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Validated All-in-One™ qPCR Primer for EGLN3(NM_022073.4) Search again
Product ID:
HQP187013
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HIFP4H3, HIFPH3, PHD3
Gene Description:
egl-9 family hypoxia inducible factor 3
Target Gene Accession:
NM_022073.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Gene References into function
- siRNA targeted degradation of HIF-1alpha and HIF-2alpha results in decreased hypoxia-induced PHD3 expression
- PHD1, PHD2, and PHD3 have roles in the regulation of hypoxia-inducible factor
- results indicate that PHD3 is a TRiC substrate, providing another step at which PHD3 activity may be regulated
- EglN3 acts downstream of c-Jun and is specifically required among the three EglN family members for neuronal apoptosis.
- Mechanism underlying the regulation of PHD3 availability and activity in hypoxia by the E3 ligase Siah2.
- The role of Siah2 phosphorylation in the regulation of its activity toward PHD3 is reported.
- PHD-dependent oxygen-sensing recruits both the hypoxia-inducible factor (HIF) and ATF-4 systems.
- The data demonstrates the cellular oxygen sensor PHD3 as a regulator of protein aggregation in response to varying oxygen availability.
- Chronic hypoxia not only increases the pool of PHDs but also overactivates the three PHD isoforms.
- Overexpression of the oxygen sensor PHD-3 is associated with tumor aggressiveness in pancreatic endocrine tumors.
- Data show that PDK1 and HIF prolyl hydroxylase 3 mRNA expressions are lowest in children of chronic mountain sickness fathers at altitude.