growth of cells, was analysed in same system using BrdU incorporation (in water treatment of mice and ex-vivo one hour treatment of cells) and cells were subsequently analysed for BrdU positivity. Work I performed on that knock-in mice was part of figure 4 F/G and figure 5 A,B and C.
- Non-English
- No
- English abstract
- -