p66Shc deficiency in the Eμ-TCL1 mouse model of chronic lymphocytic leukemia enhances leukemogenesis by altering the chemokine receptor landscape.
Journal
Haematologica
ISSN: 1592-8721
Titre abrégé: Haematologica
Pays: Italy
ID NLM: 0417435
Informations de publication
Date de publication:
10 2019
10 2019
Historique:
received:
22
10
2018
accepted:
22
02
2019
pubmed:
2
3
2019
medline:
8
7
2020
entrez:
2
3
2019
Statut:
ppublish
Résumé
The Shc family adaptor p66Shc acts as a negative regulator of proliferative and survival signals triggered by the B-cell receptor and, by enhancing the production of reactive oxygen species, promotes oxidative stress-dependent apoptosis. Additionally, p66Shc controls the expression and function of chemokine receptors that regulate lymphocyte traffic. Chronic lymphocytic leukemia cells have a p66Shc expression defect which contributes to their extended survival and correlates with poor prognosis. We analyzed the impact of p66Shc ablation on disease severity and progression in the Eμ-TCL1 mouse model of chronic lymphocytic leukemia. We showed that Eμ-TCL1/p66Shc
Identifiants
pubmed: 30819907
pii: haematol.2018.209981
doi: 10.3324/haematol.2018.209981
pmc: PMC6886430
doi:
Substances chimiques
Neoplasm Proteins
0
Receptors, Chemokine
0
Shc1 protein, mouse
0
Src Homology 2 Domain-Containing, Transforming Protein 1
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2040-2052Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright© 2019 Ferrata Storti Foundation.
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