Pages that link to "Q30193411"
Jump to navigation
Jump to search
The following pages link to Introduction of a loss-of-function point mutation from the SH3 region of the Caenorhabditis elegans sem-5 gene activates the transforming ability of c-abl in vivo and abolishes binding of proline-rich ligands in vitro. (Q30193411):
Displaying 14 items.
- A direct binding site for Grb2 contributes to transformation and leukemogenesis by the Tel-Abl (ETV6-Abl) tyrosine kinase (Q24563301) (← links)
- The PAG gene product, a stress-induced protein with antioxidant properties, is an Abl SH3-binding protein and a physiological inhibitor of c-Abl tyrosine kinase activity (Q24606662) (← links)
- c-ABL tyrosine kinase activity is regulated by association with a novel SH3-domain-binding protein (Q24647548) (← links)
- Bcr-Abl induces abnormal cytoskeleton remodeling, beta1 integrin clustering and increased cell adhesion to fibronectin through the Abl interactor 1 pathway (Q24676463) (← links)
- The cytostatic function of c-Abl is controlled by multiple nuclear localization signals and requires the p53 and Rb tumor suppressor gene products (Q28508496) (← links)
- Targeting RAD51 phosphotyrosine-315 to prevent unfaithful recombination repair in BCR-ABL1 leukemia (Q30010486) (← links)
- Autoinhibition of Bcr-Abl through its SH3 domain (Q30164601) (← links)
- Signal transducer and activator of transcription (STAT)5 activation by BCR/ABL is dependent on intact Src homology (SH)3 and SH2 domains of BCR/ABL and is required for leukemogenesis (Q30175784) (← links)
- The murine AIDS virus Gag precursor protein binds to the SH3 domain of c-Abl (Q30176596) (← links)
- Clinical targeting of mutated and wild-type protein tyrosine kinases in cancer (Q33602552) (← links)
- Stimulation of p53 DNA binding by c-Abl requires the p53 C terminus and tetramerization (Q33961679) (← links)
- Clinical resistance to the kinase inhibitor STI-571 in chronic myeloid leukemia by mutation of Tyr-253 in the Abl kinase domain P-loop (Q34075619) (← links)
- The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity (Q36368162) (← links)
- Abl kinases regulate actin comet tail elongation via an N-WASP-dependent pathway (Q40366591) (← links)