Fn14, formally known as fibroblast growth factor-inducible 14, is a cell surface receptor that belongs to the tumor necrosis factor receptor superfamily. This receptor is intricately involved in regulating various cellular processes, including proliferation, survival, inflammation, and tissue repair, primarily through its interaction with the cytokine TWEAK (TNF-like weak inducer of apoptosis). Fn14's expression is relatively low under normal physiological conditions but is significantly upregulated in response to tissue damage, chronic inflammation, and in the tumor microenvironment. The unique feature of Fn14 is its ability to mediate diverse signaling pathways, leading to cell survival and growth, as well as apoptosis under certain conditions. This dual role underscores the receptor's importance in maintaining cellular homeostasis and its involvement in the pathogenesis of various diseases, including cancer, autoimmune disorders, and fibrotic diseases. The activation of Fn14 by TWEAK initiates a cascade of intracellular signaling events, notably through the NF-κB and MAPK pathways, which are pivotal in regulating immune responses, promoting cell proliferation, and inhibiting apoptosis, thereby facilitating tissue regeneration and repair.
The activation mechanism of Fn14 involves the binding of its ligand, TWEAK, to the extracellular domain of the receptor, triggering conformational changes that facilitate the recruitment and activation of downstream signaling molecules. This ligand-receptor interaction is critical for the initiation of signal transduction pathways that modulate cellular behavior in response to external stimuli. Following activation, Fn14 engages several intracellular pathways, including the canonical and non-canonical NF-κB pathways, as well as various MAPK pathways (e.g., ERK1/2, JNK, and p38 MAPK), leading to the transcription of genes involved in inflammation, cell survival, and proliferation. Additionally, the activation of Fn14 can promote the expression of anti-apoptotic proteins and cytokines, further influencing the immune response and cellular resilience to stress and damage. The understanding of Fn14 activation and its signaling cascades offers valuable insights into the molecular mechanisms governing tissue homeostasis, inflammation, and the response to cellular stress, highlighting its value as a target for modulating disease processes.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Betulinic Acid | 472-15-1 | sc-200132 sc-200132A | 25 mg 100 mg | $117.00 $344.00 | 3 | |
Betulinic acid is a triterpenoid compound that activates Fn14 by modulating the NF-κB signaling pathway. It acts as an indirect activator by inhibiting the phosphorylation of IκBα, preventing its degradation and subsequent release of NF-κB. The stabilized NF-κB translocates to the nucleus, enhancing Fn14 transcription. This compound demonstrates specificity for Fn14, as it does not affect other related pathways. | ||||||
Forskolin | 66575-29-9 | sc-3562 sc-3562A sc-3562B sc-3562C sc-3562D | 5 mg 50 mg 1 g 2 g 5 g | $78.00 $153.00 $740.00 $1413.00 $2091.00 | 73 | |
Forskolin stimulates Fn14 expression through adenylate cyclase activation, leading to increased intracellular cAMP levels. Elevated cAMP activates PKA, subsequently enhancing NF-κB activity and Fn14 transcription. The compound's role in modulating the cAMP/PKA/NF-κB axis makes it a potential indirect activator of Fn14. | ||||||
Resveratrol | 501-36-0 | sc-200808 sc-200808A sc-200808B | 100 mg 500 mg 5 g | $80.00 $220.00 $460.00 | 64 | |
Resveratrol activates Fn14 by inhibiting the SIRT1-dependent deacetylation of p65, a subunit of NF-κB. By promoting p65 acetylation, resveratrol enhances the transcriptional activity of NF-κB, leading to increased Fn14 expression. This chemical's impact on the SIRT1/NF-κB/Fn14 axis positions it as a potential indirect activator of Fn14, affecting its cellular abundance. | ||||||
