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CUL4B is a member of the cullin family. Additionally we are shipping Cullin 4B Antibodies (87) and many more products for this protein.
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Results show that cul4a (show CUL4A Proteins) but not cul4b is required for the expression of tbx5a, an essential transcription factor in heart and limb development.
these results showed that knockdown of CUL4B inhibit proliferation and promotes apoptosis of colorectal cancer cells through suppressing the Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling pathway
Our data are consistent with the idea that the CUL4A (show CUL4A Proteins)/B-DDB1 (show DDB1 Proteins)-CRBN (show CRBN Proteins) complex catalyses the polyubiquitination and thus controls the degradation of CLC-1 (show CLCN1 Proteins) channels.
FBXO44 (show FBXO44 Proteins)-mediated degradation of RGS2 (show RGS2 Proteins) protein uniquely depends on a Cul4B/DDB1 (show DDB1 Proteins) complex.
results established a critical role of CUL4B in negatively regulating the p53 (show TP53 Proteins)-ROS (show ROS1 Proteins) positive feedback loop that drives cellular senescence
Results demonstrated that CUL4B promotes cell proliferation and inhibits the apoptosis of osteosarcoma cells.
Results show that CUL4A (show CUL4A Proteins)- and CUL4B-mediated polyubiquitination of gamma-tubulin (show TUBG1 Proteins) for its degradation.
Data show that CUL4B variants are associated with a wide range of cerebral malformations and suggest an important role in brain through its interaction with WDR62, a protein in which variants were identified in patients with cerebral malformations.
Cullin4B-Ring E3 ligase complex (CRL4B) is physically associated with PRC2. CRL4B possesses an intrinsic transcription repressive activity by promoting H2AK119 monoubiquitination. CUL4B promotes cancer cell proliferation, invasion, and tumorigenesis in vitro and in vivo.
CUL4B can up-regulate Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signalling in human HCC (show FAM126A Proteins) through transcriptionally repressing Wnt (show WNT2 Proteins) antagonists and thus contributes to the malignancy of HCC (show FAM126A Proteins).
The intellectual disability phenotype is caused by aberrant splicing and removal of intron 7 from CUL4B gene primary transcript.
CUL4B as a key regulator of post-meiotic sperm morphogenesis
CUL4B links two distinct spermatogenetic processes to a single E3 ligase, highlighting the significance of ubiquitin modification during spermatogenesis.
results demonstrate a critical role of CUL4B in hepatocarcinogenesis in mice
Ptgds (show PTGDS Proteins) is targeted and repressed by the CUL4B/PRC2 complex.
CUL4B knockdown alleviated in vivo tumorigenesis in glioma xenograft nude mice.
Data indicate a role of cullin family, CUL4B, in the immune system.
Data indicate that in Cul4b-deficient embryonic fibroblasts showed Jab1 (show COPS5 Proteins) accumulation.
Cul4b mutant mouse showed decrease in the number of parvalbumin (show PVALB Proteins)-positive neurons and altered dendritic properties.
Epiblast-specific deletion of Cul4b prevented embryonic lethality and gave rise to viable Cul4b null mice.
This gene is a member of the cullin family. The encoded protein forms a complex that functions as an E3 ubiquitin ligase and catalyzes the polyubiquitination of specific protein substrates in the cell. The protein interacts with a ring finger protein, and is required for the proteolysis of several regulators of DNA replication including chromatin licensing and DNA replication factor 1 and cyclin E. Multiple transcript variants encoding different isoforms have been found for this gene.