GLIS3 (GLI-similar 3) is a DNA-binding protein with five C2H2-type zinc finger motifs, structurally homologous to the Gli and Zic families . It regulates transcription by binding to consensus sequences such as 5’-GACCACCCAC-3’ and interacts with key pancreatic transcription factors like PDX1, MAFA, and NEUROD1 . GLIS3 mutations are linked to neonatal diabetes, congenital hypothyroidism, and polycystic kidney disease .
GLIS3 antibodies are polyclonal or monoclonal reagents validated for applications including:
Western blotting (WB)
Immunohistochemistry (IHC)
Immunofluorescence (IF/ICC)
ELISA
They target specific epitopes within the GLIS3 protein, such as amino acid regions 606–775 (C-terminal transactivation domain) or 101–200 (N-terminal repressive domain) .
GLIS3 antibodies have been instrumental in elucidating the transcription factor’s role in β-cell proliferation and insulin gene regulation. For example:
Loss of GLIS3 in mice causes neonatal hyperglycemia and β-cell apoptosis .
GLIS3 ChIP assays confirmed its direct binding to insulin and Ccnd2 promoters, critical for β-cell expansion under high-fat diets .
Diabetes: GLIS3 knockdown in INS-1E cells reduces INS2, MAFA, and PDX1 expression .
Germ Cell Development: GLIS3 deficiency disrupts retrotransposon silencing in fetal testes, leading to germ cell loss .
GLIS3 maintains adult β-cell function by directly activating insulin transcription .
Haploinsufficiency of GLIS3 impairs β-cell proliferation under metabolic stress .
Galunisertib, identified via GLIS3 antibody-based screens, rescues β-cell apoptosis in GLIS3−/− models .