Baicalein | 491-67-8 | sc-200494 sc-200494A sc-200494B sc-200494C | 10 mg 100 mg 500 mg 1 g | $32.00 $42.00 $162.00 $292.00 | 12 | |
Baicalein activates Fn14 by suppressing the activation of the PI3K/Akt pathway. By inhibiting Akt phosphorylation, baicalein prevents the downstream inhibition of NF-κB, allowing for increased Fn14 expression. This chemical's specific impact on the PI3K/Akt/NF-κB/Fn14 axis positions it as a potential indirect activator of Fn14, influencing its cellular abundance through modulation of key signaling components. | ||||||
Carnosol | 5957-80-2 | sc-204672 sc-204672A sc-204672B sc-204672C | 1 mg 5 mg 10 mg 50 mg | $87.00 $347.00 $602.00 $2647.00 | ||
Carnosol acts as an indirect activator of Fn14 by inhibiting the MAPK/ERK pathway. By blocking ERK phosphorylation, carnosol interferes with the downstream activation of Elk-1, which is involved in the inhibition of NF-κB. The resulting disinhibition of NF-κB enhances Fn14 transcription. Carnosol's specific impact on the MAPK/ERK/Elk-1/NF-κB/Fn14 axis establishes it as a potential modulator of Fn14 expression within the cellular context. | ||||||
Withaferin A | 5119-48-2 | sc-200381 sc-200381A sc-200381B sc-200381C | 1 mg 10 mg 100 mg 1 g | $130.00 $583.00 $4172.00 $20506.00 | 20 | |
Withaferin A activates Fn14 by inhibiting the STAT3 signaling pathway. Through direct binding to STAT3, withaferin A disrupts its transcriptional activity, leading to decreased inhibition of NF-κB and subsequent enhancement of Fn14 expression. This compound's specific impact on the STAT3/NF-κB/Fn14 axis positions it as a potential indirect activator of Fn14, influencing its cellular abundance through modulation of key signaling components. | ||||||
Celastrol, Celastrus scandens | 34157-83-0 | sc-202534 | 10 mg | $158.00 | 6 | |
Celastrol activates Fn14 by inhibiting the JAK2/STAT3 pathway. By suppressing JAK2 phosphorylation, celastrol prevents the downstream inhibition of NF-κB, allowing for increased Fn14 expression. This chemical's specific impact on the JAK2/STAT3/NF-κB/Fn14 axis positions it as a potential indirect activator of Fn14, influencing its cellular abundance through modulation of key signaling components. | ||||||
Curcumin | 458-37-7 | sc-200509 sc-200509A sc-200509B sc-200509C sc-200509D sc-200509F sc-200509E | 1 g 5 g 25 g 100 g 250 g 1 kg 2.5 kg | $37.00 $69.00 $109.00 $218.00 $239.00 $879.00 $1968.00 | 47 | |
Curcumin activates Fn14 by inhibiting the activation of the Wnt/β-catenin pathway. Through suppression of β-catenin stabilization, curcumin prevents the downstream inhibition of NF-κB, leading to increased Fn14 expression. This compound's specific impact on the Wnt/β-catenin/NF-κB/Fn14 axis establishes it as a potential indirect activator of Fn14, influencing its cellular abundance through modulation of key signaling components. | ||||||
Quercetin | 117-39-5 | sc-206089 sc-206089A sc-206089E sc-206089C sc-206089D sc-206089B | 100 mg 500 mg 100 g 250 g 1 kg 25 g | $11.00 $17.00 $110.00 $250.00 $936.00 $50.00 | 33 | |
Quercetin activates Fn14 by inhibiting the TGF-β/Smad pathway. Through interference with Smad phosphorylation, quercetin prevents the downstream inhibition of NF-κB, allowing for increased Fn14 expression. This chemical's specific impact on the TGF-β/Smad/NF-κB/Fn14 axis positions it as a potential indirect activator of Fn14, influencing its cellular abundance through modulation of key signaling components. | ||||||
Ursolic Acid | 77-52-1 | sc-200383 sc-200383A | 50 mg 250 mg | $56.00 $180.00 | 8 | |
Ursolic acid activates Fn14 by inhibiting the mTOR pathway. By suppressing mTOR phosphorylation, ursolic acid prevents the downstream inhibition of NF-κB, allowing for increased Fn14 expression. This compound's specific impact on the mTOR/NF-κB/Fn14 axis positions it as a potential indirect activator of Fn14, influencing its cellular abundance through modulation of key signaling components. | ||||||