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AMBN encodes the nonamelogenin enamel matrix protein ameloblastin. Additionally we are shipping AMBN Antibodies (17) and AMBN Proteins (7) and many more products for this protein.
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Data demonstrate the functional importance of the AMBN extracellular matrix protein in bone fracture prevention and rapid fracture healing.
AMBN facilitates rapid long bone growth and an important growth spurt (show BPIFA1 ELISA Kits) during the skeletogenesis of adolescent tooth-bearing vertebrates
Protein interaction between Ambn and Psma3 can facilitate redistribution of ameloblastin domains within forming enamel.
AMBN may function as a growth factor-like molecule solubilized in the aqueous microenvironment. In jaws (show IMPAD1 ELISA Kits), it might play a role in bone physiology through autocrine/paracrine pathways, particularly during development and stress-induced remodeling.
Ameloblastin (AMBN) expression may be regulated in a site-specific manner and identify AMBN as a putative in vivo marker of the site-specific fingerprint of bone organs
Ambn plays a crucial role in the regulation of cranial bone growth and suture closure via Msx 2 suppression and proliferation inhibition.
Blocking integrin alpha2beta1 and ERK 1 (show MAPK3 ELISA Kits)/2 pathways alleviated the effects of AMBN on osteoclast differentiation.
ERP (show PDIA3 ELISA Kits) expression follows defined developmental profiles; affects osteoblast differentiation, mineralization, calvarial bone development. with role in developing enamel matrix, ERPs retain conserved function related to bone biomineralization.
AMBN may regulate differentiation state of Hertwig's epithelial root sheath-derived cells and its expression fuctions as a trigger for normal root formation.
All lines expressing detectable levels of ameloblastin at least partially recovered the enamel phenotype. Ameloblastin is essential for dental enamel formation.
the calcium level was associated with genetic variations in AMELX (show AMELX ELISA Kits), AMNB and ESRRB. AMELX (show AMELX ELISA Kits) and AMNB are involved in enamel mineralization. Mutations in both these genes are responsible for the amelogenesis imperfecta phenotype (OMIN), which supports their link with enamel alterations as well as enamel mineralization.
these results indicate that AMBN enhances IL-1beta (show IL1B ELISA Kits) production in LPS-treated U937 cells through ERK1/2 (show MAPK1/3 ELISA Kits) phosphorylation and caspase-1 (show CASP1 ELISA Kits) activation, suggesting that AMBN upregulates the inflammatory response in human macrophages and plays an important role in innate immunity.
Association between caries experience (caries-free versus caries affected) depending on asthma status and SNPs was tested. Logistic regression showed an association between AMBN rs4694075 and caries experience. Ameloblastin is associated w/caries in asthmatic children.
Authors perform an evolutionary analysis of mammalian AMBN sequences in order to predict functionally important sites of the protein and to identify candidate disease-associated mutations responsible for the protein function and identify AMBN as a candidate for amelogenesis imperfect in humans.
Report shows for the first time that AMBN mutations cause non-syndromic human amelogenesis imperfecta and confirms that mouse models with disrupted Ambn function are valid.
two genetic variants (rs2337359 upstream of TUFT1 (show TUFT1 ELISA Kits) and missense rs7439186 in AMBN) involved in gene-by-fluoride interactions.
We found a trend for association between variation in AMBN and MIH in both cohorts, which may suggest that variation in the regulation of AMBN is a mechanism that leads to MIH.
AMBN ribbons exhibited lengths ranging from tens to hundreds of nm. Deletion analysis and NMR spectroscopy revealed that N-terminal segment encoded by exon 5 comprises two short independently structured regions and plays a role in self-assembly of AMBN
AMBN does not influence osteogenic activity in vitro under the conditions used
This gene encodes the nonamelogenin enamel matrix protein ameloblastin. The encoded protein may be important in enamel matrix formation and mineralization. This gene is located in the calcium-binding phosphoprotein gene cluster on chromosome 4. Mutations in this gene may be associated with dentinogenesis imperfect and autosomal dominant amylogenesis imperfect.
, ameloblastin, enamel matrix protein