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oxygen via Phd2 has a decisive influence on the formation of the vascular network during vertebrate embryogenesis.
comparative analysis of phd1 (Montrer EGLN2 Protéines), 2, and 3 expression in Xenopus laevis
PHD2 and PHD3 (Montrer EGLN3 Protéines) are essential for normal kidney development as the combined inactivation of stromal PHD2 and PHD3 (Montrer EGLN3 Protéines) resulted in renal failure that was associated with reduced kidney size, decreased numbers of glomeruli, and abnormal postnatal nephron formation.
aberrant hypoxic responses due to dysfunction of PHD2 caused both glomerular and tubular damages in HFD-induced obese mice. Phd2-inactivation provides a novel strategy against obesity-induced kidney injury
the expression of PHD2 in endothelial cells plays a critical role in renal fibrosis and vascular remodelling in adult mice.
Phd2 expressed in chondrocytes inhibits endochondral ossification at the epiphysis by suppressing HIF signaling pathways.
brain tissue protection and increased angiogenesis upon sub-acute ischemic stroke was completely absent in Phd2 knockout mice that were additionally deficient for both Hif1a (Montrer HIF1A Protéines) and Hif2a (Montrer EPAS1 Protéines)
expression of PHD2 in endothelial cells plays a critical role in preventing pulmonary arterial remodeling in mice
PHD-2 knockdown mesenchymal stromal cells overexpressed HIF-1alpha (Montrer HIF1A Protéines) and multiple angiogenic factors compared to control. Wounds treated with PHD-2 knockdown mesenchymal stromal cells healed at a significantly accelerated rate compared with wounds treated with shScramble mesenchymal stromal cells.
data identify the PHD2:HIF-2alpha:EPO axis as a so far unknown regulator of osteohematology by controlling bone homeostasis.
miR (Montrer MLXIP Protéines)-21 contributes to the protection of delayed ischemic preconditioning against renal ischemia reperfusion injury in mice, which is at least in part mediated by targeting of PHD2 and subsequently up-regulating HIF-1alpha (Montrer HIF1A Protéines)/VEGF (Montrer VEGFA Protéines) pathway.
Phd2 is the dominant HIF-hydroxylase in neutrophils under normoxic conditions; intrinsic regulation of glycolysis and glycogen (Montrer GYS1 Protéines) stores is linked to the resolution of neutrophil-mediated inflammatory responses
This study elucidates the molecular basis of the c-Myc (Montrer MYC Protéines)/EGLN1-mediated induction of LSH (Montrer HELLS Protéines) expression that inhibits ferroptosis
In vitro studies showed that a complement C1q-A chain peptide is not a substrate for PHD2 but is a substrate for CP4H1.
GPT2 (Montrer GPT2 Protéines) reduced alpha-ketoglutarate level in cells leading to the inhibition of proline hydroxylase 2 (PHD2) activity involved in the regulation of HIF1alpha (Montrer HIF1A Protéines) stability. Accumulation of HIF1alpha (Montrer HIF1A Protéines), resulting from GPT2 (Montrer GPT2 Protéines)-alpha-ketoglutarate-PHD2 axis, constitutively activates sonic hedgehog (Shh (Montrer SHH Protéines)) signaling pathway.
Studied the association between SNPs around the EGLN1 genomic region, possibly involved in high-altitude adaptation, and physiological changes to hypobaric hypoxia exposure in a cohort of Japanese lowlanders.
the expression of prolyl hydroxylase domain 2 (PHD2) is selectively increased in CKD-AT-MSCs and its inhibition can restore the expression of HIF-1alpha (Montrer HIF1A Protéines) and the wound healing function of CKD-AT-MSCs. These results indicate that more studies about the functions of MSCs from CKD patients are required before they can be applied in the clinical setting
Functionally active PHD2 SNP rs516651 , located in the key pathway for the hypoxic-inflammatory response, is associated with increased 30-day mortality in Acute Respiratory Distress Syndrome (ARDS) patients. In contrast, the PHD2 SNP rs480902 is not. Furthermore, the HIF-2alpha (Montrer EPAS1 Protéines) SNP [ch2 (Montrer Acyp1 Protéines): 46441523(hg18)] GG-genotype was neither present in our ARDS patients of Caucasian heritage nor in healthy Caucasian blood donors.
We genotyped 347 Tibetan individuals from varying altitudes for both the Tibetan-specific EGLN1 haplotype and 10 candidate SNPs in the EPAS1 haplotype and correlated their association with hemoglobin levels.
PHD2 is a direct binding partner of EGFR (Montrer EGFR Protéines) and show that PHD2 regulates EGFR (Montrer EGFR Protéines) stability as well as its subsequent signaling in breast carcinoma cells.
A mechanism of PHD2 regulation that involves the mTOR (Montrer FRAP1 Protéines) and PP2A (Montrer PPP2R4 Protéines) pathways.
These data unravel B55alpha (Montrer PPP2R2A Protéines) as a PHD2 substrate and highlight a role for PHD2-B55alpha (Montrer PPP2R2A Protéines) in the response to nutrient deprivation.
The protein encoded by this gene catalyzes the post-translational formation of 4-hydroxyproline in hypoxia-inducible factor (HIF) alpha proteins. HIF is a transcriptional complex that plays a central role in mammalian oxygen homeostasis. This protein functions as a cellular oxygen sensor, and under normal oxygen concentration, modification by prolyl hydroxylation is a key regulatory event that targets HIF subunits for proteasomal destruction via the von Hippel-Lindau ubiquitylation complex. Mutations in this gene are associated with erythrocytosis familial type 3 (ECYT3).
egl nine homolog 1 (C. elegans)
, egl nine homolog 1
, egl nine homolog 1-like
, egl nine homolog 2
, HIF-prolyl hydroxylase 2
, hypoxia-inducible factor prolyl hydroxylase 2
, prolyl hydroxylase domain-containing protein 2
, HIF prolyl hydroxylase 2
, egl nine-like protein 1
, zinc finger MYND domain-containing protein 6