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TRADD Human shRNA Plasmid Kit (Locus ID 8717)

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SKU
TR320590
TRADD - Human, 4 unique 29mer shRNA constructs in retroviral untagged vector, 5µg of each construct provided
  $883.00
2 Weeks*

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Specifications
Specifications
Product Data
Locus ID 8717
Synonyms Hs.89862
Vector pRS
E. coli Selection Ampicillin
Mammalian Cell Selection Puromycin
Format Retroviral plasmids
Components TRADD - Human, 4 unique 29mer shRNA constructs in retroviral untagged vector(Gene ID = 8717). 5µg purified plasmid DNA per construct
29-mer scrambled shRNA cassette in pRS Vector, TR30012, included for free.
RefSeq NM_003789, NM_153425, NM_001323552, NM_003789.1, NM_003789.2, NM_003789.3, BC004491, BC004491.2, NM_003789.4
UniProt ID Q15628
Summary The protein encoded by this gene is a death domain containing adaptor molecule that interacts with TNFRSF1A/TNFR1 and mediates programmed cell death signaling and NF-kappaB activation. This protein binds adaptor protein TRAF2, reduces the recruitment of inhibitor-of-apoptosis proteins (IAPs) by TRAF2, and thus suppresses TRAF2 mediated apoptosis. This protein can also interact with receptor TNFRSF6/FAS and adaptor protein FADD/MORT1, and is involved in the Fas-induced cell death pathway. provided by RefSeq, Jul 2008
shRNA Design These shRNA constructs were designed against multiple splice variants at this gene locus. To be certain that your variant of interest is targeted, please contact techsupport@origene.com. If you need a special design or shRNA sequence, please utilize our custom shRNA service.
Storage Store at -20°C
Shipping Ambient
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Documents
Resources

file-alt Citations

Esophageal cancer cells convert the death signal from TRAIL into a stimulus for survival during acid/bile exposure
Chang, Dang, Che et al
Dig Liver Dis (2020) 52 (10), 1195-1200 DOI: 10.1016/j.dld.2020.04.013
Cited by 12
AI Summary: In this study, OriGene products—including TRADD (Cat# RC213682) and c-FLIP (Cat# RC211744) expression plasmids—were used to investigate how esophageal cancer cells resist TRAIL-induced cell death by overexpressing these proteins and altering apoptotic signaling pathways.
Showing 1-1 of 1 papers.
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