SEC16B

RGPR-p117, which was named as a regucalcin gene promoter region-related protein, was originally discovered as a novel transcription factor that specifically binds to a nuclear factor I (NFI) consensus motif TTGGC(N)6CC that is located on the 5’-flanking region of the regucalcin gene (rgn) in 2001.[6][8] This gene is a highly conserved a leucine zipper motif, and it was also named as the leucine zipper transcription regulator 2 (LZTR2). In 2007, RGPR-p117 was also renamed as Sec16 homologue B (SEC16B), an endoplasmic reticulum export factor.[9]

The gene consists of 26 exons spanning approximately 4.1 kbp and is localized on human chromosome 1q25.2.[6] This gene expression is stimulated through various signaling factors in cells.[10][11] RGPR-p117 is present in the plasma membranes, cytoplasm, mitochondria, microsomes and nucleus of the cells.[11] Cytoplasm RGPR-p117 is translocated to nucleus.[10] Phosphorylated RGPR-p117 specifically binds to the TTGGC motif in the promoter region of various genes to enhance the gene expression of various proteins, and plays a crucial role as a transcription factor in the cells.[11][12][13]

In the role in the regulation of cell regulation, RGPR-p117 possesses protective effects on apoptotic cell death induced by various signaling factors.[12] Overexpression of RGPR-p117 did not cause an alteration of cell proliferation and led to significant decreases in protein and DNA contents in cloned normal rat kidney proximal tubular epithelial NRK52E cells.[14] It also plays a role as an endoplasmic reticulum export factor to deliver to newly synthesized proteins and lipids to the Golgi.[9][15][16] RGPR-p117/SEC16B may be involved in human obesity to possess an association between single nucleotide polymorphisms and different measures of obesity.[17][18][19]

Model organisms have been used in the study of SEC16B function. A conditional knockout mouse line, called Sec16b^{tm1a(KOMP)Wtsi}[25][26] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.[27][28][29]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[23][30] Twenty one tests were carried out on mutant mice and one significant abnormality was observed: homozygote mutants had decreased circulating cholesterol levels.[23]