Ameloblastin (Enamel Matrix Protein) (AMBN) ELISA Kits

Mouse (Murine) Ameloblastin (Enamel Matrix Protein) (AMBN) Interaktionspartner

1. Data demonstrate the functional importance of the AMBN extracellular matrix protein in bone fracture prevention and rapid fracture healing.

2. AMBN facilitates rapid long bone growth and an important growth spurt during the skeletogenesis of adolescent tooth-bearing vertebrates

3. Protein interaction between Ambn and Psma3 can facilitate redistribution of ameloblastin domains within forming enamel.

4. AMBN may function as a growth factor-like molecule solubilized in the aqueous microenvironment. In jaws, it might play a role in bone physiology through autocrine/paracrine pathways, particularly during development and stress-induced remodeling.

5. 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

6. Ambn plays a crucial role in the regulation of cranial bone growth and suture closure via Msx 2 suppression and proliferation inhibition.

7. Blocking integrin alpha2beta1 and ERK 1/2 pathways alleviated the effects of AMBN on osteoclast differentiation.

8. ERP 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.

9. AMBN may regulate differentiation state of Hertwig's epithelial root sheath-derived cells and its expression fuctions as a trigger for normal root formation.

10. All lines expressing detectable levels of ameloblastin at least partially recovered the enamel phenotype. Ameloblastin is essential for dental enamel formation.

11. study may implicate the role of the ameloblastin gene locus in the etiology of a number of undiagnosed autosomally dominant cases of amelogenesis imperfecta

12. Ameloblastin is a cell adhesion molecule essential for amelogenesis, and it plays a role in maintaining the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting proliferation.

13. Ameloblastin is an important regulator to maintain the differentiation state of ameloblasts.

14. no mutation could be detected in the ameloblastin gene [in amelogenesis imperfecta]

15. the ameloblastin 37-kDa isoform interacts with amelogenin during early tooth development.

16. Results indicate that absence of full-length ameloblastin and/or expression of an incomplete protein have direct/indirect effects beyond structuring of mineral during enamel formation.

17. Enamel matrix proteins such as amelogenins and ameloblastin are not only required for the formation of a proper matrix for well-orchestrated enamel biomineralization, but also have synergistic cellular functions during enamel development.

Human Ameloblastin (Enamel Matrix Protein) (AMBN) Interaktionspartner

1. Single nucleotide polymorphisms in the AMELX and AMBN genes may be genetic variants that contribute to developmental defects of enamel in primary dentition of Polish children.

2. the calcium level was associated with genetic variations in AMELX, AMNB and ESRRB. AMELX 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.

3. these results indicate that AMBN enhances IL-1beta production in LPS-treated U937 cells through ERK1/2 phosphorylation and caspase-1 activation, suggesting that AMBN upregulates the inflammatory response in human macrophages and plays an important role in innate immunity.

4. 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.

5. Protein interaction between Ambn and Psma3 can facilitate redistribution of ameloblastin domains within forming enamel.

6. 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.

7. 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.

8. two genetic variants (rs2337359 upstream of TUFT1 and missense rs7439186 in AMBN) involved in gene-by-fluoride interactions.

9. 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.

10. 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

11. AMBN does not influence osteogenic activity in vitro under the conditions used

12. Findings suggest a role for this protein in early bone formation and repair.

13. ameloblastin is expressed in osteoblasts and functions as a promoting factor for osteogenic differentiation via a novel pathway through the interaction between CD63 and integrin beta1

14. found to induce, directly and indirectly, signal transducer and activator of transcription (STAT) 1 and 2 and downstream factors in the interferon pathway

15. The identification of a fibronectin-binding domain in ameloblastin might permit interesting applications for dental implantology.

16. The frequently detected AMBN alterations in ameloblastomas are polymorphisms, which appear to be unrelated to the occurrence of ameloblastomas.

17. a bipolar calcium-binding molecule [with] a possible role in protein-protein interactions

18. Mutation of ameloblastin gene is associated with calcifying epithelial odontogenic tumor.