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The establishment of a new model of concurrent tissue-selective CBL/CBL-B deletion should allow a clear assessment of the tumor-intrinsic roles of CBL/CBL-B in non-myeloid malignancies and help test the potential for CBL/CBL-B inactivation in immunotherapy of tumors.
These findings highlight a hitherto unexplored and novel role for Cbl and PI3K in modulating the osteogenic response of periosteal cells during the early stages of fracture repair.
c-Cbl negatively regulates IFN-beta (show IFNB1 Proteins) signaling and cellular antiviral response by promoting IRF3 (show IRF3 Proteins) ubiquitination and degradation.
This study demonstrate an unprecedented role for c-Cbl in microglia-mediated neuroinflammation involving PI3K/Akt (show AKT1 Proteins)/NF-kappaB (show NFKB1 Proteins) pathway.
These studies reveal a novel, cell-autonomous requirement of CBL and CBL-B in epithelial stem cell maintenance during organ development and remodeling through modulation of mTOR (show FRAP1 Proteins) signaling.
mutant CBL proteins effectively compete with the remaining wild type CBL-B and juxtapose tyrosine kinase (show TYRO3 Proteins)-binding domain-associated protein tyrosine kinases with proline-rich region-associated signaling proteins to hyper-activate signaling downstream of hematopoietic growth factor (show IL-3 Proteins) receptors
results demonstrate that c-Cbl mediates the ubiquitination/degradation of integrin beta1, which leads to COMP (show COMP Proteins) deficiency-induced dilated cardiomyopathy.
Gem (show GEM Proteins), a gene encoding a GTPase (show RACGAP1 Proteins) that is upregulated by Cbl(Q367P) , enhanced hematopoietic stem cell activity and induced myeloid cell proliferation. In addition, Evi1 (show MECOM Proteins), a gene encoding a transcription factor, was found to cooperate with Cbl(Q367P) and progress CMML to AML (show RUNX1 Proteins).
Fasudil, a clinically safe ROCK inhibitor, decreases disease burden in a Cbl/Cbl-b deficiency-driven murine model of myeloproliferative disorders.
Cbl down-regulation protects mice against high-fat diet-induced obesity and insulin (show INS Proteins) resistance.
Patients harbouring ASXL1 (show ASXL1 Proteins) and/or CBL mutations (n = 8, 8 deaths, median OS = 11 months) had a significantly worse OS as compared to those without either mutation (n = 11, 4 deaths, median OS = 84 months) (P = 0.0002) (Fig 1a).
the loss of c-Cbl activity significantly enhanced nuclear beta-catenin (show CTNNB1 Proteins) and colorectal cancer tumor growth in cell culture and a mouse xenograft model.
we have shown that c-CBL plays a supportive role in the proliferation, migration and invasion of human melanoma cells.
Findings show for this first time that ATG9A (show ATG9A Proteins) loss in trastuzumab resistant cells allowed Her2 (show ERBB2 Proteins) to escape from lysosomal targeted degradation through K63 poly-ubiquitination via c-Cbl.
These results suggest MET overexpression is related to altered c-CBL expression in head and neck squamous cell carcinoma, which may influence tumorigenesis
This study identified a new regulatory axis in which miR (show MLXIP Proteins)-124-3p and CBL regulate the proliferation and invasion of breast cancer cells.
The viral entry receptor Nectin-1 (show PVRL1 Proteins) is also internalized during HSV-1 infection in a Cbl-dependent mechanism, and that increases the opportunity of the virus to spread to uninfected cells.
mutant CBL proteins effectively compete with the remaining wild type CBL-B and juxtapose tyrosine kinase (show TXK Proteins)-binding domain-associated protein tyrosine kinases with proline-rich region-associated signaling proteins to hyper-activate signaling downstream of hematopoietic growth factor (show IL-3 Proteins) receptors
we report that two JMML patients survived >20 years without HSCT and both patients had uniparental disomy of 11q23 where CBL is located without the phenomenon found in neither Noonan syndrome nor Noonan syndrome-like disorder. We think that some JMML patients with CBL mutation might show the good prognosis in later life after remission of JMML.
This gene is a proto-oncogene that encodes a RING finger E3 ubiquitin ligase. The encoded protein is one of the enzymes required for targeting substrates for degradation by the proteasome. This protein mediates the transfer of ubiquitin from ubiquitin conjugating enzymes (E2) to specific substrates. This protein also contains an N-terminal phosphotyrosine binding domain that allows it to interact with numerous tyrosine-phosphorylated substrates and target them for proteasome degradation. As such it functions as a negative regulator of many signal transduction pathways. This gene has been found to be mutated or translocated in many cancers including acute myeloid leukaemia. Mutations in this gene are also the cause of Noonan syndrome-like disorder.
E3 ubiquitin-protein ligase CBL
, casitas B-lineage lymphoma proto-oncogene
, proto-oncogene c-CBL
, signal transduction protein CBL
, Cas-Br-M (murine) ecotropic retroviral transforming sequence
, RING finger protein 55
, fragile site, folic acid type, rare, fra(11)(q23.3)
, oncogene CBL2
, proto-oncogene c-Cbl
, Casitas B-lineage lymphoma