|Positive WB detected in||MCF-7 cells, HeLa cells, HSC-T6 cells, T-47D cells, NCCIT cells, COLO 320 cells|
|Positive IF detected in||HepG2 cells|
|Western Blot (WB)||WB : 1:2000-1:10000|
|Immunofluorescence (IF)||IF : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
67192-1-Ig targets VDR in WB, IF, ELISA applications and shows reactivity with Human, mouse, rat samples.
|Tested Reactivity||Human, mouse, rat|
|Cited Reactivity||human, rat|
|Host / Isotype||Mouse / IgG2a|
|Immunogen||VDR fusion protein Ag28188|
|Full Name||vitamin D (1,25- dihydroxyvitamin D3) receptor|
|Calculated molecular weight||48 kDa|
|Observed molecular weight||48-55 kDa|
|GenBank accession number||BC060832|
|Gene ID (NCBI)||7421|
|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. Aliquoting is unnecessary for -20oC storage.|
The vitamin D receptor (VDR), also known as NR1I1 (nuclear receptor subfamily 1, group I, member 1), is a member of the nuclear receptor family of transcription factors. Upon activation by vitamin D, the VDR forms a heterodimer with the retinoid-X receptor and binds to hormone response elements on DNA resulting in expression or trans-repression of specific gene products.It is an intracellular hormone receptor that specifically binds 1,25(OH)2D3 and mediates its effects. Downstream targets of this nuclear hormone receptor are principally involved in mineral metabolism though the receptor regulates a variety of other metabolic pathways, such as those involved in the immune response and cancer. Defects in VDR are the cause of rickets vitamin D-dependent type 2A (VDDR2A). A disorder of vitamin D metabolism results in severe rickets, hypocalcemia and secondary hyperparathyroidism. Most patients have total alopecia in addition to rickets. The VDR exists two isoform with the MV 48 kDa and 54 kDa.
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