Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher tous les synonymes
Sélectionnez vos espèces d'intérêt
oxygen via Phd2 has a decisive influence on the formation of the vascular network during vertebrate embryogenesis.
comparative analysis of phd1, 2, and 3 expression in Xenopus laevis
Deletion of Phd2 in combination with expression of BRaf(V600E) in melanocytes (Tyr::CreER;Phd2(lox/lox);BRaf(CA)) leads to the development of melanoma with 100% penetrance and frequent lymph node metastasis.
Oxygen sensing by PHD2 in osteocytes negatively regulates bone mass through epigenetic regulation of sclerostin and targeting PHD2 elicits an osteo-anabolic response in osteoporotic mouse models.
Data show that deletion of prolyl hydroxylase 2 (PHD2) in intestinal epithelial cells (IECs) did not lead to spontaneous enteritis or colitis in mice.
PHD2 and PHD3 are essential for normal kidney development as the combined inactivation of stromal PHD2 and PHD3 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 and Hif2a
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 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-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/VEGF pathway.
Phd2 is the dominant HIF-hydroxylase in neutrophils under normoxic conditions; intrinsic regulation of glycolysis and glycogen stores is linked to the resolution of neutrophil-mediated inflammatory responses
Epo transcription in brain pericytes was HIF-2 dependent and cocontrolled by PHD2 and PHD3, oxygen- and 2-oxoglutarate-dependent prolyl-4-hydroxylases that regulate HIF activity.
Notch ligand genes Jag1, Jag2, and Dll1 and target Hes1 became downregulated upon aging HIF-2alpha dependently.
Results identified a critical role of PHD2 for a reversible glycolytic reprogramming in macrophages with a direct impact on their function.
Results found that loss of endothelial PHD2 induced pulmonary arterial hypertension and vascular remodeling in a HIF-2-dependent fashion.
This study demonstrated that the Neuronal prolyl-4-hydroxylase 2 deficiency improves cognitive abilities in a murine model of cerebral hypoperfusion.
We conclude that the activation of the HIF pathway induced by PHD2 deficiency enhances the effect of running training
deleting Phd1-3 genes in osteoblasts increased osteoclast formation in vitro and in bone.
During the transition of nevi to melanoma, the expression of PHD2 protein is significantly decreased, and lower expression of PHD2 in melanoma is associated with worse clinical outcome. Knockdown of PHD2 leads to elevated Akt phosphorylation in melanocytes.
This study elucidates the molecular basis of the c-Myc/EGLN1-mediated induction of LSH 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 reduced alpha-ketoglutarate level in cells leading to the inhibition of proline hydroxylase 2 (PHD2) activity involved in the regulation of HIF1alpha stability. Accumulation of HIF1alpha, resulting from GPT2-alpha-ketoglutarate-PHD2 axis, constitutively activates sonic hedgehog (Shh) 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 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 SNP [ch2: 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 and show that PHD2 regulates EGFR stability as well as its subsequent signaling in breast carcinoma cells.
A mechanism of PHD2 regulation that involves the mTOR and PP2A pathways.
These data unravel B55alpha as a PHD2 substrate and highlight a role for PHD2-B55alpha in the response to nutrient deprivation.
prolyl hydroxylase 2 plays an important tumor suppressive role in liver cancer
Genetic variants in HIF-1alpha and PHD2 genes exist in Caucasians but do not appear to alter 30-day mortality in sepsis
Tuning the Transcriptional Response to Hypoxia by Inhibiting Hypoxia-inducible Factor (HIF) Prolyl and Asparaginyl Hydroxylases.
The role of PHD-2 in breast cancer [review]
Sulfur mustard negatively affects hypoxia-stimulated HIF-1alpha signaling in keratinocytes and fibroblasts and thus possibly contributes to delayed wound healing in SM-injured patients, which could be treated with PHD-2 inhibitors.
The HIFalpha subunit is usually prolyl-hydroxylated by EglN family members under normoxic conditions, causing its rapid degradation. Study confirmed that triple-negative breast cancer cells secrete glutamate, which is both necessary and sufficient for the paracrine induction of HIF1alpha in such cells under normoxic conditions.
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