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1. |
Iinhibition of PI3K/Akt signaling by Cbl is involved in As2O3-induced apoptosis of acute promyelocytic leukemia cells & G2/M phase arrest of gastric cancer cells. It did this probably via its regulating PI3K/Akt pathway, modulating p53 activation. |
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2. |
Without the G306E mutation the c-Cbl unites CD38 with the signaling complex and delivers a MAPK signal that drives RA-induced differentiation. |
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3. |
CBL exon8/9 mutants occur in genetically defined myeloid leukemia/myelodysplastic syndrome subtypes and transform hematopoietic cells by constitutively activating the FLT3 pathway. |
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4. |
The expression of c-Cbl blocks the ability of mixed lineage kinases to signal to downstream components of the kinase cascade leading to JNK activation and protects neuronal cells from death induced by mixed lineage kinases. |
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5. |
CBL mutations occur frequently in juvenile myelomonocytic leukemia |
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6. |
gain-of-function mutations of c-cbl tumour suppressor associated with acquired uniparental disomy in the pathogenesis of some myeloid cancers |
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7. |
c-Cbl promoted LMP2A degradation through ubiquitination, specifically degraded the Syk protein tyrosine kinase in the presence of LMP2A, and inhibited LMP2A induction of the EBV lytic cycle |
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8. |
Frequent CBL mutations are associated with 11q acquired uniparental disomy in myeloproliferative neoplasms. |
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9. |
Characterization of the Cbl selectivity of piceatannol-induced protein loss revealed that this compound was also able to induce the functional loss of specific Cbl-associated proteins involved in signaling pathways commonly associated with cancer. |
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10. |
These results indicate that Cbl regulates STAP-2 protein levels and Brk/STAP-2-mediated STAT3 activation. |
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11. |
the interplay between Nedd4-2-related E3 ligases that regulate ACK1 levels and Cbl that modifies EGF receptor impinges on cell receptor dynamics. |
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12. |
detailed high-resolution solution structural study of CIN85A and CIN85B binding to proline-arginine peptides derived from the cognate ligands Cbl and Cbl-b |
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13. |
c-Cbl mediates the ubiquitination of stimulated FcgammaRIIa |
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14. |
Mapping minimally overlapping segmental UPD regions helps target the search for pathogenic mutations, including newly identified missense mutations in the proto-oncogene c-Cbl in 7 of 12 patients with UPD11q. |
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15. |
TEAD1 and the ubiquitin ligase c-Cbl were identified as novel basal cell markers in prostate cancer |
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16. |
Ubc4/5 and c-Cbl continue to ubiquitinate EGF receptor after internalization to facilitate polyubiquitination and degradation |
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17. |
findings show that low levels of Lck caused a dramatic reduction in c-Cbl phosphorylation and a general reduction in protein ubiquitination after TCR stimulation |
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18. |
Results identify a molecular mechanism by which activated FGFR2 recruits Cbl in raft micro-domains to trigger PI3K ubiquitination and proteasome degradation, and reveal a role for PI3K/Akt in the control of osteoblast survival by FGFR2 signaling. |
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19. |
Observational study of gene-disease association. (HuGE Navigator) |
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20. |
c-Cbl is a critical regulator of the functional responses of memory T cell subsets; role in a mechanism controlling the functional heterogeneity of memory CD4 cells. |
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21. |
c-Cbl is a new ligase for insulin-like growth factor-I receptor with distinct roles from Mdm2 in receptor ubiquitination and endocytosis |
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22. |
two Cbls accounted for total receptor ubiquitination and that while c-Cbl and Cbl-b are each alone sufficient to effect EGFR degradation, both are involved in the physiological, EGF-mediated process of receptor downregulation. |
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23. |
Lyn activation is BCR-ABL independent, it is complexed with the Gab2 and c-Cbl adapter/scaffold proteins, and it mediates persistent Gab2 and BCR-ABL tyrosine phosphorylation in the presence or absence of imatinib. |
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24. |
recruiment to endosomes is regulated by epidermal growth factors and amphiregulin |
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25. |
endogenous hSPRY2-mediated regulation of apoptosis requires c-Cbl and is manifested by the ability of hSPRY2 to sequester c-Cbl and thereby augment signaling via growth factor receptors |
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26. |
An obligatory, intrapeptidyl H-bond between the phosphotyrosine and the conserved asparagine or adjacent arginine is essential for binding and orientates peptides into a positively charged pocket on c-Cbl. |
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27. |
H-Ras interacts with Spry2-binding partners, c-Cbl and CIN85, in a Spry2-dependent manner. |
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28. |
myoferlin forms a complex with dynamin-2 and VEGFR-2, which prevents CBL-dependent VEGFR-2 polyubiquitination and proteasomal degradation. |
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29. |
Cbl-dependent negative regulation of PDGFRbeta involves a dual mechanism that concurrently promotes ubiquitin-dependent lysosomal sorting of the receptor and competitively reduces the recruitment of a positive mediator of receptor signaling |
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30. |
novel mutations in c-CBL and CBL-b have been identified in human acute myeloid leukemia |
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31. |
a role of Cbl dimerization in terminating signaling following activation of receptor tyroine kinase. |
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32. |
STAP-2 associates with FAK and enhances its degradation, proteasome inhibitors block FAK degradation, and STAP-2 recruits an endogenous E3 ubiquitin ligase, Cbl, to FAK. |
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33. |
a new role for CIN85 in regulating Syk protein levels in RBL-2H3 cells through the activation of the ubiquitin-proteasome pathway and provide a mechanism for this regulation involving c-Cbl ligase activity. |
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34. |
