Menin (multiple endocrine neoplasia I, MEN1, MEAI, SCG2) is a nuclear tumor suppressor that is mutated in patients with multiple endocrine neoplasia type I (MEN1;Menin can activate the transcription of differentiation-regulating genes by covalent histone modification. In osteoblasts, the interaction of menin and the TGFβ/Smad3 pathway negatively regulates BMP2/Smad1/5- and Runx2-dependent transcription activities leading to inhibition of late-stage differentiation. Menin regulates the expression of IGFBP-2 by influencing the IGFBP-2 promoter. Ectopic overexpression of menin via adenoviruses induces apoptosis in murine embryonic fibroblasts in a Bax/Bak-dependent manner. Two mRNA exist and two variants of the shorter mRNA have alternative splicing that changes the CDS. Five variants where alternative splicing takes place in the 5' UTR have been identified.
Recommended Dilutions: Western Blot: 1:500-1:2000
Reactivity: Human, Mouse, Rat