Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
| Cat.No. | Product Name | Price |
|---|---|---|
| CSC-DC005199 | Panoply™ Human FAF1 Knockdown Stable Cell Line | Inquiry |
| CSC-SC005199 | Panoply™ Human FAF1 Over-expressing Stable Cell Line | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| AD05718Z | Human FAF1 adenoviral particles | Inquiry |
| LV12115L | human FAF1 (NM_007051) lentivirus particles | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| SHH044561 | shRNA set against Rat Faf1(NM_130406.1) | Inquiry |
| SHH044615 | shRNA set against Human FAF1(NM_007051.2) | Inquiry |
| SHH044579 | shRNA set against Mouse Faf1(NM_007983.2) | Inquiry |
| SHH288757 | shRNA set against Human FAF1 (NM_007051.2) | Inquiry |
| SHH288761 | shRNA set against Mouse FAF1 (NM_007983.2) | Inquiry |
| SHH288765 | shRNA set against Rat FAF1 (NM_130406.1) | Inquiry |
| SHW018107 | shRNA set against Danio rerio FAF1 (NM_212973) | Inquiry |
| Cat.No. | Product Name | Price |
|---|---|---|
| CDFG022312 | Mouse Faf1 cDNA Clone(BC065098) | Inquiry |
| CDFH006280 | Human FAF1 cDNA Clone(NM_007051.2) | Inquiry |
| CDFR013881 | Rat Faf1 cDNA Clone(NM_130406.1) | Inquiry |
| MiUTR1H-03378 | FAF1 miRNA 3'UTR clone | Inquiry |
| MiUTR1M-04564 | FAF1 miRNA 3'UTR clone | Inquiry |
| MiUTR1R-01816 | FAF1 miRNA 3'UTR clone | Inquiry |
| CDCB179582 | Danio rerio FAF1 ORF Clone (NM_212973) | Inquiry |
| CDCB186717 | Rabbit FAF1 ORF clone (XM_008265271.1) | Inquiry |
| CDCR062234 | Human FAF1 ORF clone (NM_007051.2) | Inquiry |
| CDCR062236 | Mouse Faf1 ORF clone (NM_007983.2) | Inquiry |
| CDCR380915 | Rat Faf1 ORF Clone(NM_130406.1) | Inquiry |
FAS-associated factor 1 (FAF1) is an evolutionarily conserved protein with many protein interaction domains. Even FAF1 was initially confirmed as one member of FAS death-inducing signaling complex, following work about it further demonstrated its functions in diverse biological processes. Convincing evidence supports that FAF1 involves in the regulation of apoptosis and NFκB activity as well as ubiquitination and proteasomal degradation, as a tumor suppressor, and highlights that FAF1's contribution to NFκB signaling transmission has critical connotations for human cancer treatment. Programmed cell death or apoptosis in a number of tissues is mediated by interactions among FAS and its corresponding ligands, which allow the occurrence of death-inducing signaling complex (DISC). FAF1 was recently characterized as effective regulator of cell survival, so how it works in the process of cancer or Parkinson's disease remains to be with more deeply elucidations. Disappearance or abnormity of FAF1 genes in human cancers suggests that it may be a tumor suppressor for its pro-apoptotic efficacy. There is still a long way to the full revelation of linkages between the FAF1 status and NFκB pathway in tumor, and answer the question of whether loss of FAF1 influences other signaling pathways in cancer due to its diversative protein interacting domains.
An adaptor of innate immune receptor retinoic acid inducible gene1 (RIG-I), Mitochondrial antiviral signaling protein (MAVS), can connect the viral RNA recognition with antiviral signaling by accumulation of E3 ligase TRIM31 initiated lysine 63-linked poly-ubiquitination activating downstream signaling effectors. Aggregation of scaffold protein FAF1 gives a negative regulation to MAVS. Poly-ubiquitination and aggregation of MAVS were antagonized by FAF1 through its competition for the MAVS association with TRIM31. FAF1 knockout mice and FAF1 deficient myeloid cells are both shown with reduced viral load in vivo. Interaction with RIG-1 and lysine 63 poly-ubiquitination are vital for MAVS aggregation at the mitochondria, which acts as a critical step forward the initiation of antiviral responses. A recent date demonstrates repression of RNA virus induced MAVS-Lys63 poly-ubiquitination and aggregation and upcoming IFN-b birth and innate antiviral immunity by FAF1 is mitochondria relevant, moreover, mitochondria associated FAF1 come into aggregates together in cells associated with MAVS and without virus infection, while it is dismissed by IKKε-mediated-phosphorylation triggered acetylation and lysosomal degradation upon virus infection.
Fig 1. Signaling pathways intersections answer FAF1 role in Chondrogenesis (Miikka et al. 2011)
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