|Positive WB detected in||K562 cells, HepG2 cells, BxPC-3 cells, human brain tissue, HEK-293 cells, RAW 264.7 cells, A431 cells|
|Positive IP detected in||K-562 cells|
|Western Blot (WB)||WB : 1:500-1:2000|
|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|
60084-1-Ig targets DGCR8 in WB, RIP, IP,ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse|
|Host / Isotype||Mouse / IgG2a|
|Immunogen||DGCR8 fusion protein Ag4871|
|Full Name||DiGeorge syndrome critical region gene 8|
|Calculated molecular weight||773 aa, 86 kDa|
|Observed molecular weight||120 kDa|
|GenBank accession number||BC009323|
|Gene ID (NCBI)||54487|
|Purification Method||Protein A 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.|
DGCR8 is a RNA-binding protein that assists the Rnase III enzyme Drosha in the processing of microRNAs (miRNAs), which regulate the expression of a large number of protein-coding genes[PMID: 22580560]. DGCR8, which contains two double-stranded RNA (dsRNA)-binding domains, may be an essential component of the primary miRNAs processing complex, along with Drosha, promoting the processing of primary microRNA to precursor microRNA. It is ubiquitous expressed in human and mouse tissues, and is deleted in DiGeorge syndrome. The calculated molecular weight of DGCR8 is 82-86 kDa, but the post-modified DGCR8 is about 120 kDa.
Primary microRNA precursor transcripts are localized at post-synaptic densities in adult mouse forebrain.
Identification of microprocessor-dependent cancer cells allows screening for growth-sustaining micro-RNAs.
Nucleic Acids Res
SUMOylation at K707 of DGCR8 controls direct function of primary microRNA.
DGCR8/ZFAT-AS1 Promotes CDX2 Transcription in a PRC2 Complex-Dependent Manner to Facilitate the Malignant Biological Behavior of Glioma Cells.