TICAM1 Knockout A-549 Cell Line

TICAM1 Knockout A-549 Cell Line
15% OFF
Cat.No.:

EDC07592

Species:

Human

Cell Name:

A-549

Gene:

TICAM1

Gene ID:

148022

Size:

1×10⁶cells

TICAM1 Knockout Cell Line (A549) is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performance Cas9 Protein and Hassle-Free Cell Selection.
Cat.No. EDC07592
Product Name TICAM1 Knockout A549 Cell Line
Cell Line A-549
Cellosaurus ID CVCL_0023
Cell Line Synonyms A 549, A549, NCI-A549, A549/ATCC, A549 ATCC, A549ATCC, hA549
Gene TICAM1
NCBI Gene ID
Gene Synonyms IIAE6|MyD88-3|PRVTIRB|TICAM-1|TRIF
Summary
This gene encodes an adaptor protein containing a Toll/interleukin-1 receptor (TIR) homology domain, which is an intracellular signaling domain that mediates protein-protein interactions between the Toll-like receptors (TLRs) and signal-transduction components. This protein is involved in native immunity against invading pathogens. It specifically interacts with toll-like receptor 3, but not with other TLRs, and this association mediates dsRNA induction of interferon-beta through activation of nuclear factor kappa-B, during an antiviral immune response. Mutations in this gene are associated with encephalopathy, acute, infection-induced. [provided by RefSeq, Jul 2020]
Associated Diseases Non-Small Cell Lung Carcinoma
Morphology Adherent
Passage Ratio 1/5-1/4 ,2days
Complete Culture Medium F-12K + 10% FBS
Freezing Medium 95% Complete culture medium + 5% DMSO
QC Indels validated by Sanger sequencing; sterility confirmed via microbial testing.
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
LociSTR Info (Sample Cell)
Sample Cell Line: A-549
STR Info (Cell bank)
Cell Line: A-549
Allele1Allele2Allele1Allele2
Amelogenin X Y X Y
CSF1PO 10 12 10 12
D2S1338 24 24
D3S1358 16 16
D5S818 11 11
D7S820 8 11 8 11
D8S1179 13 14 13 14
D13S317 11 11
D16S539 11 12 11 12
D18S51 14 17 14 17
D19S433 13 13
D21S11 29 29
FGA 23 23
Penta D 9 9
Penta E 7 11 7 11
TH01 8 9.3 8 9.3
TPOX 8 11 8 11
vWA 14 14
D6S1043 11 13
D12S391 18 18
D2S441 10 13 10 13
* STR authentication data of this cell line matches with that of cell lines sourced from ATCC, DSMZ, JCRB, and RIKEN databases.
Conclusion: The STR identification of this cell is correct.

FAQ

The choice depends on whether you are studying TLR3/TLR4 MyD88-independent signaling or TICAM1's role in antiviral and inflammatory responses. The Knockout line is appropriate for asking whether TICAM1 (TRIF) is required for type I IFN induction downstream of TLR3 (dsRNA sensing) and TLR4 (LPS sensing — endosomal arm). Overexpression is useful for testing whether elevated TICAM1 is sufficient to drive IFN responses. For antiviral immunity research, the EDITGENE TICAM1 Knockout in A-549 is highly relevant — A-549 is widely used in respiratory virus infection studies, and TICAM1 mediates IFN induction following dsRNA detection during many viral infections. Rescue with wild-type or TIR-domain-deleted TICAM1 separates adaptor function from other signaling roles.
Primary applications: • TLR3 signaling: poly(I:C)-induced type I IFN and ISG expression analysis in the absence of TICAM1. • Antiviral response: viral infection studies in A-549 (influenza, respiratory syncytial virus, others) to assess TICAM1's contribution to host antiviral defense. • TLR4 endosomal arm: LPS-induced TRAM/TRIF-dependent IFN responses, distinguishable from MyD88-dependent inflammatory signaling. • Apoptosis pathway studies: TICAM1-mediated apoptosis through the RIP1-FADD-caspase-8 axis following TLR3 stimulation. EDITGENE recommends this model for researchers investigating TLR3/TLR4 signaling, antiviral immunity in respiratory epithelium, and TRIF-dependent innate immune responses.
Yes. TICAM1 rescue experiments require attention to TIR domain function and adaptor recruitment: • Construct design: use a codon-modified TICAM1 sequence with a C-terminal tag (FLAG, HA). TICAM1 contains an N-terminal TIR domain critical for TLR3/TLR4 receptor binding. • TIR domain mutant rescue: TIR-domain point mutations (e.g., P434H) disrupt receptor binding and serve as specificity controls for adaptor function. • Functional readout: rescue should restore poly(I:C)-induced IFN-β reporter activation and ISG expression in A-549. • Combined assay design: rescue should be tested under TLR3 (poly(I:C)) and TLR4 (LPS) stimulation conditions to confirm both signaling pathways are restored. A-549 transduces efficiently with lentivirus and supports stable rescue line generation in the respiratory virus research context.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.

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