cDNA, FLJ95281, highly similar to Homo sapiens a disintegrin-like and metalloprotease (reprolysintype) with thrombospondin type 1 motif, 1 (ADAMTS1), mRNA
A disintegrin and metalloproteinase with thrombospondin type motifs 1 rs402007 and tissue inhibitor of metalloproteinase-3 rs9619311 polymorphisms are associated with essential hypertension in a Chinese Han population and there was a positive interaction among rs402007 rs9619311 and smoking.
Melatonin-triggered post-transcriptional and post-translational modifications of ADAMTS1 coordinately retard tumorigenesis and metastasis of renal cell carcinoma.
JNK1 siRNA knockdown assay confirmed that ADAMTS-1 was regulated through JNK pathway and lauric acid interfered with this pathway to down-regulate ADAMTS-1 expression.
The results of the present study indicated that ADAMTS-1 and ADAMTS-9 as well as PRs are downregulated in the human CCs (cumulus cells) in PCOS polycystic ovary syndrome) patients which could be associated with impaired oocyte maturation and may result in a lower oocyte recovery and oocyte maturity rates as well as lower fertilization rate.
expressed 2.56-fold less in Sertoli cells in nonobstructive azoospermia than in obstructive azoospermia; insufficient expression in Sertoli cells may have an important role in the etiology of male infertility
ADAMTS 1 4 12 and 13 levels in the maternal and cord blood were lower in the preeclampsia group than in the control group. ADAMTS 1 4 and 12 levels in placental tissues were higher in the preeclampsia group.
Increased levels of ADAMTS-1 could be a potential marker for the etiopathogenesis of PCOS in adolescents and younger-aged females and predict the development of CVD [cardiovascular disease ]
Significant differences in gene expression profiles were observed between patients with post-kidney transplant bladder tumors and those with conventional bladder tumors. ADAMTS1 expression was significantly lower in first group than in the second.
Taken together our findings suggested that miR-362-3p inhibits the proliferation and migration of VSMCs by directly targeting ADAMTS1 which might provide novel insight into the molecular mechanisms underlying the action of miR-362-3p in atherosclerosis.
we identified Adamts1 as the modulator of a potent pathway that converts changes in diet into a cellular signal in adipose tissue that controls APC activity in vivo
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