Leveraging protein quaternary structure to identify oncogenic driver mutations
- Standort
-
Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
-
1471-2105
- Umfang
-
Online-Ressource
- Sprache
-
Englisch
- Anmerkungen
-
online resource.
- Erschienen in
-
Leveraging protein quaternary structure to identify oncogenic driver mutations ; volume:17 ; number:1 ; day:22 ; month:3 ; year:2016 ; pages:1-13 ; date:12.2016
BMC bioinformatics ; 17, Heft 1 (22.3.2016), 1-13, 12.2016
- Urheber
-
Ryslik, Gregory A.
- Beteiligte Personen und Organisationen
-
Cheng, Yuwei
Modis, Yorgo
Zhao, Hongyu
SpringerLink (Online service)
- DOI
-
10.1186/s12859-016-0963-3
- URN
-
urn:nbn:de:1111-2016032814741
- Rechteinformation
-
Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
-
14.08.2025, 11:03 MESZ
Datenpartner
Dieses Objekt wird bereitgestellt von:
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Deutsche Nationalbibliothek. Bei Fragen zum Objekt wenden Sie sich bitte an den Datenpartner.
Beteiligte
- Ryslik, Gregory A.
- Cheng, Yuwei
- Modis, Yorgo
- Zhao, Hongyu
- SpringerLink (Online service)
Ähnliche Objekte (12)
Oncogenic potential of rare RRAS2 mutations
Small molecule inhibitors of RAS proteins with oncogenic mutations
Proteomic alterations in extracellular vesicles induced by oncogenic PIK3CA mutations
Oncogenic and drug-sensitive RET mutations in human epithelial ovarian cancer
Accumulation of Oncogenic Mutations During Progression from Healthy Tissue to Cancer
Leveraging genetically simple traits to identify small-effect variants for complex phenotypes
Leveraging unstructured data to identify hereditary angioedema patients in electronic medical records
VaryMinions: leveraging RNNs to identify variants in variability-intensive systems’ logs
Discovery of oncogenic ROS1 missense mutations with sensitivity to tyrosine kinase inhibitors
Identification of oncogenic driver mutations by genome-wide CRISPR-Cas9 dropout screening
Vav1 mutations identified in human cancers give rise to different oncogenic phenotypes
Overexpression of wild type RRAS2, without oncogenic mutations, drives chronic lymphocytic leukemia
Oncogenic potential of rare RRAS2 mutations
Small molecule inhibitors of RAS proteins with oncogenic mutations
Proteomic alterations in extracellular vesicles induced by oncogenic PIK3CA mutations
Oncogenic and drug-sensitive RET mutations in human epithelial ovarian cancer
Accumulation of Oncogenic Mutations During Progression from Healthy Tissue to Cancer
Leveraging genetically simple traits to identify small-effect variants for complex phenotypes
Leveraging unstructured data to identify hereditary angioedema patients in electronic medical records
VaryMinions: leveraging RNNs to identify variants in variability-intensive systems’ logs
Discovery of oncogenic ROS1 missense mutations with sensitivity to tyrosine kinase inhibitors
Identification of oncogenic driver mutations by genome-wide CRISPR-Cas9 dropout screening
Vav1 mutations identified in human cancers give rise to different oncogenic phenotypes
Overexpression of wild type RRAS2, without oncogenic mutations, drives chronic lymphocytic leukemia
Oncogenic potential of rare RRAS2 mutations
Small molecule inhibitors of RAS proteins with oncogenic mutations
Proteomic alterations in extracellular vesicles induced by oncogenic PIK3CA mutations
Oncogenic and drug-sensitive RET mutations in human epithelial ovarian cancer
Accumulation of Oncogenic Mutations During Progression from Healthy Tissue to Cancer
Leveraging genetically simple traits to identify small-effect variants for complex phenotypes
Leveraging unstructured data to identify hereditary angioedema patients in electronic medical records
VaryMinions: leveraging RNNs to identify variants in variability-intensive systems’ logs
Discovery of oncogenic ROS1 missense mutations with sensitivity to tyrosine kinase inhibitors
Identification of oncogenic driver mutations by genome-wide CRISPR-Cas9 dropout screening
Vav1 mutations identified in human cancers give rise to different oncogenic phenotypes