|Institutional Source||Beutler Lab|
|Gene Name||matrix metallopeptidase 9|
|Synonyms||gelatinase B, MMP-9, Gelatinase B, B/MMP9, Gel B, Clg4b|
|Is this an essential gene?||Non essential (E-score: 0.000)|
|Stock #||R7822 (G1)|
|Chromosomal Location||164940780-164955850 bp(+) (GRCm38)|
|Type of Mutation||nonsense|
|DNA Base Change (assembly)||A to T at 164949036 bp|
|Amino Acid Change||Lysine to Stop codon at position 115 (K115*)|
|Ref Sequence||ENSEMBL: ENSMUSP00000017881 (fasta)|
|Gene Model||predicted gene model for transcript(s): [ENSMUST00000017881] [ENSMUST00000137626]|
|Predicted Effect||probably null
AA Change: K115*
AA Change: K115*
|Predicted Effect||probably benign
|Coding Region Coverage||
FUNCTION: This gene encodes a member of the matrix metalloproteinase family of extracellular matrix-degrading enzymes that are involved in tissue remodeling, wound repair, progression of atherosclerosis and tumor invasion. The encoded preproprotein undergoes proteolytic processing to generate a mature, zinc-dependent endopeptidase enzyme that degrades collagens of type IV, V and XI, and elastin. Mice lacking the encoded protein exhibit an abnormal pattern of skeletal growth plate vascularization and ossification, reduced keratinocyte hyperproliferation at all neoplastic stages, a decreased incidence of invasive tumors, and resistance to experimental autoimmune encephalomyelitis. [provided by RefSeq, Feb 2016]
PHENOTYPE: Null mutants have short long bones with compensatory growth via delayed ossification and apoptosis of hypertrophic chondroctyes. Mutants are protected against ischemic brain injury, damage caused by myocardial infarction, and allergic airway inflammation. [provided by MGI curators]
|Allele List at MGI|
|Other mutations in this stock||
|Other mutations in Mmp9||
(F):5'- GAACTCTGTGATGTCTCTGCCC -3'
(R):5'- AGCTACACCACGATCGCTTC -3'
(F):5'- ACAGGCATACTTGTACCGCTATGG -3'
(R):5'- GCTTCAAAACACACAGGGCTG -3'