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Validated All-in-One™ qPCR Primer for TICAM1(NM_182919.3) Search again
Product ID:
HQP003420
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
IIAE6, MyD88-3, PRVTIRB, TICAM-1, TRIF
Gene Description:
TIR domain containing adaptor molecule 1
Target Gene Accession:
NM_182919.3(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.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
TRIF, or TICAM1, is a Toll/IL1R (MIM 147810) (TIR) domain-containing adaptor molecule, like MYD88 (MIM 602170) and TIRAP (MIM 606252), that induces interferon-beta (IFNB; MIM 147640), specifically interacts with TLR3 (MIM 603029), and activates nuclear factor kappa-B (NFKB; see MIM 164011).[supplied by OMIM].
Gene References into function
- TRIF is identified and characterized as a novel adaptor protein containing the Toll/IL-1 receptor domain, with a specific role in TLR3 signaling.
- identified an alternative adaptor, designated Toll-interleukin 1 receptor domain (TIR)-containing adaptor molecule (TICAM)-1, that can physically bind the TIR domain of TLR3
- LPS-TLR4 signaling to IRF-3/7 and NF-kappaB involves the toll adapters TRAM and TRIF.
- the adapter complex of TICAM-2 and TICAM-1 plays a crucial role in lipopolysaccharide-TLR4-mediated activation of IFN-beta
- TRIF associates with TNF receptor-associated factor 6 (TRAF6) and TANK-binding kinase (TBK)-1 independently and activates two distinct transcription factors, NF-kappa B and IFN regulatory factor-3, respectively.
- the TRIF-induced IFN-stimulated response element and NF-kappaB activation and apoptosis pathways are uncoupled
- TRIF has a distal region with the ability to negatively regulate basal transcription & a proximal region containing an Sp1 site that confers approx. 75% of basal transcriptional activity. TRIF appears to be regulated primarily by NF-kappaB.
- double-stranded RNA-induced TLR3/TRIF-mediated NF-kappaB and IRF3 activation diverge at TRIF
- TRIF-induced ISRE and NF-kappaB activation are inhibited by PIASy
- studies of the molecular properties of TRIF which contribute to its ability to function as a substrate for the NS3/4A protease; a polyproline II interaction with the 3(10) helix likely facilitates NS3/4A recognition of TRIF
- TRIF-induced cell death required caspase activity initiated by the Fas/Apo-1-associated DD protein-caspase-8 axis
- SARM associated with TRIF, and 'knockdown' of endogenous SARM expression by interfering RNA led to enhanced TRIF-dependent cytokine and chemokine induction.
- the spatiotemporal mobilization of TICAM-1 in response to dsRNA and the formation of the TICAM-1 speckles containing RIP1 and NAP1 are important for the activation of the TLR3-TICAM-1 pathway.
- activation and formation of TICAM-1 signalosomes with NF-kappaB and interferon regulatory factor-3 requires oligomerization induced at two different sites and RIP1 binding
- PTP1B is a physiological negative regulator of TLR signaling via suppression of both MyD88- and TRIF-dependent production of proinflammatory cytokine and IFN-beta in macrophages.
- Inactivation of Trif and Cardif can also occur through cellular caspases activated by various pro-apoptotic signals.
- PKR, in addition to IPS-1 and IRF3 but not TRIF, was required for maximal type I IFN-beta induction and the induction of apoptosis by both transfected PRNAs and polyinosinic-polycytidylic acid.