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The protein encoded by MGP is secreted and likely acts as an inhibitor of bone formation. Additionally we are shipping Matrix Gla Protein Kits (39) and Matrix Gla Protein Proteins (29) and many more products for this protein.
Showing 10 out of 62 products:
Human Polyclonal MGP Primary Antibody for IHC, WB - ABIN2784506
Yao, Shahbazian, Boström: Proline and gamma-carboxylated glutamate residues in matrix Gla protein are critical for binding of bone morphogenetic protein-4. in Circulation research 2008
Human Polyclonal MGP Primary Antibody for IHC, IHC (p) - ABIN4334178
Lorenzen, Martino, Scheffner, Bröcker, Leitolf, Haller, Gwinner: Fetuin, matrix-Gla protein and osteopontin in calcification of renal allografts. in PLoS ONE 2013
Usefulnees of nonmammalian model systems to elucidate the complex regulation of MGP gene transcription.
These data also indicate that MGP is under dual regulation by runx2 (show RUNX2 Antibodies) through the use of various isoforms and context-dependent formation of transcriptional complexes.
MGP is a multi-functional inhibitor of normal and abnormal angiogenesis that may function by coordinating with both Notch and BMP signaling pathways
In contrast with results obtained for previously studied marine fishes, in zebrafish and Senegal sole Mgp accumulates in both calcified tissues and non-mieralized vessel walls of the vascular system.
The substitution of threonine by alanine due to MGP exon 4 Thr83Ala polymorphism is related to a decrease in the likelihood of arterial calcification in female persons in the Ukrainian population
Correlations of plasma desphosphorylated uncarboxylated matrix Gla protein (dp-ucMGP) with vascular calcification and vascular stiffness in chronic kidney disease. Plasma dp-ucMGP was positively associated with vascular calcification and might be utilized as an early marker for vascular calcification in CKD patients.
It is assumed that Lp-PLA2 (show Lp-PLA2 Antibodies) is involved in vascular calcification and that dp-ucMGP is a more appropriate biomarker of residual risk than Lp-PLA2 (show Lp-PLA2 Antibodies) itself.
Data shoed increased GAS6 (show GAS6 Antibodies) and decreased MGP levels in hemodialysis patients, as mediators of induction or prevention of vascular calcification.
Altering NOTCH1 (show NOTCH1 Antibodies) levels affected MGP mRNA and protein.
Uncarboxylated MGP in synovial fluid might serve as a novel biomarker for assessing knee osteoarthritis progression.
MGP expression is significantly lower in diseased relative to normal aortic valve interstitial cells. Lack of this important "anti-calcification" protein may contribute to calcification of the aortic valve.
Higher plasma dephosphorylated uncarboxylated MGP (reflective of lower vitamin K status) was associated with higher odds of meniscus damage, osteophytes, bone marrow lesions, and subarticular cysts.
High levels of desphospho-uncarboxylated MGP are independently and positively associated with arterial stiffness after adjustment for common cardiovascular risk factors, renal function, and age.
The association has been found between the ischemic atherothrombotic stroke and polymorphic variants of genes MGP and VKORC1 (show VKORC1 Antibodies).
loss of MGP causes dysregulation of early endothelial differentiation.
Matrix Gla protein limits pulmonary arteriovenous malformations in ALK1 (show ACVRL1 Antibodies) deficiency.
expression of MGP and OCN increased gradually in the murine developing tibial epiphysis, and the two mineral-associated proteins may occur at the same location during a particular period, but at different levels.
Elastin (show ELN Antibodies) haploinsufficiency impedes the progression of arterial calcification in MGP-deficient mice.
The arterial calcification, not MGP deficiency itself, causes the low bone mass phenotype in Mgp-/- mice.
Two sides of MGP null arterial disease: chondrogenic lesions dependent on transglutaminase 2 (show TGM2 Antibodies) and elastin (show ELN Antibodies) fragmentation associated with induction of adipsin (show CFD Antibodies).
Mgp gene deletion may have a role in arteriovenous malformations
MGP is a known inhibitor of mineralization, and mice deficient in Mgp show severe vascular calcification and premature bone mineralization.
Inorganic phosphate(Pi) regulates MGP expression in growth plate chondrocytes, thereby suggesting a key role for Pi and ERK1/2 (show MAPK1/3 Antibodies) in the regulation of bone formation.
High DNA methylation (show HELLS Antibodies) resulting in the down regulation of matrix Gla protein is associated with osteochondrosis.
Selective CaSR (show CASR Antibodies) activation, either by extracellular calcium or AMG (show AMELX Antibodies) 641, increased MGP expression in vivo in the arterial wall and in vitro in bovine vascular smooth muscle cells.
the effect of MGP on calcification and osteogenic differentiation is determined by availability of BMP-2 (show BMP2 Antibodies)
MGP plays a role in endothelial cell function, by increasing transforming growth factor-beta1 activity and stimulating VEGF expression
MGP has a novel binding activity for vitronectin (show VTN Antibodies)
Heat shock protein 70 (show HSP70 Antibodies) enhances vascular bone morphogenetic protein-4 (show BMP4 Antibodies) signaling by binding matrix Gla protein.
The protein encoded by this gene is secreted and likely acts as an inhibitor of bone formation. The encoded protein is found in the organic matrix of bone and cartilage. Defects in this gene are a cause of Keutel syndrome (KS). Two transcript variants encoding different isoforms have been found for this gene.
matrix Gla protein
, Matrix Gla protein
, cell growth-inhibiting gene 36 protein
, matrix gamma-carboxyglutamate (gla) protein