Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on curation of immunofluorescence data
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Combined Automated Annotation using Multiple IEA Methods
Inactivation of menin, a Smad3-interacting protein, blocks transforming growth factor type beta signaling.
Menin, a gene product responsible for multiple endocrine neoplasia type 1, interacts with the putative tumor metastasis suppressor nm23.
Menin interacts directly with the homeobox-containing protein Pem.
The tumor suppressor protein menin interacts with NF-kappaB proteins and inhibits NF-kappaB-mediated transactivation.
Menin uncouples Elk-1, JunD and c-Jun phosphorylation from MAP kinase activation.
The 32-kilodalton subunit of replication protein A interacts with menin, the product of the MEN1 tumor suppressor gene.
Multiple tumor suppressor pathways negatively regulate telomerase.
Menin associates with FANCD2, a protein involved in repair of DNA damage.
Menin, a tumor suppressor, associates with nonmuscle myosin II-A heavy chain.
Menin associates with a trithorax family histone methyltransferase complex and with the hoxc8 locus.
Leukemia proto-oncoprotein MLL forms a SET1-like histone methyltransferase complex with menin to regulate Hox gene expression.
Direct binding of DNA by tumor suppressor menin.
Menin suppresses osteoblast differentiation by antagonizing the AP-1 factor, JunD.
Menin and MLL cooperatively regulate expression of cyclin-dependent kinase inhibitors.
Physical association and coordinate function of the H3 K4 methyltransferase MLL1 and the H4 K16 acetyltransferase MOF.
Menin localizes to chromatin through an ATR-CHK1 mediated pathway after UV-induced DNA damage.
Multiple endocrine neoplasia type 1 interacts with forkhead transcription factor CHES1 in DNA damage response.
PTIP associates with MLL3- and MLL4-containing histone H3 lysine 4 methyltransferase complex.
c-Myb, Menin, GATA-3, and MLL form a dynamic transcription complex that plays a pivotal role in human T helper type 2 cell development.
The same pocket in menin binds both MLL and JUND but has opposite effects on transcription.
Structural insights into inhibition of the bivalent menin-MLL interaction by small molecules in leukemia.
Quantitative dissection and stoichiometry determination of the human SET1/MLL histone methyltransferase complexes.
HTLV-1 bZIP factor impedes the menin tumor suppressor and upregulates JunD-mediated transcription of the hTERT gene.
Human-chromatin-related protein interactions identify a demethylase complex required for chromosome segregation.
The same site on the integrase-binding domain of lens epithelium-derived growth factor is a therapeutic target for MLL leukemia and HIV.
A High-Density Map for Navigating the Human Polycomb Complexome.
Systematic discovery of mutation-directed neo-protein-protein interactions in cancer.
Menin, the product of the MEN1 gene, is a nuclear protein.
Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription.
MEN1 binds SMAD2/3:SMAD4 heterotrimer
Recruitment of MLL2 methyltransferase complex
MLL2 complex trimethylates H3K4 at the MYC gene
APC promotes disassembly of beta-catenin transactivation complex
IQGAP1 binds CDH1:CTTNB1:CTTNA1 and MEN1
FAM20C phosphorylates FAM20C substrates
PSIP1 binds MLL1 and MEN1
HCFC1, HCFC2 bind the MLL1:MEN1 complex
PSIP1 binds MEN1 associated with MLL2 complex
The menin tumor suppressor protein is an essential oncogenic cofactor for MLL-associated leukemogenesis.
MEN1 tumor-suppressor protein localizes to telomeres during meiosis.
Menin induces apoptosis in murine embryonic fibroblasts.
STAT6-mediated displacement of polycomb by trithorax complex establishes long-term maintenance of GATA3 expression in T helper type 2 cells.
UniProt entry O00255 (MEN1_HUMAN)