Validation Data Gallery
|Positive WB detected in||HeLa cells, COLO 320 cells, HepG2 cells, K-562 cells, mouse kidney tissue, Raji cells|
|Positive IP detected in||HEK-293 cells|
|Western Blot (WB)||WB : 1:500-1:1000|
|Immunoprecipitation (IP)||IP : 0.5-4.0 ug for IP and 1:500-1:1000 for WB|
|Sample-dependent, check data in validation data gallery|
14343-1-AP targets NUB1 in WB, IP, IHC, IF, ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||NUB1 fusion protein Ag5668|
|Full Name||negative regulator of ubiquitin-like proteins 1|
|Calculated molecular weight||71 kDa|
|Observed molecular weight||69 kDa|
|GenBank accession number||BC046354|
|Gene ID (NCBI)||51667|
|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.|
Proteasome-associated protein NEDD8 ultimate buster 1 (NUB1) is an interferon-inducible protein that down-regulates NEDD8 expression and its conjugation system. Over-expression of NUB1 induces a growth-inhibitory effect in cells, and it mediates anti-proliferative actions and apoptosis in renal cell carcinoma cells through cell-cycle regulation. Expression of NUB1 leads to decreased modification of p53 with NEDD8 and stimulation of p53 ubiquitination. Recent finding revealed that NUB1, by regulating GSK3β levels, modulates tau phosphorylation and aggregation, and is a key player in neurodegeneration associated with tau pathology.
Biochem Biophys Res Commun
The role of NUB1 in α-synuclein degradation in Lewy body disease model mice.
Ubiquitin-negative, eosinophilic neuronal cytoplasmic inclusions associated with stress granules and autophagy: an immunohistochemical investigation of two cases.
Phosphorylated NUB1 distinguishes α-synuclein in Lewy bodies from that in glial cytoplasmic inclusions in multiple system atrophy