SREBF1

Polyclonal antibody produced in rabbits immunized with a synthetic peptide corresponding to a region of Mouse Srebf1.

Transcription Factor Antibodies

Transcriptional activator required for lipid homeostasis. Regulates transcription of the LDL receptor gene as well as the fatty acid and to a lesser degree the cholesterol synthesis pathway. Binds to the sterol regulatory element 1 (SRE-1) (5\' -ATCACCCCAC-3\' ). Has dual sequence specificity binding to both an E-box motif (5\' -ATCACGTGA-3\' ) and to SRE-1 (5\' -ATCACCCCAC-3\' ). Isoform SREBP-1A is much more active than isoform SREBP-1C in stimulating transcription from SRE-1-containing promoters.

Endoplasmic reticulum membrane; Multi-pass membrane protein. Golgi apparatus membrane; Multi-pass membrane protein. Cytoplasmic vesicle COPII-coated vesicle membrane; Multi-pass membrane protein. Note=Moves from the endoplasmic reticulum to the Golgi in the absence of sterols.

Isoform SREBP-1C predominates in liver adrenal gland brain and adipose tissue whereas isoform SREBP-1A predominates in spleen. Isoform SREBP-1A and isoform SREBP-1C are found in kidney thymus testis muscle jejunum and ileum.

Mice lacking Srepf1 show high embryonic lethality around day 11 dpc. Surviving mice show a 2-3-fold increase in processed Srebpf2 protein in liver nuclei 3-fold increase in cholesterol synthesis and 50% increase in cholesterol content of the liver. Mice lacking isoform SREBP-1C show a lack of up-regulation of several lipogenic enzymes in response to high insulin or LXR activation. Mice overexpressing processed isoform SREBP-1A in adipocytes show enlarged white and brown adipocytes increased rate of fatty acid synthesis and secretion leading to a fatty liver. Mice overexpressing processed isoform SREBP-1C in adipocytes show inhibition of adipocyte differentiation leading to a syndrome similar to human lipodystrophy with loss of peripheral white adipose tissue diabetes and fatty liver.

Contains 1 basic helix-loop-helix (bHLH) domain. Briancon. N. (2006) EMBO J. 25 (6). 1253-1262.