scholarly article | Q13442814 |
P356 | DOI | 10.1074/JBC.M305656200 |
P698 | PubMed publication ID | 12881521 |
P50 | author | Brian Druker | Q373427 |
Robert Rottapel | Q51814787 | ||
P2093 | author name string | Vimla Band | |
Hamid Band | |||
Lei Duan | |||
Hideki Shimura | |||
Alexander Tsygankov | |||
Navin L Rao | |||
Alagarsamy L Reddi | |||
Yuko Miura-Shimura | |||
P2860 | cites work | hSiah2 is a new Vav binding protein which inhibits Vav-mediated signaling pathways | Q22009420 |
Biological and regulatory properties of Vav-3, a new member of the Vav family of oncoproteins | Q22010673 | ||
Familial Parkinson disease gene product, parkin, is a ubiquitin-protein ligase | Q22254584 | ||
Structure and functions of the 20S and 26S proteasomes | Q24328777 | ||
Structure of the amino-terminal domain of Cbl complexed to its binding site on ZAP-70 kinase | Q27617539 | ||
Structure of a c-Cbl-UbcH7 complex: RING domain function in ubiquitin-protein ligases | Q27626747 | ||
Structural basis for relief of autoinhibition of the Dbl homology domain of proto-oncogene Vav by tyrosine phosphorylation | Q27627224 | ||
The ubiquitin system | Q27860803 | ||
Phosphotyrosine-dependent activation of Rac-1 GDP/GTP exchange by the vav proto-oncogene product | Q28114879 | ||
The tyrosine kinase negative regulator c-Cbl as a RING-type, E2-dependent ubiquitin-protein ligase | Q28145635 | ||
Ligand-induced ubiquitination of the epidermal growth factor receptor involves the interaction of the c-Cbl RING finger and UbcH7 | Q28146026 | ||
Tyrosine phosphorylation of the vav proto-oncogene product in activated B cells | Q28186886 | ||
Negative regulation of Lck by Cbl ubiquitin ligase | Q28208259 | ||
Coordinated regulation of the tyrosine phosphorylation of Cbl by Fyn and Syk tyrosine kinases | Q28267092 | ||
A novel phosphotyrosine-binding domain in the N-terminal transforming region of Cbl interacts directly and selectively with ZAP-70 in T cells | Q28289338 | ||
Cbl-mediated negative regulation of the Syk tyrosine kinase. A critical role for Cbl phosphotyrosine-binding domain binding to Syk phosphotyrosine 323 | Q28291812 | ||
Functional and physical interactions of Syk family kinases with the Vav proto-oncogene product | Q28300755 | ||
The non-receptor tyrosine kinase Syk is a target of Cbl-mediated ubiquitylation upon B-cell receptor stimulation. | Q28366332 | ||
Cbl-b is a negative regulator of receptor clustering and raft aggregation in T cells | Q28585061 | ||
Fyn, Yes, and Syk Phosphorylation Sites in c-Cbl Map to the Same Tyrosine Residues That Become Phosphorylated in Activated T Cells | Q28609046 | ||
Lck regulates Vav activation of members of the Rho family of GTPases | Q28610619 | ||
The structure of an antigenic determinant in a protein | Q29547829 | ||
Ubiquitin ligase activity and tyrosine phosphorylation underlie suppression of growth factor signaling by c-Cbl/Sli-1 | Q29617290 | ||
The Lck SH3 domain negatively regulates localization to lipid rafts through an interaction with c-Cbl | Q30167736 | ||
Cbl-b, a RING-type E3 ubiquitin ligase, targets phosphatidylinositol 3-kinase for ubiquitination in T cells. | Q30168616 | ||
The Cbl proto-oncogene product negatively regulates the Src-family tyrosine kinase Fyn by enhancing its degradation | Q30175273 | ||
Defective T-cell receptor signalling and positive selection of Vav-deficient CD4+ CD8+ thymocytes | Q30193572 | ||
Defective antigen receptor-mediated proliferation of B and T cells in the absence of Vav. | Q30193575 | ||
RING finger mutations that abolish c-Cbl-directed polyubiquitination and downregulation of the EGF receptor are insufficient for cell transformation | Q32138771 | ||
The Cbl phosphotyrosine-binding domain selects a D(N/D)XpY motif and binds to the Tyr292 negative regulatory phosphorylation site of ZAP-70. | Q32170429 | ||
The Cbl protooncoprotein: a negative regulator of immune receptor signal transduction | Q33702164 | ||
Tissue hyperplasia and enhanced T-cell signalling via ZAP-70 in c-Cbl-deficient mice | Q33776192 | ||
Signal transduction in T lymphocytes using a conditional allele of Sos | Q33871535 | ||
Vav-Rac1-mediated activation of the c-Jun N-terminal kinase/c-Jun/AP-1 pathway plays a major role in stimulation of the distal NFAT site in the interleukin-2 gene promoter | Q33968015 | ||
