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results suggest that adam12 plays a significant role in the regulation of body growth during juvenile stage in zebrafish, although the precise molecular mechanisms await further study.
In conclusion, MiR29a regulates endothelial cell ADAM12 upregulation in ischemia and this is impaired in hyperglycemia.
It was concluded that TNF-alpha (show TNF Proteins)-induced changes in extracellular matix components increased expression of ADAM12 among other changes that were temporally related with the onset of myocyte function.
ADAM12 and ADAM17 (show ADAM17 Proteins) are essential molecules for the impairment of barrier function of retinal vasculature under hypoxia.
Augmentation of ADAM12 expression in vivo improved outcomes in Balb/c mice, whereas knockdown of ADAM12 made outcomes worse in C57Bl/6 mice. In vitro, ADAM12 expression modulates endothelial cell proliferation, survival, and angiogenesis.
The effect of insulin-like growth factor-I (show IGF1 Proteins) on ADAM12 expression during the course of myogenesis is reported.
Nitric oxide synthase deficiency has differential effects on ADAM12 expression in growing mouse brain.
Inhibition of Erbb2 (show ERBB2 Proteins) suppressed the increase in metalloproteinase ADAM12 expression in skin tumors.
TGF-beta (show TGFB1 Proteins) stimulation of renal cells results in a significant up-regulation of Adams 10, 17, 12, and 19
ADAM12 enhanced ephrin-A1 (show EFNA1 Proteins) cleavage in response to transforming growth factor-betra1 in primary tumors.
The endogenous SnoN (show SKIL Proteins) plays a role in regulating ADAM12 expression in response to TGFbeta1 (show TGFB1 Proteins).
A novel regulator, myoferlin, of ADAM12 is discovered in HeLa cells and this protein increases ADAM12 expression level, stability, and its enzymatic activity, leading to the reduction of its substrate, E-cadherin (show CDH1 Proteins), which plays important roles in the regulation of cell adhesion and tumor metastasis.
Our data support a role for ADAM12 in NHL cell proliferation, adhesion, and drug resistance, and it may pave the way for a novel therapeutic approach for CAM-DR in NHL.
The rs3740199 polymorphism in the ADAM12 gene was associated with knee osteoarthritis genetic susceptibility.
These results indicate that ADAM12 actively supports the CSC phenotype in claudin-low breast cancer cells via modulation of the EGFR (show EGFR Proteins) pathway.
We conclude that ADAM12 and MMP-14 (show MMP14 Proteins) are associated with cavernous sinus invasion in pituitary adenomas, which qualifies these proteins in diagnosis and therapy.
ADAM12 expression is significantly upregulated in human masticatory mucosa during wound healing
Stromal expression patterns for both ADAM12 and CDCP1 (show CDCP1 Proteins).
The first trimester maternal ADAM12-s levels were statistically significantly higher in the entire ART group, IVF (show SCN5A Proteins) and ICSI groups, and normal cycle-frozen embryo transfer group when compared with those in the controls.
The level of ADAM12 was upregulated in tumor tissues of breast cancer compared to that of adjacent normal tissues. patients with higher level of ADAM12 exhibited shorter survival time compared to that of low level of ADAM12
The siRNA-directed loss of ADAM12 impedes spontaneous fusion of primary cytotrophoblasts, whereas overexpression of the secreted variant, ADAM12S, potentiates cell fusion in the Bewo trophoblast cell line.
These findings suggest ADAM12 is upregulated in muscles with more slow-oxidative myofibres, such as the LM, and is linked to type I myofibers in cattle.
The 5'- and 3'-regions of bovive ADAM12 have been analysed and compared to the human gene, and the promoter region has been cloned and sequenced.
This gene encodes a member of the ADAM (a disintegrin and metalloprotease) protein family. Members of this family are membrane-anchored proteins structurally related to snake venom disintegrins, and have been implicated in a variety of biological processes involving cell-cell and cell-matrix interactions, including fertilization, muscle development, and neurogenesis. This gene has two alternatively spliced transcripts: a shorter secreted form and a longer membrane-bound form. The shorter form is found to stimulate myogenesis.
ADAM metallopeptidase domain 12
, ADAM metallopeptidase domain 12 (meltrin alpha)
, a disintegrin and metalloproteinase domain 12 (meltrin alpha)
, ADAM 12
, a disintegrin and metalloprotease domain 12
, disintegrin and metalloproteinase domain-containing protein 12
, meltrin alpha
, ADAM12 short isoform
, disintegrin and metalloprotease 12
, a disintegrin and metallopeptidase domain 12 (meltrin alpha)