Given that phospholipase gamma 2 (PLC gamma 2) function is also influenced by c-Cbl hypophosphorylation, the ratio of PLC gamma 2 to c-Cbl |
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35. |
results implicate CD45, Cbl, Cbl-b, src kinases and potentially other associated proteins as mediators of SDF-1alpha/CXCL12-induced cell migration of Jurkat T cells |
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36. |
Recruitment of CBL to lipid rafts mediates signals important for actin reorganization in growing neurites. |
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37. |
c-cbl binds to hSpry2, and this interaction is critical for its physiological function in a signal-specific context |
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38. |
Lower expression of cbl is associated with acute myeloid leukemia-M2 and higher expression of cbl is associated with acute myeloid leukemia-M5 |
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39. |
EGF-R fate is controlled by a checkpoint downstream of receptor ubiquitination whose regulation by the Cbl RF tail may require Sprouty2 degradation. |
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40. |
corecruitment of c-Cbl and PLCgamma1 to VEGFR-2 serves as a mechanism to fine-tune the angiogenic signal relay of VEGFR-2 |
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41. |
mediates ubiquitination and lysosomal degradation of PAR(2) to irrevocably terminate its signaling |
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42. |
the SH3 domain of betaPix specifically interacts with a proline-arginine motif (PxxxPR) present within the ubiquitin ligase Cbl and Pak1 kinase. Cbl and Pak1 compete for binding to betaPix. |
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43. |
CD21 activation triggered Cbl tyrosine phosphorylation, which interacts with SH2 domains of p85 subunit, SH2 domains of Crk-L and with tyrosine phosphorylated Syk kinase. CD21 activation triggers dissociation of Cbl-Vav complex. |
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44. |
MLL-CBL fusion was the result of an interstitial deletion in patients with de novo acute myeloid leukemia (FAB-M1). |
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45. |
c-Cbl-dependent ubiquitination of p75NTR involved in the regulation of p75NTR signalling. |
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46. |
Sts-1 and Sts-2 bind to Cbl and inhibit endocytosis of receptor tyrosine kinases |
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47. |
Cbl has a role, via its ubiquitin ligase activity, as a negative regulator of activated Vav |
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48. |
c-Cbl has a role in EGFR trafficking |
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49. |
Cbl-directed monoubiquitination of CIN85 is involved in regulation of ligand-induced degradation of EGF receptors. |
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50. |
complexation with ArgBP2 mediates ubiquitination and degradation of c-Abl |
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51. |
ubiquitin ligase of EGFR, namely c-Cbl, also mediates receptor modification with the ubiquitin-like molecule Nedd8 |
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52. |
Alix inhibits down-regulation of PDGFRbeta by modulating the interaction between c-Cbl and the receptor, thereby affecting the ubiquitination of the receptor |
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53. |
The interaction between c-Cbl and SLAP in v-Abl-3T3 cells positively influenced c-Cbl-mediated spreading and adhesion of these cells |
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54. |
Results suggest a novel function for c-Cbl, microtubule binding and stabilization. |
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55. |
CBL has a role in down-regulation of Lyn and Fyn in osteoblast differentiation induced by constitutive FGFR2 activation |
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56. |
the alpha5 integrin subunit has a role in the induction of apoptosis triggered by FGFR2 activation in osteoblasts, and a Cbl-dependent mechanism is involved in the coordinated regulation of cell apoptosis induced by alpha5 integrin degradation |
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57. |
dynamin, Cbl, and Src coordinately participate in signaling complexes that are important in the assembly and remodeling of the actin cytoskeleton, leading to changes in osteoclast adhesion, migration, and resorption |
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58. |
Data show that infected cell protein 0 (ICP0) binds CIN85 in a reciprocal manner and that the complexes pulled down by ICP0 also contain Cbl. |
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59. |
The endophilin-CIN85-Cbl complex mediates ligand-dependent downregulation of c-Met |
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60. |
Cbl-b protein and CIN85 downregulate receptor tyrosine kinases |
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61. |
Differences in ubiquitin-binding may reflect distinct regulatory functions of c-Cbl and Cbl-b. |
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62. |
the c-Cbl/CD2AP complex binds to activated Flt-1 and plays a crucial role in its endocytosis and subsequent degradation. |
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63. |
Cbl promotes clustering of endocytic adaptor proteins. |
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64. |
By lysing primary hemopoietic cells at high pH, BCR-ABL1 protein-degradative activity was inhibited & association between BCR-ABL1 protein in complexes with adaptor proteins CBL, CRKL & GRB2 in primary chronic myeloid leukaemia material was demonstrated |
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65. |
Twist haploinsufficiency results in decreased Cbl-mediated PI3K degradation in osteoblasts. |
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66. |
Depletion of Cbl and Cbl-b E3 ubiquitin ligases by RNA interference, or overexpression of a Cbl dominant inhibitory mutant (Cbl-N), inhibited Spred-2 ubiquitination. |
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67. |
Ron tyrosine kinase receptor desensitization mediated by c-Cbl and its binding partner Grb2. |
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68. |
Grb2-mediated recruitment of the functional RING domain of Cbl to the EGFR is essential and sufficient to support receptor endocytosis |
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69. |
Cbl-CIN85-endophilin complex mediates ligand-induced downregulation of EGF receptors |
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70. |
c-Cbl guides the epidermal growth factor receptor into clathrin-coated pits by two distinct modes of Eps15 recruitment |
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71. |
c-Cbl-dependent EphA2 protein degradation is induced by ligand binding. |
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72. |
Negative regulation of Lck by Cbl ubiquitin ligase |
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73. |
novel E3 ubiquitin-protein ligase; role in regulation of immune response - review |