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Validated All-in-One™ qPCR Primer for CBLB(NM_001321788.2) Search again
Product ID:
HQP150967
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ADMIO3, Cbl-b, Nbla00127, RNF56
Gene Description:
Cbl proto-oncogene B
Target Gene Accession:
NM_001321788.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Gene References into function
- novel E3 ubiquitin-protein ligase; role in regulation of immune response - review
- Cbl-b plays a negative role in Crk-L-C3G-mediated Rap1 and LFA-1 activation in T cells.
- Expression of Cbl-b effectively blocks the ability of Cool-2 to stimulate PAK, providing an additional mechanism, aside from catalyzing receptor ubiquitination, by which Cbl-b acts as a negative regulator for signaling activities requiring PAK activation
- Cbl-b is a negative regulator of both Lyn-Syk-LAT and Gab2mediated complementary signaling pathways in FcepsilonRI-mediated mast cell activation
- Differences in ubiquitin-binding may reflect distinct regulatory functions of c-Cbl and Cbl-b.
- genetic interaction between the CTLA4 and CBLB genes in type 1 diabetes
- NF-kappaB activity is enhanced by a PI3K signal mediated by Cbl-b and Rho
- results suggest that Cbl-b- or atrogin-1-mediated ubiquitination plays an important role in unloading-induced muscle atrophy, and that unloading stress may preferentially inhibit transcriptional responses in skeletal muscle
- In a primary analysis, no evidence for an association of the CBLB SNP rs3772534 with disease was found in either sample set in type 1 diabetes.
- the host ubiquitin ligase Cbl-b interacts with the type III-secreted effector exotoxin T (ExoT) and plays a key role in vivo in limiting bacterial dissemination mediated by ExoT
- novel mutations in c-CBL and CBL-b have been identified in human acute myeloid leukemia
- F328L mutation is involved in the development of autoimmune diseases including type 1 diabetes, and also provide insight into the structure-function relationship of CBLB protein
- 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.