|Positive WB detected in||HeLa cells, HEK-293 cells, ROS1728 cells|
|Positive IHC detected in||human gliomas tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Western Blot (WB)||WB : 1:1000-1:4000|
|Immunohistochemistry (IHC)||IHC : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
60151-1-Ig targets CUL4B in WB, IHC,ELISA applications and shows reactivity with human, rat samples.
|Tested Reactivity||human, rat|
|Host / Isotype||Mouse / IgG1|
|Immunogen||CUL4B fusion protein Ag3563|
|Full Name||cullin 4B|
|Calculated molecular weight||913 aa, 104 kDa|
|Observed molecular weight||102 kDa|
|GenBank accession number||BC036216|
|Gene ID (NCBI)||8450|
|Purification Method||Caprylic acid/ammonium sulfate precipitation|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
Cullin-RING ligases (CRLs) complexes participate in the regulation of diverse cellular processes, including cell cycle progression, transcription, signal transduction and development (PMID: 21816341)(PMID: 21554755). Serving as the scaffold protein, cullins are crucial for the assembly of ligase complexes, which recognize and target various substrates for proteosomal degradation. Two cullin 4 (CUL4) proteins, CUL4A (87 kDa) and CUL4B(104 kDa), are two members in cullin family with 83% of identity. Mutations in human CUL4B are one of the major causes of X-linked mental retardation. Cul4b knockout mice demonstrated that CUL4B is indispensable for embryonic development in the mouse (PMID: 22606329).
Int J Oncol
miR‑381 and miR‑489 suppress cell proliferation and invasion by targeting CUL4B via the Wnt/β‑catenin pathway in gastric cancer.
Pathol Res Pract
Cullin-4B promotes cell proliferation and invasion through inactivation of p53 signaling pathway in colorectal cancer.
Temporal Regulation of ESCO2 Degradation by the MCM Complex, the CUL4-DDB1-VPRBP Complex, and the Anaphase-Promoting Complex.