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Validated All-in-One™ qPCR Primer for RTN3(NM_201428.3) Search again
Product ID:
HQP167970
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
ASYIP, HAP, NSPL2, NSPLII, RTN3-A1
Gene Description:
reticulon 3
Target Gene Accession:
NM_201428.3(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.
Summary
The reticulons are a group of highly conserved genes with preferential expression in neuroendocrine tissues (see, e.g., RTN1; MIM 600865).[supplied by OMIM].
Gene References into function
- The ASYIP protein co-localizes with ASY in the endoplasmic reticulum. Characterization of the ASYIP gene helps to clarify ASY-induced apoptosis or Nogo-involved inhibition of neuronal regeneration in the central nervous system.
- RTN3 isoforms may contribute, by as yet unknown mechanisms, to neuronal survival and plasticity
- apoptosis-inducing protein, HAP, induces bacterial cell death [HAP, homolog of ASY protein]
- These results suggest that RTN3 plays a role in membrane trafficking in the early secretory pathway.
- All the results indicate that both the mitochondria and the endoplasmic reticulum (ER) are involved in apoptosis caused by HAP overexpression, and suggest that HAP overexpression may initiate an ER overload response (EOR).
- Results describe the mapping of interaction domains mediating binding between BACE1 and RTN3/Nogo proteins.
- Endoplasmic reticulum, ER-bound RTN3 protein recruited endogenous FADD to the ER membrane and subsequently initiated caspase-8 cascade, including activation of caspase-8, processing of Bid and release of cytochrome c from mitochondria.
- These findings indicate that RTN3 is directly involved in the endoplasmic reticulum-constituents trafficking events through dually acting as an essential and important ER-stress sensor, and a trigger for the Bcl-2 translocation.
- In normal HeLa cells, ectopic overexpressed Bcl-2 reduced the cell apoptosis induced by overexpressed RTN3. results suggest that RTN3 could bind with Bcl-2 and mediate its accumulation in mitochondria, which modulate the anti-apoptotic activity of Bcl-2
- the membrane topology of RTN3 has an effect on binding of RTN3 to BACE1