Version 5.4
Homo sapiens Gene: MXD4
Summary
InnateDB Gene IDBG-7451.5
Last Modified 2014-10-13 [Report errors or provide feedback]
Gene Symbol MXD4
Gene Name MAX dimerization protein 4
Synonyms bHLHc12; MAD4; MST149; MSTP149
Species Homo sapiens
Ensembl Gene ENSG00000123933
Encoded Proteins
IDBP-7455
MAX dimerization protein 4
IDBP-477871
MAX dimerization protein 4
IDBP-474450
MAX dimerization protein 4
Protein Structure
Useful resources Stemformatics EHFPI ImmGen
Entrez Gene
Summary microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop. [provided by RefSeq, Sep 2009] This gene is a member of the MAD gene family . The MAD genes encode basic helix-loop-helix-leucine zipper proteins that heterodimerize with MAX protein, forming a transcriptional repression complex. The MAD proteins compete for MAX binding with MYC, which heterodimerizes with MAX forming a transcriptional activation complex. Studies in rodents suggest that the MAD genes are tumor suppressors and contribute to the regulation of cell growth in differentiating tissues. [provided by RefSeq, Jul 2008]
This gene is a member of the MAD gene family . The MAD genes encode basic helix-loop-helix-leucine zipper proteins that heterodimerize with MAX protein, forming a transcriptional repression complex. The MAD proteins compete for MAX binding with MYC, which heterodimerizes with MAX forming a transcriptional activation complex. Studies in rodents suggest that the MAD genes are tumor suppressors and contribute to the regulation of cell growth in differentiating tissues. [provided by RefSeq, Jul 2008]
Gene Information
Type Protein coding
Genomic Location Chromosome 4:2247432-2262294
Strand Reverse strand
Band p16.3
Transcripts
ENST00000337190 ENSP00000337889
ENST00000513372
ENST00000513380 ENSP00000422660
ENST00000515378
ENST00000510822 ENSP00000421209
Interactions
Number of Interactions This gene and/or its encoded proteins are associated with 8 experimentally validated interaction(s) in this database.
They are also associated with 2 interaction(s) predicted by orthology.
Experimentally validated
Total 8 [view]
Protein-Protein 8 [view]
Protein-DNA 0
Protein-RNA 0
DNA-DNA 0
RNA-RNA 0
DNA-RNA 0
Predicted by orthology
Total 2 [view]
Gene Ontology

Molecular Function
Accession GO Term
GO:0003677 DNA binding
GO:0003714 transcription corepressor activity
GO:0005515 protein binding
GO:0046983 protein dimerization activity
Biological Process
GO:0000122 negative regulation of transcription from RNA polymerase II promoter
GO:0006351 transcription, DNA-templated
GO:0008285 negative regulation of cell proliferation
GO:0045892 negative regulation of transcription, DNA-templated
Cellular Component
GO:0005634 nucleus
Orthologs
Species
Mus musculus
Bos taurus
Gene ID
Gene Order
ENSMUSG00000037235
View Gene Order
ENSBTAG00000015209
Not yet available
Pathways
NETPATH
REACTOME
KEGG
INOH
PID NCI
myc_represspathway
Validated targets of C-MYC transcriptional repression
Cross-References
SwissProt
TrEMBL
UniProt Splice Variant
Entrez Gene
UniGene Hs.623185 Hs.655020
RefSeq NM_006454
HUGO
OMIM
CCDS CCDS3361
HPRD 10103
IMGT
EMBL
GenPept
RNA Seq Atlas

If you use InnateDB for your research, please cite the following publication:

Breuer et al., InnateDB: systems biology of innate immunity and beyond - recent updates and continuing curation. Nucl. Acids Res. (2013) 41 (D1) 

InnateDB is being developed jointly by the Brinkman Laboratory (Simon Fraser University, British Columbia, Canada), the Hancock Laboratory (University of British Columbia, Vancouver, British Columbia) and the Lynn EMBL Australia Group (South Australian Health & Medical Research Institute and Flinders University, Adelaide, Australia).

Funding is currently provided by Allergen and EMBL Australia. Previous funding has been provided by Genome Canada, the Foundation for the National Institutes of Health through the Grand Challenges in Global Health initiative and by Teagasc. InnateDB curated interactions are licensed under the Design Science License. All other data is licensed under the terms of the originating database. Contact: innatedb-mail@sfu.ca