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Proteins of the matrix metalloproteinase (MMP) family are involved in the breakdown of extracellular matrix in normal physiological processes, such as embryonic development, reproduction, and tissue remodeling, as well as in disease processes, such as arthritis and metastasis. Additionally we are shipping Matrix Metallopeptidase 17 (Membrane-inserted) Antibodies (95) and Matrix Metallopeptidase 17 (Membrane-inserted) Kits (20) and many more products for this protein.
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while Adam17 (show ADAM17 Proteins)-deficiency suppresses Ang II (show AGT Proteins)-induced SMC (show DYM Proteins) remodeling in vitro, in vivo Adam17 (show ADAM17 Proteins)-deficiency provides only a transient protective effect against Ang II (show AGT Proteins)-mediated hypertension and end-organ damage.
Mmp17-mediated osteopontin cleavage regulated vascular SMC maturation via c-JNK during aorta wall development. Mmp17 proteolytic activity regulates vascular SMC phenotype in the arterial vessel wall. Its absence predisposes to thoracic aortic aneurysm.
function and expression of MT4-MMP
MT4-MMP promotes lung metastasis by disturbing the tumour vessel integrity and thereby facilitating tumour cell intravasation
MT1 (show MT1 Proteins)-MT4-MMP chimaeras do not undergo normal trafficking and are not correctly processed to their fully active forms and, as a consequence, they are unable to activate pro-MMP-2 (show MMP2 Proteins) at the cell surface.
Three forms of MT4-MMP with molecular masses of 45 kDa, 58 kDa and 69 kDa were detected. Further, we demonstrate that the 58 kDa form is the mature protein in the cell membrane, while the 69 kDa form is its precursor found in intracellular compartments.
Low MT4-MMP expression is associated with erlotinib resistance in breast cancer.
The MT4-MMP is internalized by the clathrin-independent carriers/GPI (show GNPDA1 Proteins)-enriched early endosomal compartments pathway, a mechanism that differs from that responsible for the internalization of other membrane-type MMP members.
Screening of patients with inherited thoracic aortic aneurysms and dissections identified a missense mutation (R373H) in the MMP17 gene that prevented the expression of the protease in human transfected cells.
A functional link between MT4-MMP and the growth factor receptor (show RYK Proteins) EGFR (show EGFR Proteins).
CAV1 (show CAV1 Proteins) when found in lipid rafts does not allow the metalloproteinase MT4-MMP to localize into the lipid rafts, affecting its expression in the cell and probably its activity which is translated into the metastasis-associated activities of these cells.
It identifies MT4-MMP as a key intrinsic tumor cell determinant that contributes to the elaboration of a permissive microenvironment for metastatic dissemination.
The data presented here provide a new insight into the characteristics of MT4-MMP and highlight the common and distinct properties of the glycosylphosphatidylinositol-anchored membrane type-matrix metalloproteinases.
Studies suggest a model of hypoxia induced metastasis through expression of HIF-1alpha (show HIF1A Proteins), and SLUG regulation of MT4-MMP transcription.
Proteins of the matrix metalloproteinase (MMP) family are involved in the breakdown of extracellular matrix in normal physiological processes, such as embryonic development, reproduction, and tissue remodeling, as well as in disease processes, such as arthritis and metastasis. Most MMP's are secreted as inactive proproteins which are activated when cleaved by extracellular proteinases. The protein encoded by this gene is considered a member of the membrane-type MMP (MT-MMP) subfamily. However, this protein is unique among the MT-MMP's in that it is a GPI-anchored protein rather than a transmembrane protein. The protein activates MMP-2 by cleavage.
, MT-MMP 4
, matrix metalloproteinase 17
, matrix metalloproteinase-17
, membrane type-4 matrix metalloproteinase
, membrane-type matrix metalloproteinase 4
, membrane-type-4 matrix metalloproteinase
, matrix metalloproteinase 17 (membrane-inserted)
, matrix metallopeptidase 17 (membrane-inserted)