抗Mouse (Murine) 抗体:
抗Rat (Rattus) 抗体:
Cow (Bovine) Polyclonal EGLN2 Primary Antibody for WB - ABIN2775992
Gilbert, Banek, Bauer, Gingery, Needham: Exercise training attenuates placental ischemia-induced hypertension and angiogenic imbalance in the rat. in Hypertension 2012
Human Polyclonal EGLN2 Primary Antibody for EIA, WB - ABIN453633
Semenza: HIF-1, O(2), and the 3 PHDs: how animal cells signal hypoxia to the nucleus. in Cell 2001
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Dog (Canine) Polyclonal EGLN2 Primary Antibody for WB - ABIN2778438
Pan, Mansfield, Bertozzi, Rudenko, Chan, Giaccia, Simon: Multiple factors affecting cellular redox status and energy metabolism modulate hypoxia-inducible factor prolyl hydroxylase activity in vivo and in vitro. in Molecular and cellular biology 2007
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comparative analysis of phd1, 2, and 3 expression in Xenopus laevis
Hypoxia-inducible factor prolyl-4-hydroxylase-1 is a convergent point in the reciprocal negative regulation of NF-kappaB and p53 signaling pathways
HS-induced PPARalpha-mediated downregulation of PHD1 is a novel pathway for PHD/HIF-1alpha transcriptional regulation.
EglN2 might act as an FBW7 ubiquitin ligase substrate contributing to the progression of triple negative breast cancer.
Selective reduction of PHD1 protein using CRISPR/Cas9 technology reduced both lipid peroxidation and mitochondrial impairment, and attenuated glutamate toxicity in the cultured neurons.
Phd1 deficiency in dendritic cells significantly reduced interleukin-1beta production in response to lipopolysaccharide. Taken together, our results further support the development of selective PHD1 inhibitors for ulcerative colitis, and identify haematopoietic cells as their primary target.
This study provides new information relating to the possible mechanism of therapeutic action of hydroxylase inhibitors that has been reported in pre-clinical models of intestinal and hepatic disease.
PHD1 deficiency promotes hepatic steatosis and liver-specific insulin resistance but does not worsen the deleterious effects of HFD on metabolic homeostasis.
deleting Phd1-3 genes in osteoblasts increased osteoclast formation in vitro and in bone.
These data identify PHD1 as a regulator of neuronal metabolism and a potential therapeutic target in ischemic stroke.
PHD1 and PHD3 deletions promote angiogenesis in ischemia-injured tissue by increasing HIF1-alpha stability.
Rosiglitazone increases PHD expression in a PPARgamma-dependent manner and that this leads to the commitment of anti-adipogenic proteins to the ubiquitination-proteasomal pathway and to the subsequent induction of adipocyte differentiation.
PHD-1 deficient mouse appears to be the first animal model showing neuroepithelial bodies cell hyperplasia
Alterations in the function of all 3 isoforms of prolyl-4-hydroxylase enzymes (PHD1-3) in the first 24 h following transient focal cerebral ischaemia are reported.
Data show it is feasible to reactivate hepatic erythropoietin production using systemically delivered siRNAs targeting the EglN1, EglN2 and EglN3 prolyl hydroxylase mRNA specifically in the liver.
silencing of PHD-1 attenuates myocardial ischemia/reperfusion injury probably by enhancing HIF-1alpha/beta-catenin/endothelial nitric oxide synthase/nuclear factor-kappaB and Bcl-2 signaling pathway
role for PHD1 as a positive regulator of intestinal epithelial cell apoptosis in the inflamed colon
Prolyl hydroxylase enzyme (PHD) is the key enzyme responsible for degrading HIF-1. HIF activation is an approach to increase vascularity and bone formation following skeletal trauma.
Loss of PHD1 provided tolerance of hepatocytes to acute hypoxia and protected them against ischemia/reperfusion damage.
Egln1/2/3 play dual roles in chondrocyte growth, acting as oxygen sensors and mediators of late stage events in the cell cycle.
PHD1/3 double deficiency leads to erythrocytosis partly by activating the hepatic HIF-2alpha/erythropoietin pathway, whereas PHD2 deficiency leads to erythrocytosis by activating the renal Epo pathway
High PHD1 expression is associated with liver fibrosis.
4-bp Insertion/deletion Polymorphism within the Promoter of EGLN2 is associated with breast cancer.
Our study provided initial evidence that the insertion/deletion polymorphism rs10680577 may play a functional role in the development of CRC in the Chinese population
In advanced-stage Hodgkin's Lymphoma patients strong cytoplasmic PHD1 expression in Reed-Sternberg cells was associated with poor relapse-free survival among patients treated with involved-field radiotherapy and advanced-stage patients treated with doxorubicin, bleomycin, vinblastine and darcabazine and involved-field radiotherapy.
Tuning the Transcriptional Response to Hypoxia by Inhibiting Hypoxia-inducible Factor (HIF) Prolyl and Asparaginyl Hydroxylases.
PHD1 is phosphorylated by CDK2, CDK4 and CDK6 at Serine 130.
siRNA-mediated knockdown of PHD1 inhibited glucose-stimulated insulin secretion in pancreatic Beta cells.
EglN2 associates with the NRF1-PGC1alpha complex and controls mitochondrial function in breast cancer
rs3733829 in the EGLN2 gene is significantly associated with the risk of COPD in Chinese populations of Hainan province.
Germ-line PHD1 and PHD2 mutations detected in patients with pheochromocytoma/paraganglioma-polycythemia
study conducted to investigate the association between gastric cancer (GC) susceptibility with a 4-bp insertion/deletion polymorphism (rs10680577) in the proximal promoter of EGLN2; findings showed that the heterozygote and the homozygote 4-bp del/del confer a significantly increased risk of GC
Data indicate that the prolyl hydrolase 1 (PHD1) rs10680577 polymorphism is associated with the risk of non-small cell lung cancer in a Chinese population.
PHD-1 played an important role in hypoxic response pathway of trophoblast through modulating the level of HIF-2alpha.
PHD1 could induce cell cycle arrest in lung cancer cells, resulting in the suppression of cell proliferation.
Results show that variants in two adjacent genes, EGLN2 and CYP2A6, influence smoking behavior related to disease risk.
The diminished expression of PHD1 and PHD2 and elevated level of FIH protein in cancerous tissue compared to histopathologically unchanged colonic mucosa was not associated with DNA methylation within the CpG islands of the PHD1, PHD2 and FIH genes.
By modulating Cep192 levels, PHD1 thereby affects the processes of centriole duplication and centrosome maturation and contributes to the regulation of cell-cycle progression.
Onconeuronal antigen Cdr2 correlates with HIF prolyl-4-hydroxylase PHD1 and worse prognosis in renal cell carcinoma.
The hypoxia inducible factor (HIF) is a transcriptional complex that is involved in oxygen homeostasis. At normal oxygen levels, the alpha subunit of HIF is targeted for degration by prolyl hydroxylation. This gene encodes an enzyme responsible for this post-translational modification. Alternative splicing results in multiple transcript variants. Read-through transcription also exists between this gene and the upstream RAB4B (RAB4B, member RAS oncogene family) gene.
EGL nine homolog 2
, egl nine homolog 2
, Egl nine homolog 2
, EGL nine (C.elegans) homolog 2
, egl nine homolog 2 (C. elegans)
, egl nine homolog 2-like
, HIF-prolyl hydroxylase 1
, hypoxia-inducible factor prolyl hydroxylase 1
, immediate early response 4
, prolyl hydroxylase domain-containing protein 1
, HIF-1alpha prolyl-4-hydroxylase-1
, estrogen-induced tag 6