Proteolysis-independent regulation of PI3K by Cbl-b-mediated ubiquitination in T cells. | Q34088521 | ||
c-Cbl and Cbl-b regulate T cell responsiveness by promoting ligand-induced TCR down-modulation | Q34157660 | ||
Cbl: many adaptations to regulate protein tyrosine kinases | Q34205572 | ||
Beyond the RING: CBL proteins as multivalent adapters | Q34405560 | ||
VAV proteins as signal integrators for multi-subunit immune-recognition receptors | Q34718119 | ||
The tyrosine kinase regulator Cbl enhances the ubiquitination and degradation of the platelet-derived growth factor receptor alpha | Q36164471 | ||
A mouse with a loss-of-function mutation in the c-Cbl TKB domain shows perturbed thymocyte signaling without enhancing the activity of the ZAP-70 tyrosine kinase | Q36370638 | ||
A functional T-cell receptor signaling pathway is required for p95vav activity | Q36553748 | ||
Oncogenes, growth factors, and signal transduction | Q38715382 | ||
Tyrosine phosphorylation mediates both activation and downmodulation of the biological activity of Vav | Q39451395 | ||
The linker phosphorylation site Tyr292 mediates the negative regulatory effect of Cbl on ZAP-70 in T cells | Q40884199 | ||
Suppressor of cytokine signaling-1 inhibits VAV function through protein degradation. | Q40889649 | ||
Cbl-b regulates the CD28 dependence of T-cell activation. | Q40904107 | ||
Ubiquitin-dependent degradation of active Src. | Q40925082 | ||
Product of vav proto-oncogene defines a new class of tyrosine protein kinase substrates | Q41635684 | ||
A guanine nucleotide exchange factor-independent function of Vav1 in transcriptional activation | Q41714413 | ||
The Cbl protooncoprotein stimulates CSF-1 receptor multiubiquitination and endocytosis, and attenuates macrophage proliferation | Q42676655 | ||
Defects in actin-cap formation in Vav-deficient mice implicate an actin requirement for lymphocyte signal transduction | Q46517603 | ||
Vav is a regulator of cytoskeletal reorganization mediated by the T-cell receptor | Q57185397 | ||
The RING Finger Domain of Cbl Is Essential for Negative Regulation of the Syk Tyrosine Kinase | Q58179986 | ||
Negative regulation of lymphocyte activation and autoimmunity by the molecular adaptor Cbl-b | Q59058408 | ||
P433 | issue | 40 | |
P407 | language of work or name | English | Q1860 |
P304 | page(s) | 38495-38504 | |
P577 | publication date | 2003-07-24 | |
P1433 | published in | Journal of Biological Chemistry | Q867727 |
P1476 | title | Cbl-mediated ubiquitinylation and negative regulation of Vav | |
P478 | volume | 278 |
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Q38117477 | Plasma membrane signaling in HIV-1 infection |
Q26852269 | Protein tyrosine kinase regulation by ubiquitination: critical roles of Cbl-family ubiquitin ligases |
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Q35571851 | Scaffolding of antigen receptors for immunogenic versus tolerogenic signaling. |
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Q38721532 | Structural Determinants of the Gain-of-Function Phenotype of Human Leukemia-associated Mutant CBL Oncogene. |
Q33745662 | Synergistic signals for natural cytotoxicity are required to overcome inhibition by c-Cbl ubiquitin ligase |
Q38107331 | T cell antigen receptor activation and actin cytoskeleton remodeling |
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Q37376318 | The Sts proteins target tyrosine phosphorylated, ubiquitinated proteins within TCR signaling pathways |
Q34559351 | Vav1 fine tunes p53 control of apoptosis versus proliferation in breast cancer |
Q57295717 | Vav1 mutations identified in human cancers give rise to different oncogenic phenotypes |
Q38151844 | Wiskott-Aldrich syndrome protein--dynamic regulation of actin homeostasis: from activation through function and signal termination in T lymphocytes |
Q30852257 | bloodthirsty, an RBCC/TRIM gene required for erythropoiesis in zebrafish |
Q37672284 | c-Cbl inhibits angiogenesis and tumor growth by suppressing activation of PLCγ1 |
Q40415906 | c-Cbl regulates migration of v-Abl-transformed NIH 3T3 fibroblasts via Rac1. |
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