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Cbls were highly expressed in GC light zone (LZ) B cells, where they promoted the ubiquitination and degradation of Irf4, a transcription factor facilitating PC fate choice.
Cbl, Cbl-b, and Cbl-c have a role in protecting mammary epithelial cellsfrom proteotoxic stress-induced cell death by promoting turnover of active c-Src
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 signaling and cellular antiviral response by promoting IRF3 ubiquitination and degradation.
This study demonstrate an unprecedented role for c-Cbl in microglia-mediated neuroinflammation involving PI3K/Akt/NF-kappaB pathway.
c-Cbl's linker helix region mutations are only oncogenic when they disrupt the native state and fail to ubiquitinate protein tyrosine kinases.
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 signaling.
mutant CBL proteins effectively compete with the remaining wild type CBL-B and juxtapose tyrosine kinase-binding domain-associated protein tyrosine kinases with proline-rich region-associated signaling proteins to hyper-activate signaling downstream of hematopoietic growth factor receptors
results demonstrate that c-Cbl mediates the ubiquitination/degradation of integrin beta1, which leads to COMP deficiency-induced dilated cardiomyopathy.
Gem, a gene encoding a GTPase that is upregulated by Cbl(Q367P) , enhanced hematopoietic stem cell activity and induced myeloid cell proliferation. In addition, Evi1, a gene encoding a transcription factor, was found to cooperate with Cbl(Q367P) and progress CMML to AML.
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 resistance.
Cbl-b and c-Cbl regulate the degradation of Osterix through the ubiquitin-proteasome pathway.
Overexpression of Smad7 in human HaCaT keratinocyte cells and mouse skin tissues elevated EGF receptor (EGFR) activity by impairing ligand-induced ubiquitination and degradation of activated receptor, which is induced by the E3 ubiquitin ligase c-Cbl.
Erbin promotes tumourigenesis and tumour growth in colorectal cancer by stabilizing epidermal growth factor receptor
Whereas Cbl-PI3K interaction regulates differentiation and survival, bone resorption is predominantly regulated by Cbl-b in osteoclasts.
c-Cbl activation promotes myocyte apoptosis, inhibits angiogenesis, and causes adverse cardiac remodeling after myocardial infarction.
Data indicate a Cbl/p85/epsin-1 pathway in erythropoietin receptor (EpoR) endocytosis.
These results support the notion that the distal cytoplasmic domain of CD5, including Y463, plays a relevant role in the downmodulation of TCR signals in thymocytes via c-Cbl.
Study provided evidence suggesting that Cbl can positively control GM-CSF-induced JAK2 activation and signaling through JAK2 ubiquitination.
Cbl-b and c-Cbl downregulate PD-L1 in EGFR wild-type non-small cell lung cancer
Authors observed that delta-catenin plays a key role in EGFR stability and downstream signaling. delta-Catenin competes with c-Cbl for EGFR binding, which results in a reduction of binding between c-Cbl and EGFR and thus decreases the ubiquitination of EGFR.
its mutation is genetic predictor of tumor reduction in glucocorticoid-treated patients with chronic myelomonocytic leukemia.
c-CBL might play a role in the pathogenesis of inflammatory dermatoses and cutaneous T-cell lymphoma
Two germline de novo mutations in CBL were identified in patients with infancy-onset severe Moyamoya angiopathy who also presented subtle signs of RASopathy.
Patients harbouring ASXL1 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 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 loss in trastuzumab resistant cells allowed Her2 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-124-3p and CBL regulate the proliferation and invasion of breast cancer cells.
The viral entry receptor Nectin-1 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.
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.
we found that CQ decreased the expression of Cbl, an E3 ligase of DR5, and knock-down of Cbl markedly enhanced DR5 up-regulation. Other lysosomal inhibitors, including monensin and nigericin, also up-regulated DR5 and sensitized TRAIL-mediated apoptosis
miR-513a-5p, miR-22-3p and miR-625-5p may have an impact on the regulation of the immune response and inflammatory cytokine pathways through the regulation of their target gene(s), CBL, PPARGC1B and ESR1, which may then lead to a dust mite-induced asthma attack
Data suggest that the combination of peritumoral Cbl and EGFR serves as a much stronger indicator to make an accurate prognosis, especially during early recurrence.
H19 non coding RNA-derived miR-675 enhances tumorigenesis and metastasis of breast cancer cells by downregulating c-Cbl and Cbl-b.
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