Genome-wide CRISPR screens reveal genetic mediators of cereblon modulator toxicity in primary effusion lymphoma.
Adaptor Proteins, Signal Transducing
/ genetics
CRISPR-Cas Systems
Clustered Regularly Interspaced Short Palindromic Repeats
Cullin Proteins
/ metabolism
Drug Resistance, Neoplasm
/ genetics
Endopeptidases
/ genetics
Gene Knockdown Techniques
Genome-Wide Association Study
Humans
Lenalidomide
/ adverse effects
Lymphoma, Primary Effusion
/ drug therapy
Models, Biological
Thalidomide
/ analogs & derivatives
Ubiquitin-Protein Ligases
Journal
Blood advances
ISSN: 2473-9537
Titre abrégé: Blood Adv
Pays: United States
ID NLM: 101698425
Informations de publication
Date de publication:
23 07 2019
23 07 2019
Historique:
received:
15
01
2019
accepted:
17
05
2019
entrez:
14
7
2019
pubmed:
14
7
2019
medline:
8
7
2020
Statut:
ppublish
Résumé
Genome-wide CRISPR/Cas9 screens represent a powerful approach to studying mechanisms of drug action and resistance. Cereblon modulating agents (CMs) have recently emerged as candidates for therapeutic intervention in primary effusion lymphoma (PEL), a highly aggressive cancer caused by Kaposi's sarcoma-associated herpesvirus. CMs bind to cereblon (CRBN), the substrate receptor of the cullin-RING type E3 ubiquitin ligase CRL4
Identifiants
pubmed: 31300418
pii: bloodadvances.2019031732
doi: 10.1182/bloodadvances.2019031732
pmc: PMC6650732
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
CRBN protein, human
0
CUL4A protein, human
0
CUL4B protein, human
0
Cullin Proteins
0
Thalidomide
4Z8R6ORS6L
pomalidomide
D2UX06XLB5
Ubiquitin-Protein Ligases
EC 2.3.2.27
Endopeptidases
EC 3.4.-
SENP8 protein, human
EC 3.4.22.-
Lenalidomide
F0P408N6V4
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2105-2117Subventions
Organisme : NCI NIH HHS
ID : R21 CA210904
Pays : United States
Informations de copyright
© 2019 by The American Society of Hematology.
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