MAD1L1
Sign in to saveAlso known as PIG9, TP53I9, TXBP181, MAD1, MAD1 mitotic arrest deficient like 1, mitotic arrest deficient 1 like 1
Mitotic spindle assembly checkpoint protein MAD1 is a protein that in humans is encoded by the MAD1L1 gene.
Gene data
MAD1L1- Name
- mitotic arrest deficient 1 like 1
- Type
- protein-coding
- Position
- 1,815,787–2,233,243 (−)
- Aliases
- MAD1, MVA7, PIG9, TP53I9, TXBP181
- Ensembl
- ENSG00000002822
- RefSeq RNA
- NM_001013836.2, NM_001013837.2, NM_001304523.2, NM_001304524.2, NM_001304525.2
- RefSeq protein
- NP_001013858.1, NP_001013859.1, NP_001291452.1, NP_001291453.1, NP_001291454.1
MAD1L1 is a component of the mitotic spindle-assembly checkpoint that prevents the onset of anaphase until all chromosome are properly aligned at the metaphase plate. MAD1L1 functions as a homodimer and interacts with MAD2L1. MAD1L1 may play a role in cell cycle control and tumor suppression. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Jan 2015].
Gene Ontology
Biological process
Molecular function
Pathways
via MyGene.info
Gene · Ensembl
mitotic arrest deficient 1 like 1
- Symbol
- MAD1L1
- Biotype
- Protein coding
- Organism
- Homo sapiens
- Location
- 7:1,815,787-2,233,243
- Strand
- Reverse (−)
- Assembly
- GRCh38
via Ensembl · EMBL-EBI
Wikidata facts
- Instance of
- gene
- Image
- Protein MAD1L1 PDB 1go4.png
Show 8 more facts
- HomoloGene ID
- 74500
- genetic association
- bipolar disorder
- found in taxon
- Homo sapiens
- exact match
- identifiers.org/ncbigene/8379
- genomic end
- 2272878
- genomic start
- 1855429
- chromosome
- human chromosome 7
- cytogenetic location
- 7p22.3
via Wikidata · CC0
~1 min read
Encyclopedic overview
4 sectionsContents
- Function
- Interactions
- See also
- References
Mitotic spindle assembly checkpoint protein MAD1 is a protein that in humans is encoded by the MAD1L1 gene.
MAD1L1 is also known as Human Accelerated Region 3. It may have played a key role in the evolution of humans from apes.
Excerpted from Wikipedia’s “MAD1L1” article, available under the CC BY-SA 4.0 licence.