Oncogene-induced senescence in hematopoietic progenitors features myeloid restricted hematopoiesis, chronic inflammation and histiocytosis.
Animals
Bone Marrow
/ pathology
Cell Cycle Checkpoints
/ genetics
Cellular Senescence
/ genetics
Chronic Disease
Cyclin-Dependent Kinase Inhibitor p16
/ metabolism
Gene Expression Regulation
Green Fluorescent Proteins
/ metabolism
Hematopoiesis
/ genetics
Hematopoietic Stem Cells
/ metabolism
Histiocytosis
/ complications
Humans
Inflammation
/ complications
Lentivirus
/ genetics
Mice
Mutation
/ genetics
Myeloid Cells
/ pathology
Oncogenes
Paracrine Communication
Principal Component Analysis
Proto-Oncogene Proteins B-raf
/ genetics
Tumor Necrosis Factor-alpha
/ antagonists & inhibitors
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
27 07 2021
27 07 2021
Historique:
received:
22
01
2020
accepted:
12
07
2021
entrez:
28
7
2021
pubmed:
29
7
2021
medline:
5
8
2021
Statut:
epublish
Résumé
Activating mutations in the BRAF-MAPK pathway have been reported in histiocytoses, hematological inflammatory neoplasms characterized by multi-organ dissemination of pro-inflammatory myeloid cells. Here, we generate a humanized mouse model of transplantation of human hematopoietic stem and progenitor cells (HSPCs) expressing the activated form of BRAF (BRAF
Identifiants
pubmed: 34315896
doi: 10.1038/s41467-021-24876-1
pii: 10.1038/s41467-021-24876-1
pmc: PMC8316479
doi:
Substances chimiques
Cyclin-Dependent Kinase Inhibitor p16
0
Tumor Necrosis Factor-alpha
0
Green Fluorescent Proteins
147336-22-9
Proto-Oncogene Proteins B-raf
EC 2.7.11.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
4559Informations de copyright
© 2021. The Author(s).
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