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Metalloproteinase which specifically cleaves IGFBP-5.
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This review evaluates the current data concerning PAPP-A2 function, and particularly the effect of PAPP-A2 mutation on growth.
Locally-produced Pappa2 in osteoblasts, epiphysis, and metaphysis, is required for normal postnatal bone growth.
Despite a dramatic disruption of the balance between circulating IGF-I (show IGF1 ELISA Kits), IGFBP-3 (show IGFBP3 ELISA Kits) and -5, we found no effects of Pappa2 deletion on glucose metabolism, weight gain or adiposity on a high-fat diet.
Pappa2 deletion had no effect on female reproduction and subtle effects on male fertility.
Pappa2 is responsible for the effects of the previously-identified QTL, demonstrating that natural variation in the Pappa2 gene contributes to variation in postnatal growth in mice
investigation of biological role of PAPP-A2 using knockout mice, heterozygotes, primary fibroblasts: The most striking phenotype of PAPP-A2 KO mice was postnatal growth retardation. PAPP-A2 KO mice were fertile, but exhibited compromised fecundity.
Elevated PAPPA2 levels are a consequence rather than a cause of pregnancy complications.
The refinement of the target region to four genes and the finding that the QTL affects IGFBP-5 (show IGFBP5 ELISA Kits) levels suggest that PAPPA2 may be involved with normal postnatal growth
Pappa2 expression also shows specific localization within the mouse embryo and therefore may play roles in fetal development, independent of its action in the placenta
PAPP-A2 is increased in Hemodialysis patients and interacts with PAPP-A (show PAPPA ELISA Kits) on patients prognosis.
These patients provide important insights into the regulation of longitudinal growth in humans, documenting the critical role of PAPP-A2 in releasing IGF-I (show IGF1 ELISA Kits) from its binding proteins.
Short-term treatment with progressive doses of rhIGF1 (recombinant human insulin-like growth factor-1 (show IGF1 ELISA Kits)) improved growth in two siblings with deficiency of PAPP-A2 (pregnancy-associated plasma protein-A2) [due to a homozygous loss-of-function frameshift mutation in exon 3 of the PAPP-A2 gene (p.D643fs25*)] that resulted in postnatal growth failure due to resulting decrease in IGF1 (show IGF1 ELISA Kits) bioavailability. [CASE REPORT]
in situ hybridization (ISH (show ANTXR2 ELISA Kits)) and immunohistochemistry (IHC) were employed to examine the spatial and temporal expression of PAPPA2 in the human fetomaternal interface.
PAPP-A2 is differentially expressed in different trophoblast populations and shows strong down regulation in the mid second trimester in chorionic villous samples.
The association between this PAPPA2 single nucleotide polymorphism and developmental dysplasia of the hip was evaluated.
The upregulation of PAPP-A2 observed in preeclampsia at term occurs early in pregnancy, before the symptoms develop.
PAPPA2 may be upregulated in severe pre-eclampsia and, functionally, this may be mediated via increased placental hypoxia known to occur with this pregnancy disorder.
The existence of this assay will enable an assessment of the biomarker potential of PAPP-A2 in pre-eclampsia as well as other clinical conditions.
Variants in the pregnancy-associated plasma protein-A2 gene on Bos taurus autosome 16 are associated with daughter calving ease and productive life in Holstein cattle.
Papp-a2 modulates Bmp and Notch (show NOTCH1 ELISA Kits) signaling by independent mechanisms in zebrafish embryos to control cranial cartilage development and angiogenesis.
Metalloproteinase which specifically cleaves IGFBP-5. Shows limited proteolysis toward IGFBP-3.
, pregnancy-associated plasma preproprotein-A2
, pregnancy-associated plasma protein-E
, pregnancy-associated plasma protein E1
, pappalysin 2