The serum and glucocorticoid inducible kinase SGK1 increases the activity of Orai1, the pore forming unit of store operated Ca²⁺ -entry (SOCE) and thus influences Ca²⁺ dependent cellular functions such as migration. SGK1 further regulates transcription factor NF-kB. The present study explored whether SGK1 influences transcription of Orai1 and/or STIM1, the Orai1 activating Ca²⁺-sensor. Orai1 and STIM1 transcript levels were decreased in mast cells from SGK1 knockout mice and increased in HEK293 cells by transfection with active ^S422DSGK1 but not with inactive ^K127NSGK1 or in ^S422DSGK1-transfected cells treated with the NF-kB inhibitor Wogonin (100 mM). Treatment with the stem cell factor enhanced transcript levels of STIM1 and Orai1 in sgk1^+/+ but not in sgk1^-/- mast cells and not in sgk1^+/+ cells treated with Wogonin. Orai1 and STIM1 transcript levels were further increased in sgk1^+/+ and sgk1^-/- mast cells by transfection with active NF-kB subunit p65 as well as in HEK293 cells by transfection with NF-kB subunits p65/p50 or p65/p52. They were decreased by silencing of NF-kB subunits p65, p50 or p52 or by NF-kB inhibitor Wogonin (100 mM). SOCE was similarly increased by overexpression of p65/p50 or p65/p52 and decreased by treatment with Wogonin. Transfection of HEK293 cells with p65/p50 or p65/p52 further augmented migration. The present observations reveal powerful genomic regulation of Orai1/STIM1 by SGK1 dependent NF-kB signaling.