Recombinant Rabbit monoclonal primary
MMP9 Recombinant Rabbit Monoclonal Antibody [JA80-73] (ET1704-69)
Synthetic peptide within human mmp9 aa 71-120 / 707.
Rat spleen tissue lysates, Hela, SHG-44, human tonsil tissue, mouse placenta tissue, A431.
Store at +4C after thawing. Aliquot store at -20C or -80C. Avoid repeated freeze / thaw cycles.
1*TBS (pH7.4), 0.05% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
Protein A affinity purified.
82 kDa matrix metalloproteinase-9 antibody; 92 kDa gelatinase antibody; 92 kDa type IV collagenase antibody; CLG 4B antibody; CLG4B antibody; Collagenase Type 4 beta antibody; Collagenase type IV 92 KD antibody; EC 184.108.40.206 antibody; Gelatinase 92 KD antibody; Gelatinase B antibody; Gelatinase beta antibody; GelatinaseB antibody; GELB antibody; Macrophage gelatinase antibody; MANDP2 antibody; Matrix metallopeptidase 9 (gelatinase B, 92kDa gelatinase, 92kDa type IV collagenase) antibody; Matrix Metalloproteinase 9 antibody; MMP 9 antibody; MMP-9 antibody; MMP9 antibody; MMP9_HUMAN antibody; Type V collagenase antibody
Belongs to the peptidase M10A family.
Detected in neutrophils (at protein level). Produced by normal alveolar macrophages and granulocytes.
Processing of the precursor yields different active forms of 64, 67 and 82 kDa. Sequentially processing by MMP3 yields the 82 kDa matrix metalloproteinase-9.; N- and O-glycosylated.
The matrix metalloproteinases (MMPs) are a family of peptidase pathway responsible for the degradation of extracellular matrix components, including collagen, gelatin, fibronectin, laminin and proteoglycan. Transcription of MMP genes is is differentially activated by phorbol ester, lipopolysaccharide (LPS) or staphylococcal enterotoxin MMP-9 (also designated 92 kDa type IV collagenase or gelatinase B) has been shown to degrade bone collagens in concert with MMP-1 (also specified interstitial collagenase, fibroblast collagenase or Collagenase-1), and cysteine proteases and may play a role in bone osteoclastic resorption. MMP-1 is downregulated by p53, and abnormality of p53 expression can contribute to joint degradation in rheumatoid arthritis by regulating MMP-1 expression.
Tang, Li et al.
Deficiency of DICER reduces the invasion ability of trophoblasts and impairs the pro-angiogenic effect of trophoblast-derived microvesicles. | Journal of Cellular and Molecular Medicine 
Zhou, Yuzhen et al.
FOXM1c promotes oesophageal cancer metastasis by transcriptionally regulating IRF1 expression. | Cell Proliferation 
Luo, P., Yan, H., Chen, ......
Luo, P., Yan, H., Chen, X., Zhang, Y., Zhao, Z., Cao, J., Zhu, Y., Du, J., Xu, Z., Zhang, X., Zeng, S., Yang, B., Ma, S., & He, Q. (2020). s-HBEGF/SIRT1 circuit-dictated crosstalk between vascular endothelial cells and keratinocytes mediates sorafenib-induced hand-foot skin reaction that can be reversed by nicotinamide. Cell research, 30(9), 779–793.
Lin, Yinuo et al.
Exosomes derived from HeLa cells break down vascular integrity by triggering endoplasmic reticulum stress in endothelial cells. | Journal of Extracellular Vesicles