|Positive WB detected in||HEK-293 cells|
|Western Blot (WB)||WB : 1:500-1:2000|
|Sample-dependent, check data in validation data gallery|
13738-1-AP targets CUL7 in WB, ELISA applications and shows reactivity with human samples.
|Host / Isotype||Rabbit / IgG|
|Immunogen||CUL7 fusion protein Ag4675|
|Full Name||cullin 7|
|Calculated molecular weight||1698 aa, 191 kDa|
|Observed molecular weight||185 kDa|
|GenBank accession number||BC033647|
|Gene ID (NCBI)||9820|
|Purification Method||Antigen affinity purification|
|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. 20ul sizes contain 0.1% BSA.|
The cullin family proteins are scaffold proteins for the Ring finger type E3 ligases, participating in the proteolysis through the ubiquitin-proteasome pathway. Humans express seven cullin proeins: CUL1-3, CUL4A, CUL4B, CUL5, and CUL7. Each cullin protein can form an E3 ligase similar to the prototype Ring-type E3 ligase Skp1-CUL1-F-box complex. The Cullin-RING-finger type E3 ligases are important regulators in early embryonic development, as highlighted by genetic studies demonstrating that knock-out of CUL1, CUL3, or CUL4A in mice results in early embryonic lethality. CUL7 was originally discovered as 185-kDa protein associated with the large T antigen of simian virus 40 (SV40). CUL7-deficient mice exhibit neonatal lethality with reduced size and vascular defects. CUL7 presumably plays a role in the DNA damage response by limiting p53 activity. CUL7 mutations have also been identified in 3-Msyndrome and the Yakuts short stature syndrome, both of which are characterized by pre- and post-natal growth retardation but with relatively normal mental and endocrine functions, suggesting that CUL7 may also be crucial for human placental development.